Perspectives

I was surprised when the name came up on my hospital census as a new consult.

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Many years ago he’d been one of my attendings in residency. Someone I’d trained under. He’d been patient, almost grandfatherly, in the way he taught residents on his service. Never angry or impatient. I’d genuinely liked him as a person and respected him as a teacher.

And here he was now, a new consult on my daily hospital patient list.

A quick look at his chart brought the irony that I’m the same age now that he was when I worked under him. Time flies.

He didn’t remember me, nor did I expect him to. In my training from 1993 to 1997, I’d only dealt with him directly for a few months here and there. He’d seen a lot of residents come and go over his career.

He was, like me, older now. I wouldn’t have recognized him if I didn’t know the name in advance. He was frail now, seemingly smaller than I remembered, his mind and health damaged by his own neurologic issues.

Like all of us, I’ve taken care of other physicians, but this was the first time I’d encountered one of my former teachers in that role, and felt bad that he was in a situation I really couldn’t do much about.

I wrote some orders and moved on to the next consult, but haven’t stopped thinking about him.

Time comes for all of us sooner or later, though it’s never easy to reflect on. I’d certainly do what I could to help him, but was well aware (as I’m sure he was) that there was only so much I could.

When I came back the next day he’d left. At his own insistence, he wanted us to stop what we were doing and opted to be kept comfortable. It was certainly not an easy choice to make for any of us, but in character with the person and physician I still liked and respected.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I was surprised when the name came up on my hospital census as a new consult.

andresr/Getty Images

Many years ago he’d been one of my attendings in residency. Someone I’d trained under. He’d been patient, almost grandfatherly, in the way he taught residents on his service. Never angry or impatient. I’d genuinely liked him as a person and respected him as a teacher.

And here he was now, a new consult on my daily hospital patient list.

A quick look at his chart brought the irony that I’m the same age now that he was when I worked under him. Time flies.

He didn’t remember me, nor did I expect him to. In my training from 1993 to 1997, I’d only dealt with him directly for a few months here and there. He’d seen a lot of residents come and go over his career.

He was, like me, older now. I wouldn’t have recognized him if I didn’t know the name in advance. He was frail now, seemingly smaller than I remembered, his mind and health damaged by his own neurologic issues.

Like all of us, I’ve taken care of other physicians, but this was the first time I’d encountered one of my former teachers in that role, and felt bad that he was in a situation I really couldn’t do much about.

I wrote some orders and moved on to the next consult, but haven’t stopped thinking about him.

Time comes for all of us sooner or later, though it’s never easy to reflect on. I’d certainly do what I could to help him, but was well aware (as I’m sure he was) that there was only so much I could.

When I came back the next day he’d left. At his own insistence, he wanted us to stop what we were doing and opted to be kept comfortable. It was certainly not an easy choice to make for any of us, but in character with the person and physician I still liked and respected.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I was surprised when the name came up on my hospital census as a new consult.

andresr/Getty Images

Many years ago he’d been one of my attendings in residency. Someone I’d trained under. He’d been patient, almost grandfatherly, in the way he taught residents on his service. Never angry or impatient. I’d genuinely liked him as a person and respected him as a teacher.

And here he was now, a new consult on my daily hospital patient list.

A quick look at his chart brought the irony that I’m the same age now that he was when I worked under him. Time flies.

He didn’t remember me, nor did I expect him to. In my training from 1993 to 1997, I’d only dealt with him directly for a few months here and there. He’d seen a lot of residents come and go over his career.

He was, like me, older now. I wouldn’t have recognized him if I didn’t know the name in advance. He was frail now, seemingly smaller than I remembered, his mind and health damaged by his own neurologic issues.

Like all of us, I’ve taken care of other physicians, but this was the first time I’d encountered one of my former teachers in that role, and felt bad that he was in a situation I really couldn’t do much about.

I wrote some orders and moved on to the next consult, but haven’t stopped thinking about him.

Time comes for all of us sooner or later, though it’s never easy to reflect on. I’d certainly do what I could to help him, but was well aware (as I’m sure he was) that there was only so much I could.

When I came back the next day he’d left. At his own insistence, he wanted us to stop what we were doing and opted to be kept comfortable. It was certainly not an easy choice to make for any of us, but in character with the person and physician I still liked and respected.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I agree wholeheartedly with Dr. William G. Wilkoff’s doubts that an increase in medical schools/students and/or foreign medical graduates is the answer to the physician shortage felt by many areas of the country (Letters From Maine, “Help Wanted,” Nov. 2019, page 19). All you have to do is look at the glut of physicians – and just about any other profession – in metropolitan areas versus rural America, and ask basic questions regarding why those doctors practice where they do. You will quickly discover that most are willing to trade the possibility of a higher salary in areas where their presence is more needed to achieve more school choices, jobs for a spouse, and likely a more favorable call schedule. Something more attractive than salary or the prospect of more “elbow room” is desired.

Here in Mississippi we may have found an answer to the problem. A few years ago our state legislature started the Mississippi Rural Health Scholarship Program that pays for recipients to attend a state-run medical school on scholarship in exchange for agreeing to practice at least 4 years in a rural area of the state (less than 20k population) following their primary care residency (family medicine, pediatrics, ob.gyn., med-peds, internal medicine, and, recently added, psychiatry). Although a recent increase in the number of pediatric residency slots at our state’s sole program will no doubt also have a positive effect to this end, such a scholarship program as the one implemented by Mississippi is the best way to compete with the various intangibles that lead people to choose bigger cities over rural areas of the state to practice their trade. Once there, many – like myself – will find that such a practice is not only a good business decision but often is a wonderful place to raise a family. Meanwhile, our own practice just added a fourth physician as a result of said Rural Health Scholarship Program, and we could not be more satisfied with the result.
 

I agree wholeheartedly with Dr. William G. Wilkoff’s doubts that an increase in medical schools/students and/or foreign medical graduates is the answer to the physician shortage felt by many areas of the country (Letters From Maine, “Help Wanted,” Nov. 2019, page 19). All you have to do is look at the glut of physicians – and just about any other profession – in metropolitan areas versus rural America, and ask basic questions regarding why those doctors practice where they do. You will quickly discover that most are willing to trade the possibility of a higher salary in areas where their presence is more needed to achieve more school choices, jobs for a spouse, and likely a more favorable call schedule. Something more attractive than salary or the prospect of more “elbow room” is desired.

Here in Mississippi we may have found an answer to the problem. A few years ago our state legislature started the Mississippi Rural Health Scholarship Program that pays for recipients to attend a state-run medical school on scholarship in exchange for agreeing to practice at least 4 years in a rural area of the state (less than 20k population) following their primary care residency (family medicine, pediatrics, ob.gyn., med-peds, internal medicine, and, recently added, psychiatry). Although a recent increase in the number of pediatric residency slots at our state’s sole program will no doubt also have a positive effect to this end, such a scholarship program as the one implemented by Mississippi is the best way to compete with the various intangibles that lead people to choose bigger cities over rural areas of the state to practice their trade. Once there, many – like myself – will find that such a practice is not only a good business decision but often is a wonderful place to raise a family. Meanwhile, our own practice just added a fourth physician as a result of said Rural Health Scholarship Program, and we could not be more satisfied with the result.
 

I agree wholeheartedly with Dr. William G. Wilkoff’s doubts that an increase in medical schools/students and/or foreign medical graduates is the answer to the physician shortage felt by many areas of the country (Letters From Maine, “Help Wanted,” Nov. 2019, page 19). All you have to do is look at the glut of physicians – and just about any other profession – in metropolitan areas versus rural America, and ask basic questions regarding why those doctors practice where they do. You will quickly discover that most are willing to trade the possibility of a higher salary in areas where their presence is more needed to achieve more school choices, jobs for a spouse, and likely a more favorable call schedule. Something more attractive than salary or the prospect of more “elbow room” is desired.

Here in Mississippi we may have found an answer to the problem. A few years ago our state legislature started the Mississippi Rural Health Scholarship Program that pays for recipients to attend a state-run medical school on scholarship in exchange for agreeing to practice at least 4 years in a rural area of the state (less than 20k population) following their primary care residency (family medicine, pediatrics, ob.gyn., med-peds, internal medicine, and, recently added, psychiatry). Although a recent increase in the number of pediatric residency slots at our state’s sole program will no doubt also have a positive effect to this end, such a scholarship program as the one implemented by Mississippi is the best way to compete with the various intangibles that lead people to choose bigger cities over rural areas of the state to practice their trade. Once there, many – like myself – will find that such a practice is not only a good business decision but often is a wonderful place to raise a family. Meanwhile, our own practice just added a fourth physician as a result of said Rural Health Scholarship Program, and we could not be more satisfied with the result.
 

The time has come for good men and women to unite and rise up against a common foe. For too long nurses and doctors have labored under the tyranny of a dictator who claimed to help them provide high-quality care for their patients while at the same time cutting their paperwork to nil. But like most autocrats he failed to engage his subjects in a meaningful dialogue as each new version of his promised improvements rolled off the drawing board. When the caregivers were slow to adopt these new nonsystems he offered them financial incentives and issued threats to their survival. Although they were warned that there might be uncomfortable adjustment periods, the caregivers were promised that the steep learning curves would level out and their professional lives would again be valued and productive.

Of course, the dictator is not a single person but a motley and disorganized conglomerate of user- and patient-unfriendly electronic health record nonsystems. Ask almost any nurse or physician for her feelings about computer-based medical record systems, and you will hear tales of long hours, disengagement, and frustration. Caregivers are unhappy at all levels, and patients have grown tired of their nurses and physicians spending most of their time looking at computer screens.

You certainly have heard this all before. But you are hearing it in hospital hallways and grocery store checkout lines as a low rumble of discontent emerging from separate individuals, not as a well-articulated and widely distributed voice of physicians as a group. To some extent this relative silence is because there is no such group, at least not in same mold as a labor union. The term “labor union” may make you uncomfortable. But given the current climate in medicine, unionizing may be the best and only way to effect change.

But organizing to effect change in the workplace isn’t part of the physician genome. In the 1960s, a group of house officers in Boston engaged in a heal-in to successfully improve their salaries and working conditions. But over the ensuing half century physicians have remained tragically silent in the face of a changing workplace landscape in which they have gone from being independent owner operators in control of their destinies to becoming employees feeling powerless to improve their working conditions. This perceived impotence has escalated in the face of the challenge posed by the introduction of dysfunctional EHRs.

Ironically, a solution is at almost every physician’s elbow. In a recent New York Times opinion piece Theresa Brown and Stephen Bergman acknowledge that physicians don’t seem prepared to mount a meaningful response to the challenge to the failed promise of EHRs (“Doctors, Nurses and the Paperwork Crisis That Could Unite Them,” Dec. 31, 2019). They point out that, over the last half century, physicians have remained isolated on the sidelines, finding just enough voice to grumble. Nurses have in a variety of situations organized to effect change in their working conditions – in some cases by forming labor unions.

The authors of this op-ed piece, a physician and a nurse, make a strong argument that the time has come for nurses and doctors shake off the shackles of their stereotypic roles and join in creating a loud, forceful, and effective voice to demand a working environment in which the computer functions as an asset and no longer as the terrible burden it has become. Neither group has the power to do it alone, but together they may be able to turn the tide. For physicians it will probably mean venturing several steps outside of their comfort zone. But working shoulder to shoulder with nurses may provide the courage to speak out.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

The time has come for good men and women to unite and rise up against a common foe. For too long nurses and doctors have labored under the tyranny of a dictator who claimed to help them provide high-quality care for their patients while at the same time cutting their paperwork to nil. But like most autocrats he failed to engage his subjects in a meaningful dialogue as each new version of his promised improvements rolled off the drawing board. When the caregivers were slow to adopt these new nonsystems he offered them financial incentives and issued threats to their survival. Although they were warned that there might be uncomfortable adjustment periods, the caregivers were promised that the steep learning curves would level out and their professional lives would again be valued and productive.

Of course, the dictator is not a single person but a motley and disorganized conglomerate of user- and patient-unfriendly electronic health record nonsystems. Ask almost any nurse or physician for her feelings about computer-based medical record systems, and you will hear tales of long hours, disengagement, and frustration. Caregivers are unhappy at all levels, and patients have grown tired of their nurses and physicians spending most of their time looking at computer screens.

You certainly have heard this all before. But you are hearing it in hospital hallways and grocery store checkout lines as a low rumble of discontent emerging from separate individuals, not as a well-articulated and widely distributed voice of physicians as a group. To some extent this relative silence is because there is no such group, at least not in same mold as a labor union. The term “labor union” may make you uncomfortable. But given the current climate in medicine, unionizing may be the best and only way to effect change.

But organizing to effect change in the workplace isn’t part of the physician genome. In the 1960s, a group of house officers in Boston engaged in a heal-in to successfully improve their salaries and working conditions. But over the ensuing half century physicians have remained tragically silent in the face of a changing workplace landscape in which they have gone from being independent owner operators in control of their destinies to becoming employees feeling powerless to improve their working conditions. This perceived impotence has escalated in the face of the challenge posed by the introduction of dysfunctional EHRs.

Ironically, a solution is at almost every physician’s elbow. In a recent New York Times opinion piece Theresa Brown and Stephen Bergman acknowledge that physicians don’t seem prepared to mount a meaningful response to the challenge to the failed promise of EHRs (“Doctors, Nurses and the Paperwork Crisis That Could Unite Them,” Dec. 31, 2019). They point out that, over the last half century, physicians have remained isolated on the sidelines, finding just enough voice to grumble. Nurses have in a variety of situations organized to effect change in their working conditions – in some cases by forming labor unions.

The authors of this op-ed piece, a physician and a nurse, make a strong argument that the time has come for nurses and doctors shake off the shackles of their stereotypic roles and join in creating a loud, forceful, and effective voice to demand a working environment in which the computer functions as an asset and no longer as the terrible burden it has become. Neither group has the power to do it alone, but together they may be able to turn the tide. For physicians it will probably mean venturing several steps outside of their comfort zone. But working shoulder to shoulder with nurses may provide the courage to speak out.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

The time has come for good men and women to unite and rise up against a common foe. For too long nurses and doctors have labored under the tyranny of a dictator who claimed to help them provide high-quality care for their patients while at the same time cutting their paperwork to nil. But like most autocrats he failed to engage his subjects in a meaningful dialogue as each new version of his promised improvements rolled off the drawing board. When the caregivers were slow to adopt these new nonsystems he offered them financial incentives and issued threats to their survival. Although they were warned that there might be uncomfortable adjustment periods, the caregivers were promised that the steep learning curves would level out and their professional lives would again be valued and productive.

Of course, the dictator is not a single person but a motley and disorganized conglomerate of user- and patient-unfriendly electronic health record nonsystems. Ask almost any nurse or physician for her feelings about computer-based medical record systems, and you will hear tales of long hours, disengagement, and frustration. Caregivers are unhappy at all levels, and patients have grown tired of their nurses and physicians spending most of their time looking at computer screens.

You certainly have heard this all before. But you are hearing it in hospital hallways and grocery store checkout lines as a low rumble of discontent emerging from separate individuals, not as a well-articulated and widely distributed voice of physicians as a group. To some extent this relative silence is because there is no such group, at least not in same mold as a labor union. The term “labor union” may make you uncomfortable. But given the current climate in medicine, unionizing may be the best and only way to effect change.

But organizing to effect change in the workplace isn’t part of the physician genome. In the 1960s, a group of house officers in Boston engaged in a heal-in to successfully improve their salaries and working conditions. But over the ensuing half century physicians have remained tragically silent in the face of a changing workplace landscape in which they have gone from being independent owner operators in control of their destinies to becoming employees feeling powerless to improve their working conditions. This perceived impotence has escalated in the face of the challenge posed by the introduction of dysfunctional EHRs.

Ironically, a solution is at almost every physician’s elbow. In a recent New York Times opinion piece Theresa Brown and Stephen Bergman acknowledge that physicians don’t seem prepared to mount a meaningful response to the challenge to the failed promise of EHRs (“Doctors, Nurses and the Paperwork Crisis That Could Unite Them,” Dec. 31, 2019). They point out that, over the last half century, physicians have remained isolated on the sidelines, finding just enough voice to grumble. Nurses have in a variety of situations organized to effect change in their working conditions – in some cases by forming labor unions.

The authors of this op-ed piece, a physician and a nurse, make a strong argument that the time has come for nurses and doctors shake off the shackles of their stereotypic roles and join in creating a loud, forceful, and effective voice to demand a working environment in which the computer functions as an asset and no longer as the terrible burden it has become. Neither group has the power to do it alone, but together they may be able to turn the tide. For physicians it will probably mean venturing several steps outside of their comfort zone. But working shoulder to shoulder with nurses may provide the courage to speak out.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

Sequencing Therapies

Mark Klein, MD. The last few years, there have been several new trials in prostate cancer for people in a metastatic setting or more advanced local setting, such as the STAMPEDE, LATITUDE, and CHAARTED trials.^1-4 In addition, recently a few trials have examined apalutamide and enzalutamide for people who have had PSA (prostate-specific antigen) levels rapidly rising within about 10 months or so. One of the questions that arises is, how do we wrap our heads around sequencing these therapies. Is there a sequence that we should be doing and thinking about upfront and how do the different trials compare?

Julie Graff, MD. It just got more complicated. There was news today (December 20, 2018) that using enzalutamide early on in newly diagnosed metastatic prostate cancer may have positive results. It is not yet approved by the US Food and Drug Administration (FDA), but for patients who present with metastatic prostate cancer, we may have 4 potential treatments. We could have androgen deprivation therapy (ADT) alone, ADT plus docetaxel, enzalutamide, or abiraterone.

When I see patients in this situation, I talk to them about their options, the pros and cons of each option, and try to cover all the trials that look at these combinations. It can be quite a long visit. I talk to the patient about who benefits most, whether it is patients with high-risk factors or high-volume cancers. Also, I talk with the patient about all the adverse effects (AEs), and I look at my patients’ comorbid conditions and come up with a plan.

I encourage any patient who has high-volume or high-risk disease to consider more than just ADT alone. For many patients, I have been using abiraterone plus ADT. I have a wonderful pharmacist. As a medical oncologist, I can’t do it on my own. I need someone to follow patients’ laboratory results and to be available for medication questions and complications.

Elizabeth Hansen, PharmD. With the increasing number of patients on oral antineoplastics, monitoring patients in the outpatient setting has become an increasing priority and one of my major roles as a pharmacist in the clinic at the Chalmers P. Wylie VA Ambulatory Care Center in Columbus, Ohio. This is especially important as some of these treatments require frequent laboratory monitoring, such as abiraterone with liver function tests every 2 weeks for the first 3 months of treatment and monthly thereafter. Without frequent-follow up it’s easy for these patients to get lost in the shuffle.

Abhishek Solanki, MD. You could argue that a fifth option is prostate-directed radiation for patients who have limited metastases based on the STAMPEDE trial, which we’ve started integrating into our practice at the Edward Hines, Jr. Veterans Affairs Hospital in Chicago, Illinois.⁴

Mark Klein. Do you have a feel for the data and using radiation in oligometastatic (≤ 5 metastatic tumors) disease in prostate cancer and how well that might work?

Abhishek Solanki. The best data we have are from the multi-arm, multistage STAMPEDE trial systemic therapies and local therapy in the setting of high-risk localized disease and metastatic disease.⁶ The most recent publication looked specifically at the population with newly diagnosed metastatic disease and compared standard ADT (and docetaxel in about 18% of the patients) with or without prostate-directed radiation therapy. There was no survival benefit with radiation in the overall population, but in the subgroup of patients with low metastatic burden, there was an 8% survival benefit at 3 years.

It’s difficult to know what to make of that information because, as we’ve discussed already, there are other systemic therapy options that are being used more and more upfront such as abiraterone. Can you see the same benefit of radiation in that setting? The flip side is that in this study, radiation just targeted the prostate; could survival be improved even more by targeting all sites of disease in patients with oligometastatic disease? These are still open questions in prostate cancer and there are clinical trials attempting to define the clinical benefit of radiation in the metastatic setting for patients with limited metastases.

Mark Klein. How do you select patients for radiation in this particular situation; How do you approach stratification when radiation is started upfront?

Abhishek Solanki. In the STAMPEDE trial, low metastatic burden was defined based on the definition in the CHAARTED trial, which was those patients who did not have ≥ 4 bone metastases with ≥ 1 outside the vertebral bodies or pelvis, and did not have visceral metastases.⁷ That’s tough, because this definition could be a patient with a solitary bone metastasis but also could include some patients who have involved nodes extending all the way up to the retroperitoneal nodes—that is a fairly heterogeneous population. What we have done at our institution is select patients who have 3 to 5 metastases, administer prostate radiation therapy, and add stereotactic body radiation therapy (SBRT) for the other sites of disease, invoking the oligometastasis approach.

We have been doing this more frequently in the last few months. Typically, we’ll do 3 to 5 fractions of SBRT to metastases. For the primary, if the patient chooses SBRT, we’ll take that approach. If the patient chooses a more standard fractionation, we’ll do 20 treatments, but from a logistic perspective, most patients would rather come in for 5 treatments than 20. We also typically would start these patients on systemic hormonal therapy.

Mark Klein. At that point, are they referred back to medical oncology for surveillance?

Abhishek Solanki. Yes, they are followed by medical oncology and radiation oncology, and typically would continue hormonal therapy.

Mark Klein. Julie, how have you thought about presenting the therapeutic options for those patients who would be either eligible for docetaxel with high-bulk disease or abiraterone? Do you find patients prefer one or the other?

Julie Graff. I try to be very open about all the possibilities, and I present both. I don’t just decide for the patient chemotherapy vs abiraterone, but after we talk about it, most of my patients do opt for the abiraterone. I had a patient referred from the community—we are seeing more and more of this because abiraterone is so expensive—whose ejection fraction was about 38%. I said to that patient, “we could do chemotherapy, but we shouldn’t do abiraterone.” But usually it’s not that clear-cut.

Elizabeth Hansen. There was also an update from the STAMPEDE trial published recently comparing upfront abiraterone and prednisone to docetaxel (18 weeks) in advanced or metastatic prostate cancer. Results from this trial indicated a nearly identical overall survival (OS) (hazard ratio [HR] = 1.16; 95% CI, 0.82-1.65; P = .40). However, the failure-free survival (HR = 0.51; 95% CI, 0.39-0.67; P < .001) and progression-free survival (PFS) (HR= 0.65; 95% CI, 0.0.48-0.88; P = .005) favored abiraterone.^8,9 The authors argue that while there was no change in OS, this trial demonstrates an important difference in the pattern of treatment failure.

Julie, do you think there will be any change in the treatment paradigm between docetaxel and abiraterone with this new update?

Julie Graff. I wasn’t that impressed by that study. I do not see it as practice changing, and it makes sense to me that the PFS is different in the 2 arms because we give chemotherapy and take a break vs giving abiraterone indefinitely. For me, there’s not really a shift.

Patients With Rising PSAs

Mark Klein. Let’s discuss the data from the recent studies on enzalutamide and apalutamide for the patients with fast-rising PSAs. In your discussions with other prostate researchers, will this become a standard part of practice or not?

Julie Graff. I was one of the authors on the SPARTAN apalutamide study.¹⁰ For a long time, we have had patients without metastatic disease but with a PSA relapse after surgery or radiation; and the PSA levels climb when the cancer becomes resistant to ADT. We haven’t had many options in that setting except to use bicalutamide and some older androgen receptor (AR) antagonists. We used to use estrogen and ketoconazole as well.

But now 2 studies have come out looking at a primary endpoint of metastases-free survival. Patients whose PSA was doubling every 10 months or shorter were randomized to either apalutamide (SPARTAN¹⁰) or enzalutamide (PROSPER¹¹), both second-generation AR antagonists. There was a placebo control arm in each of the studies. Both studies found that adding the second-generation AR targeting agent delayed the time to metastatic disease by about 2 years. There is not any signal yet for statistically significant OS benefit, so it is not entirely clear if you could wait for the first metastasis to develop and then give 1 of these treatments and have the same OS benefit.

At the VA Portland Health Care System (VAPORHCS), it took a while to make these drugs available. My fellows were excited to give these drugs right away, but I often counsel patients that we don’t know if the second-generation AR targeting agents will improve survival. They almost certainly will bring down PSAs, which helps with peace of mind, but anything we add to the ADT can cause more AEs.

I have been cautious with second-generation AR antagonists because patients, when they take one of these drugs, are going to be on it for a long time. The FDA has approved those 2 drugs regardless of PSA doubling time, but I would not give it for a PSA doubling time > 10 months. In my practice about a quarter of patients who would qualify for apalutamide or enzalutamide are actually taking one, and the others are monitored closely with computed tomography (CT) and bone scans. When the disease becomes metastatic, then we start those drugs.

Mark Klein. Why 10 months, why not 6 months, a year, or 18 months? Is there reasoning behind that?

Julie Graff. There was a publication by Matthew Smith showing that the PSA doubling time was predictive of the development of metastatic disease and cancer death or prostate cancer death, and that 10 months seemed to be the cutoff between when the prostate cancer was going to become deadly vs not.¹² If you actually look at the trial data, I think the PSA doubling time was between 3 and 4 months for the participants, so pretty short.

Adverse Effects

Mark Klein. What are the AEs people are seeing from using apalutamide, enzalutamide, and abiraterone? What are they seeing in their practice vs what is in the studies? When I have had to stop people on abiraterone or drop down the dose, almost always it has been for fatigue. We check liver function tests (LFTs) repeatedly, but I can’t remember ever having to drop down the dose or take it away even for that reason.

Elizabeth Hansen. The toxicities of these 3 agents are very different. In my practice I have seen a few patients develop hepatotoxicity with abiraterone, and I think this reflects the known incidence of transaminitis (grade 3/4) seen in clinical trials, reported at 6%. Generally, we’ve been able to restart treatment by withholding abiraterone until liver function returns to baseline and then subsequently dose reducing. Like Julie mentioned, abiraterone should be used with caution and/or avoided in patients with serious cardiac disease, recent myocardial infarction, or heart failure. I also always check blood pressure history, to ensure it is well controlled prior to initiation, and order a home blood pressure cuff for monitoring. With enzalutamide one of the main concerns is fatigue, which occurred in > 10% of patients in clinical trials. In my experience this has been dose limiting and can be managed with dose reductions. Seizures also occurred in 0.4% of patients on enzalutamide, so I always ask about seizure history and screen the medication list for concomitant medications that may lower the seizure threshold or other risk factors such as brain metastasis. Last, enzalutamide is a strong CYP3A4 inducer, so there is a strong possibility for drug interactions with other medications, and it is associated with increased cardiac events. With apalutamide you have the cardiac concerns, thyroid dysfunction, fracture risk, and drug interactions to worry about as well. To be honest, we have not used this agent yet at my practice.

Mark Klein. At the Minneapolis VA Health Care System (MVAHCS) when apalutamide first came out, for the PSA rapid doubling, there had already been an abstract presenting the enzalutamide data. We have chosen to recommend enzalutamide as our choice for the people with PSA doubling based on the cost. It’s significantly cheaper for the VA. Between the 2 papers there is very little difference in the efficacy data. I’m wondering what other sites have done with regard to that specific point at their VAs?

Elizabeth Hansen. In Columbus, we prefer to use either abiraterone and enzalutamide because they’re essentially cost neutral. However, this may change with generic abiraterone coming to market. Apalutamide is really cost prohibitive currently.

Julie Graff. I agree.

Patient Education

Mark Klein. At MVAHCS, the navigators handle a lot of upfront education. We have 3 navigators, including Kathleen Nelson who is on this roundtable. She works with patients and provides much of the patient education. How have you handled education for patients?

Kathleen Nelson. For the most part, our pharmacists do the drug-specific education for the oral agents, and the nurse navigators provide more generic education. We did a trial for patients on IV therapies. We learned that patients really don’t report in much detail, but if you call and ask them specific questions, then you can tease out some more detail.

Elizabeth Hansen. It is interesting that every site is different. One of my main roles is oral antineoplastic monitoring, which includes many patients on enzalutamide or abiraterone. At least initially with these patients, I try to follow them closely—abiraterone more so than enzalutamide. I typically call every 2 to 4 weeks, in between clinic visits, to follow up the laboratory tests and manage the AEs. I always try to ask direct and open-ended questions: How often are you checking your blood pressure? What is your current weight? How has your energy level changed since therapy initiation?

The VA telehealth system is amazing. For patients who need to monitor blood pressure regularly, it’s really nice for them to have those numbers come directly back to me in CPRS (Computerized Patient Record System). That has worked wonders for some of our patients to get them through therapy.

Mark Klein. What do you tend to use when the prostate cancer is progressing for a patient? And how do you determine that progression? Some studies will use PSA rise only as a marker for progression. Other studies have not used PSA rise as the only marker for progression and oftentimes require some sort of bone scan criteria or CT imaging criteria for progression.

Julie Graff. We have a limited number of treatment options. Providers typically use enzalutamide or abiraterone as there is a high degree of resistance between the 2. Then there is chemotherapy and then radium, which quite a few people don’t qualify for. We need to be very thoughtful when we change treatments. I look at the 3 factors of biochemical progression or response—PSA, radiographic progression, and clinical progression. If I don’t see 2 out of 3, I typically don’t change treatments. Then after enzalutamide or abiraterone, I wait until there are cancer-related symptoms before I consider chemotherapy and closely monitor my patients.

Imaging Modalities

Abhishek Solanki. Over the last few years the Hines VA Hospital has used fluciclovine positron emission tomography (PET), which is one of the novel imaging modalities for prostate cancer. Really the 2 novel imaging modalities that have gained the most excitement are prostate-specific membrane antigen (PSMA) PET and fluciclovine PET. Fluciclovine PET is based on a synthetic amino acid that’s taken up in multiple tissues, including prostate cancer. It has changed our practice in the localized setting for patients who have developed recurrence after radiation or radical prostatectomy. We have incorporated the scan into our workup of patients with recurrent disease, which can give us some more information at lower PSAs than historically we could get with CT, bone scan, or magnetic resonance imaging.

Our medical oncologists have started using it more and more as well. We are getting a lot of patients who have a negative CT or bone scan but have a positive fluciclovine PET. There are a few different disease settings where that becomes relevant. In patients who develop biochemical recurrence after radiation or salvage radiation after radical, we are finding that a lot of these patients who have no CT or bone scan findings of disease ultimately are found to have a PET-positive lesion. Sometimes it’s difficult to know how best to help patients with PET-only disease. Should you target the disease with an oligometastasis approach or just pursue systemic therapy or surveillance? It is challenging but more and more we are moving toward metastasis-directed therapy. There are multiple randomized trials in progress testing whether metastasis-directed therapy to the PET areas of recurrence can improve outcomes or delay systemic ADT. The STOMP trial randomized surveillance vs SBRT or surgery for patients with oligometastatic disease that showed improvement in biochemical control and ADT-free survival.¹³ However this was a small trial that tried to identify a signal. More definitive trials are necessary.

The other setting where we have found novel PET imaging to be helpful is in patients who have become castration resistant but don’t have clear metastases on conventional imaging. We’re identifying more patients who have only a few sites of progression, and we’ll pursue metastasis-directed therapy to those areas to try to get more mileage out of the systemic therapy that the patient is currently on and to try to avoid having to switch to the next line with the idea that, potentially, the progression site is just a limited clone that is progressing despite the current systemic therapy.
 

Mark Klein. I find that to be a very attractive approach. I’m assuming you do that for any systemic therapy where people have maybe 1 or 2 sites and they do not have a big PSA jump. Do you have a number of sites that you’re willing to radiate? And then, when you do that, what radiation fractionation and dosing do you use? Is there any observational data behind that for efficacy?

Abhishek Solanki. It is a patient by patient decision. Some patients, if they have a very rapid pace of progression shortly after starting systemic therapy and metastases have grown in several areas, we think that perhaps this person may benefit less from aggressive local therapy. But if it’s somebody who has been on systemic therapy for a while and has up to 3 sites of disease growth, we consider SBRT for oligoprogressive disease. Typically, we’ll use SBRT, which delivers a high dose of radiation over 3 to 5 treatments. With SBRT you can give a higher biologic dose and use more sophisticated treatment machines and image guidance for treatments to focus the radiation on the tumor area and limit exposure to normal tissue structures.

In prostate cancer to the primary site, we will typically do around 35 to 40 Gy in 5 fractions. For metastases, it depends on the site. If it’s in the lung, typically we will do 3 to 5 treatments, giving approximately 50 to 60 Gy in that course. In the spine, we use lower doses near the spinal cord and the cauda equina, typically about 30 Gy in 3 fractions. In the liver, similar to the lung, we’ll typically do 50-54 Gy in 3-5 fractions. There aren’t a lot of high-level data guiding the optimal dose/fractionation to metastases, but these are the doses we’ll use for various malignancies.

Treatment Options for Patients With Adverse Events

Mark Klein. I was just reviewing the 2004 study that randomized patients to mitoxantrone or docetaxel for up to 10 cycles.^14,15 Who are good candidates for docetaxel after they have exhausted abiraterone and enzalutamide? How long do you hold to the 10-cycle rule, or do you go beyond that if they’re doing well? And if they’re not a good candidate, what are some options?

Julie Graff. The best candidates are those who are having a cancer-related AE, particularly pain, because docetaxel only improves survival over mitoxantrone by about 2.5 months. I don’t talk to patients about it as though it is a life extender, but it seems to help control pain—about 70% of patients benefited in terms of pain or some other cancer-related symptom.¹⁴

I have a lot of patients who say, “Never will I do chemotherapy.” I refer those patients to hospice, or if they’re appropriate for radium-223, I consider that. I typically give about 6 cycles of chemotherapy and then see how they’re doing. In some patients, the cancer just doesn’t respond to it.

I do tell patients about the papers that you mentioned, the 2 studies of docetaxel vs mitoxantrone where they use about 10 cycles, and some of my patients go all 10.^14,15 Sometimes we have to stop because of neuropathy or some other AE. I believe in taking breaks and that you can probably start it later.

Elizabeth Hansen. I agree, our practice is similar. A lot of our patients are not very interested in chemotherapy. You have to take into consideration their ECOG (Eastern Cooperative Oncology Group) status, their goals, and quality of life when talking to them about these medications. And a lot of them tend to choose more of a palliative route. Depending on their AEs and how things are going, we will dose reduce, hold treatment, or give treatment holidays.

Mark Klein. If patients are progressing on docetaxel, what are options that people would use? Radium-223 certainly is available for patients with nonvisceral metastases, as well as cabazitaxel, mitoxantrone, estramustine and other older drugs.

Julie Graff. We have some clinical trials for patients postdocetaxel. We have the TRITON2 and TRITON3 studies open at the VA. (NCT02952534 and NCT02975934, respectively) A lot of patients would get a biopsy, and we’d look for a BRCA 1 or 2 and ATM mutation. For those patients who don’t have those mutations—and maybe 80% of them don’t—we talk about radium-223 for the patients without visceral metastases and bone pain. I have had a fair number of patients go on cabazitaxel, but I have not used mitoxantrone since cabazitaxel came out. It’s not off the table, but it hasn’t shown improvement in survival.

Elizabeth Hansen. One of our challenges, because we’re an ambulatory care center, is that we are unable to give radium-223 in house, and these services have to be sent out to a non-VA facility. It is doable, but it takes more legwork and organization on our part.

Julie Graff. We have not had radium-223, although we’re working to get that online. And we are physically connected to Oregon Health Science University (OHSU), so we send our patients there for radium. It is a pain because the doctors at OHSU don’t have CPRS access. I’m often in the middle of making sure the complete blood counts (CBCs) are sent to OHSU and to get my patients their treatments.

Mark Klein. The Minneapolis VAMC has radium-223 on site, and we have used it for patients whose cancer has progressed while on docetaxel without visceral metastases. Katie, have you had an opportunity to coordinate that care for patients?

Kathleen Nelson. Radium is administered at our facility by one of our nuclear medicine physicians. A complete blood count is checked at least 3 days prior to the infusion date but no sooner than 6 days. Due to the cost of the material, ordering without knowing the patient’s counts are within a safe range to administer is prohibitive. This adds an additional burden of 2 visits (lab with return visit) to the patient. We have treated 12 patients. Four patients stopped treatment prior to completing the 6 planned treatments citing debilitating fatigue and/or nonresolution of symptoms as their reason to stop treatment. One patient died. The 7 remaining patients subjectively reported varying degrees of pain relief.

Elizabeth Hansen. Another thing to mention is the lack of a PSA response from radium-223 as well. Patients are generally very diligent about monitoring their PSA, so this can be a bit distressing.

Mark Klein. Julie, have you noticed a PSA flare with radium-223? I know it has been reported.

Julie Graff. I haven’t. But I put little stock in PSAs in these patients. I spend 20 minutes explaining to patients that the PSA is not helpful in determining whether or not the radium is working. I tell them that the bone marker alkaline phosphatase may decrease. And I think it’s important to note, too, that radium-223 is not a treatment we have on the shelf. We order it from Denver I believe. It is weight based, and it takes 5 days to get.

Clinical Trials

Mark Klein. That leads us into clinical trials. What is the role for precision oncology in prostate cancer right now, specifically looking at particular panels? One would be the DNA repair enzyme-based genes and/or also the AR variants and any other markers.

Elizabeth Hansen. The National Comprehensive Cancer Network came out with a statement recommending germ-line and somatic-mutation testing in all patients with metastatic prostate cancer. This highlights the need to offer patients the availability of clinical trials.

Julie Graff. I agree. We occasionally get to a place in the disease where patients are feeling fine, but we don’t have anything else to offer. The studies by Robinson¹⁶ and then Matteo¹⁷ showed that (a) these DNA repair defects are present in about a quarter of patients; and (b) that PARP inhibitors can help these patients. At least it has an anticancer effect.

What’s interesting is that we have TRITON2, and TRITON3, which are sponsored by Clovis,for patients with BRCA 1/2 and ATM mutations and using the PARP-inhibitor rucaparib. Based on the data we have available, we thought a quarter of patients would have the mutation in the tumor, but they’re finding that it is more like 10% to 15%. They are screening many patients but not finding it.

I agree that clinical trials are the way to go. I am hopeful that we’ll get more treatments based on molecular markers. The approval for pembrolizumab in any tumor type with microsatellite instability is interesting, but in prostate cancer, I believe that’s about 3%. I haven’t seen anyone qualify for pembrolizumab based on that. Another plug for clinical trials: Let’s learn more and offer our patients potentially beneficial treatments earlier.

Mark Klein. The first interim analysis from the TRITON2 study found about 12% of patients had alterations in BRCA 1/2. But in those that met the RECIST criteria, they were able to have evaluable disease via that standard with about a 44% response rate so far and a 51% PSA response rate. It is promising data, but it’s only 85 patients so far. We’ll know more because the TRITON2 study is of a more pretreated population than the TRITION3 study at this point. Are there any data on precision medicine and radiation in prostate cancer?

Abhishek Solanki. In the prostate cancer setting, there are not a lot of emerging data specifically looking at using precision oncology biomarkers to help guide decisions in radiation therapy. For example, genomic classifiers, like GenomeDx Decipher (Vancouver, BC) and Myriad Genetics Prolaris (Salt Lake City, UT) are increasingly being utilized in patients with localized disease. Decipher can help predict the risk of recurrence after radical prostatectomy. The difficulty is that there are limited data that show that by using these genomic classifiers, one can improve outcomes in patients over traditional clinical characteristics.

There are 2 trials currently ongoing through NRG Oncology that are using Decipher. The GU002 is a trial for patients who had a radical prostatectomy and had a postoperative PSA that never nadired below 0.2. These patients are randomized between salvage radiation with hormone therapy with or without docetaxel. This trial is collecting Decipher results for patients enrolled in the study. The GU006 is a trial for a slightly more favorable group of patients who do nadir but still have biochemical recurrence and relatively low PSAs. This trial randomizes between radiotherapy alone and radiotherapy and 6 months of apalutamide, stratifying patients based on Decipher results, specially differentiating between patients who have a luminal vs basal subtype of prostate cancer. There are data that suggest that patients who have a luminal subtype may benefit more from the combination of radiation and hormone therapy vs patients who have basal subtype.¹⁸ However this hasn’t been validated in a prospective setting, and that’s what this trial will hopefully do.

Immunotherapies

Mark Klein. Outside of prostate cancer, there has been a lot of research trying to determine how to improve PD-L1 expression. Where are immunotherapy trials moving? How radiation might play a role in conjunction with immunotherapy.

Julie Graff. Two phase 3 studies did not show statistically improved survival or statistically significant survival improvement on ipilimumab, an immunotherapy agent that targets CTLA4. Some early studies of the PD-1 drugs nivolumab and pembrolizumab did not show much response with monotherapy. Despite the negative phase 3 studies for ipilimumab, we periodically see exceptional responses.

In prostate cancer, enzalutamide is FDA approved. And there’s currently a phase 3 study of the PD-L1 inhibitor atezolizumab plus enzalutamide in patients who have progressed on abiraterone. That trial is fully accrued, but the results are not yet known. Soon a study will compare pembrolizumab plus enzalutamide vs enzalutamide alone. So the combinations are getting more interesting.

I just received a Prostate Cancer Foundation Challenge Award to open a VA-only study looking at fecal microbiota transplant from responders to nonresponders to see how manipulating host factors can increase potential responses to PD-1 inhibition.

Abhishek Solanki. The classic mechanism by which radiation therapy works is direct DNA damage and indirect DNA damage through hydroxyl radicals that leads to cytotoxicity. But preclinical and clinical data suggest that radiation therapy can augment the local and systemic immunotherapy response. The radiation oncologist’s dream is what is called the abscopal effect, which is the idea that when you treat one site of disease with radiation, it can induce a response at other sites that didn’t get radiation therapy through reactivation of the immune system. I like to think of the abscopal effect like bigfoot—it’s elusive. However, it seems that the setting it is most likely to happen in is in combination with immunotherapy.

One of the ways that radiation fails locally is that it can upregulate PD-1 expression, and as a result, you can have progression of the tumor because of local immune suppression. We know that T cells are important for the activity of radiation therapy. If you combine checkpoint inhibition with radiation therapy, you can not only have better local control in the area of the tumor, but perhaps you can release tumor antigens that will then induce a systemic response.

The other potential mechanism by which radiation may work synergistically with immunotherapy is as a debulking agent. There are some data that suggest that the ratio of T-cell reinvigoration to bulk of disease, or the volume of tumor burden, is important. That is, having T-cell reinvigoration may not be sufficient to have a response to immunotherapy in patients with a large burden of disease. By using radiation to debulk disease, perhaps you could help make checkpoint inhibition more effective. Ultimately, in the setting of prostate cancer, there are not a lot of data yet showing meaningful benefits with the combination of immunotherapy and radiotherapy, but there are trials that are ongoing that will educate on potential synergy.

Pharmacy

Julie Graff. Before we end I want to make sure that we applaud the amazing pharmacists and patient care navigation teams in the VA who do such a great job of getting veterans the appropriate treatment expeditiously and keeping them safe. It’s something that is truly unique to the VA. And I want to thank the people on this call who do this every day.

Elizabeth Hansen. Thank you Julie. Compared with working in the community, at the VA I’m honestly amazed by the ease of access to these medications for our patients. Being able to deliver medications sometimes the same day to the patient is just not something that happens in the community. It’s nice to see that our veterans are getting cared for in that manner.

Author disclosures
Dr. Solanki participated in advisory boards for Blue Earth Diagnostics’ fluciclovine PET and was previously paid as a consultant. Dr. Graff is a consultant for Sanofi (docetaxel) and Astellas (enzalutamide), and has received research funding (no personal funding)from Sanofi, Merck (pembrolizumab), Astellas, and Jannsen (abiraterone, apalutamide). The other authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the US Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

Sequencing Therapies

Mark Klein, MD. The last few years, there have been several new trials in prostate cancer for people in a metastatic setting or more advanced local setting, such as the STAMPEDE, LATITUDE, and CHAARTED trials.^1-4 In addition, recently a few trials have examined apalutamide and enzalutamide for people who have had PSA (prostate-specific antigen) levels rapidly rising within about 10 months or so. One of the questions that arises is, how do we wrap our heads around sequencing these therapies. Is there a sequence that we should be doing and thinking about upfront and how do the different trials compare?

Julie Graff, MD. It just got more complicated. There was news today (December 20, 2018) that using enzalutamide early on in newly diagnosed metastatic prostate cancer may have positive results. It is not yet approved by the US Food and Drug Administration (FDA), but for patients who present with metastatic prostate cancer, we may have 4 potential treatments. We could have androgen deprivation therapy (ADT) alone, ADT plus docetaxel, enzalutamide, or abiraterone.

When I see patients in this situation, I talk to them about their options, the pros and cons of each option, and try to cover all the trials that look at these combinations. It can be quite a long visit. I talk to the patient about who benefits most, whether it is patients with high-risk factors or high-volume cancers. Also, I talk with the patient about all the adverse effects (AEs), and I look at my patients’ comorbid conditions and come up with a plan.

I encourage any patient who has high-volume or high-risk disease to consider more than just ADT alone. For many patients, I have been using abiraterone plus ADT. I have a wonderful pharmacist. As a medical oncologist, I can’t do it on my own. I need someone to follow patients’ laboratory results and to be available for medication questions and complications.

Elizabeth Hansen, PharmD. With the increasing number of patients on oral antineoplastics, monitoring patients in the outpatient setting has become an increasing priority and one of my major roles as a pharmacist in the clinic at the Chalmers P. Wylie VA Ambulatory Care Center in Columbus, Ohio. This is especially important as some of these treatments require frequent laboratory monitoring, such as abiraterone with liver function tests every 2 weeks for the first 3 months of treatment and monthly thereafter. Without frequent-follow up it’s easy for these patients to get lost in the shuffle.

Abhishek Solanki, MD. You could argue that a fifth option is prostate-directed radiation for patients who have limited metastases based on the STAMPEDE trial, which we’ve started integrating into our practice at the Edward Hines, Jr. Veterans Affairs Hospital in Chicago, Illinois.⁴

Mark Klein. Do you have a feel for the data and using radiation in oligometastatic (≤ 5 metastatic tumors) disease in prostate cancer and how well that might work?

Abhishek Solanki. The best data we have are from the multi-arm, multistage STAMPEDE trial systemic therapies and local therapy in the setting of high-risk localized disease and metastatic disease.⁶ The most recent publication looked specifically at the population with newly diagnosed metastatic disease and compared standard ADT (and docetaxel in about 18% of the patients) with or without prostate-directed radiation therapy. There was no survival benefit with radiation in the overall population, but in the subgroup of patients with low metastatic burden, there was an 8% survival benefit at 3 years.

It’s difficult to know what to make of that information because, as we’ve discussed already, there are other systemic therapy options that are being used more and more upfront such as abiraterone. Can you see the same benefit of radiation in that setting? The flip side is that in this study, radiation just targeted the prostate; could survival be improved even more by targeting all sites of disease in patients with oligometastatic disease? These are still open questions in prostate cancer and there are clinical trials attempting to define the clinical benefit of radiation in the metastatic setting for patients with limited metastases.

Mark Klein. How do you select patients for radiation in this particular situation; How do you approach stratification when radiation is started upfront?

Abhishek Solanki. In the STAMPEDE trial, low metastatic burden was defined based on the definition in the CHAARTED trial, which was those patients who did not have ≥ 4 bone metastases with ≥ 1 outside the vertebral bodies or pelvis, and did not have visceral metastases.⁷ That’s tough, because this definition could be a patient with a solitary bone metastasis but also could include some patients who have involved nodes extending all the way up to the retroperitoneal nodes—that is a fairly heterogeneous population. What we have done at our institution is select patients who have 3 to 5 metastases, administer prostate radiation therapy, and add stereotactic body radiation therapy (SBRT) for the other sites of disease, invoking the oligometastasis approach.

We have been doing this more frequently in the last few months. Typically, we’ll do 3 to 5 fractions of SBRT to metastases. For the primary, if the patient chooses SBRT, we’ll take that approach. If the patient chooses a more standard fractionation, we’ll do 20 treatments, but from a logistic perspective, most patients would rather come in for 5 treatments than 20. We also typically would start these patients on systemic hormonal therapy.

Mark Klein. At that point, are they referred back to medical oncology for surveillance?

Abhishek Solanki. Yes, they are followed by medical oncology and radiation oncology, and typically would continue hormonal therapy.

Mark Klein. Julie, how have you thought about presenting the therapeutic options for those patients who would be either eligible for docetaxel with high-bulk disease or abiraterone? Do you find patients prefer one or the other?

Julie Graff. I try to be very open about all the possibilities, and I present both. I don’t just decide for the patient chemotherapy vs abiraterone, but after we talk about it, most of my patients do opt for the abiraterone. I had a patient referred from the community—we are seeing more and more of this because abiraterone is so expensive—whose ejection fraction was about 38%. I said to that patient, “we could do chemotherapy, but we shouldn’t do abiraterone.” But usually it’s not that clear-cut.

Elizabeth Hansen. There was also an update from the STAMPEDE trial published recently comparing upfront abiraterone and prednisone to docetaxel (18 weeks) in advanced or metastatic prostate cancer. Results from this trial indicated a nearly identical overall survival (OS) (hazard ratio [HR] = 1.16; 95% CI, 0.82-1.65; P = .40). However, the failure-free survival (HR = 0.51; 95% CI, 0.39-0.67; P < .001) and progression-free survival (PFS) (HR= 0.65; 95% CI, 0.0.48-0.88; P = .005) favored abiraterone.^8,9 The authors argue that while there was no change in OS, this trial demonstrates an important difference in the pattern of treatment failure.

Julie, do you think there will be any change in the treatment paradigm between docetaxel and abiraterone with this new update?

Julie Graff. I wasn’t that impressed by that study. I do not see it as practice changing, and it makes sense to me that the PFS is different in the 2 arms because we give chemotherapy and take a break vs giving abiraterone indefinitely. For me, there’s not really a shift.

Patients With Rising PSAs

Mark Klein. Let’s discuss the data from the recent studies on enzalutamide and apalutamide for the patients with fast-rising PSAs. In your discussions with other prostate researchers, will this become a standard part of practice or not?

Julie Graff. I was one of the authors on the SPARTAN apalutamide study.¹⁰ For a long time, we have had patients without metastatic disease but with a PSA relapse after surgery or radiation; and the PSA levels climb when the cancer becomes resistant to ADT. We haven’t had many options in that setting except to use bicalutamide and some older androgen receptor (AR) antagonists. We used to use estrogen and ketoconazole as well.

But now 2 studies have come out looking at a primary endpoint of metastases-free survival. Patients whose PSA was doubling every 10 months or shorter were randomized to either apalutamide (SPARTAN¹⁰) or enzalutamide (PROSPER¹¹), both second-generation AR antagonists. There was a placebo control arm in each of the studies. Both studies found that adding the second-generation AR targeting agent delayed the time to metastatic disease by about 2 years. There is not any signal yet for statistically significant OS benefit, so it is not entirely clear if you could wait for the first metastasis to develop and then give 1 of these treatments and have the same OS benefit.

At the VA Portland Health Care System (VAPORHCS), it took a while to make these drugs available. My fellows were excited to give these drugs right away, but I often counsel patients that we don’t know if the second-generation AR targeting agents will improve survival. They almost certainly will bring down PSAs, which helps with peace of mind, but anything we add to the ADT can cause more AEs.

I have been cautious with second-generation AR antagonists because patients, when they take one of these drugs, are going to be on it for a long time. The FDA has approved those 2 drugs regardless of PSA doubling time, but I would not give it for a PSA doubling time > 10 months. In my practice about a quarter of patients who would qualify for apalutamide or enzalutamide are actually taking one, and the others are monitored closely with computed tomography (CT) and bone scans. When the disease becomes metastatic, then we start those drugs.

Mark Klein. Why 10 months, why not 6 months, a year, or 18 months? Is there reasoning behind that?

Julie Graff. There was a publication by Matthew Smith showing that the PSA doubling time was predictive of the development of metastatic disease and cancer death or prostate cancer death, and that 10 months seemed to be the cutoff between when the prostate cancer was going to become deadly vs not.¹² If you actually look at the trial data, I think the PSA doubling time was between 3 and 4 months for the participants, so pretty short.

Adverse Effects

Mark Klein. What are the AEs people are seeing from using apalutamide, enzalutamide, and abiraterone? What are they seeing in their practice vs what is in the studies? When I have had to stop people on abiraterone or drop down the dose, almost always it has been for fatigue. We check liver function tests (LFTs) repeatedly, but I can’t remember ever having to drop down the dose or take it away even for that reason.

Elizabeth Hansen. The toxicities of these 3 agents are very different. In my practice I have seen a few patients develop hepatotoxicity with abiraterone, and I think this reflects the known incidence of transaminitis (grade 3/4) seen in clinical trials, reported at 6%. Generally, we’ve been able to restart treatment by withholding abiraterone until liver function returns to baseline and then subsequently dose reducing. Like Julie mentioned, abiraterone should be used with caution and/or avoided in patients with serious cardiac disease, recent myocardial infarction, or heart failure. I also always check blood pressure history, to ensure it is well controlled prior to initiation, and order a home blood pressure cuff for monitoring. With enzalutamide one of the main concerns is fatigue, which occurred in > 10% of patients in clinical trials. In my experience this has been dose limiting and can be managed with dose reductions. Seizures also occurred in 0.4% of patients on enzalutamide, so I always ask about seizure history and screen the medication list for concomitant medications that may lower the seizure threshold or other risk factors such as brain metastasis. Last, enzalutamide is a strong CYP3A4 inducer, so there is a strong possibility for drug interactions with other medications, and it is associated with increased cardiac events. With apalutamide you have the cardiac concerns, thyroid dysfunction, fracture risk, and drug interactions to worry about as well. To be honest, we have not used this agent yet at my practice.

Mark Klein. At the Minneapolis VA Health Care System (MVAHCS) when apalutamide first came out, for the PSA rapid doubling, there had already been an abstract presenting the enzalutamide data. We have chosen to recommend enzalutamide as our choice for the people with PSA doubling based on the cost. It’s significantly cheaper for the VA. Between the 2 papers there is very little difference in the efficacy data. I’m wondering what other sites have done with regard to that specific point at their VAs?

Elizabeth Hansen. In Columbus, we prefer to use either abiraterone and enzalutamide because they’re essentially cost neutral. However, this may change with generic abiraterone coming to market. Apalutamide is really cost prohibitive currently.

Julie Graff. I agree.

Patient Education

Mark Klein. At MVAHCS, the navigators handle a lot of upfront education. We have 3 navigators, including Kathleen Nelson who is on this roundtable. She works with patients and provides much of the patient education. How have you handled education for patients?

Kathleen Nelson. For the most part, our pharmacists do the drug-specific education for the oral agents, and the nurse navigators provide more generic education. We did a trial for patients on IV therapies. We learned that patients really don’t report in much detail, but if you call and ask them specific questions, then you can tease out some more detail.

Elizabeth Hansen. It is interesting that every site is different. One of my main roles is oral antineoplastic monitoring, which includes many patients on enzalutamide or abiraterone. At least initially with these patients, I try to follow them closely—abiraterone more so than enzalutamide. I typically call every 2 to 4 weeks, in between clinic visits, to follow up the laboratory tests and manage the AEs. I always try to ask direct and open-ended questions: How often are you checking your blood pressure? What is your current weight? How has your energy level changed since therapy initiation?

The VA telehealth system is amazing. For patients who need to monitor blood pressure regularly, it’s really nice for them to have those numbers come directly back to me in CPRS (Computerized Patient Record System). That has worked wonders for some of our patients to get them through therapy.

Mark Klein. What do you tend to use when the prostate cancer is progressing for a patient? And how do you determine that progression? Some studies will use PSA rise only as a marker for progression. Other studies have not used PSA rise as the only marker for progression and oftentimes require some sort of bone scan criteria or CT imaging criteria for progression.

Julie Graff. We have a limited number of treatment options. Providers typically use enzalutamide or abiraterone as there is a high degree of resistance between the 2. Then there is chemotherapy and then radium, which quite a few people don’t qualify for. We need to be very thoughtful when we change treatments. I look at the 3 factors of biochemical progression or response—PSA, radiographic progression, and clinical progression. If I don’t see 2 out of 3, I typically don’t change treatments. Then after enzalutamide or abiraterone, I wait until there are cancer-related symptoms before I consider chemotherapy and closely monitor my patients.

Imaging Modalities

Abhishek Solanki. Over the last few years the Hines VA Hospital has used fluciclovine positron emission tomography (PET), which is one of the novel imaging modalities for prostate cancer. Really the 2 novel imaging modalities that have gained the most excitement are prostate-specific membrane antigen (PSMA) PET and fluciclovine PET. Fluciclovine PET is based on a synthetic amino acid that’s taken up in multiple tissues, including prostate cancer. It has changed our practice in the localized setting for patients who have developed recurrence after radiation or radical prostatectomy. We have incorporated the scan into our workup of patients with recurrent disease, which can give us some more information at lower PSAs than historically we could get with CT, bone scan, or magnetic resonance imaging.

Our medical oncologists have started using it more and more as well. We are getting a lot of patients who have a negative CT or bone scan but have a positive fluciclovine PET. There are a few different disease settings where that becomes relevant. In patients who develop biochemical recurrence after radiation or salvage radiation after radical, we are finding that a lot of these patients who have no CT or bone scan findings of disease ultimately are found to have a PET-positive lesion. Sometimes it’s difficult to know how best to help patients with PET-only disease. Should you target the disease with an oligometastasis approach or just pursue systemic therapy or surveillance? It is challenging but more and more we are moving toward metastasis-directed therapy. There are multiple randomized trials in progress testing whether metastasis-directed therapy to the PET areas of recurrence can improve outcomes or delay systemic ADT. The STOMP trial randomized surveillance vs SBRT or surgery for patients with oligometastatic disease that showed improvement in biochemical control and ADT-free survival.¹³ However this was a small trial that tried to identify a signal. More definitive trials are necessary.

The other setting where we have found novel PET imaging to be helpful is in patients who have become castration resistant but don’t have clear metastases on conventional imaging. We’re identifying more patients who have only a few sites of progression, and we’ll pursue metastasis-directed therapy to those areas to try to get more mileage out of the systemic therapy that the patient is currently on and to try to avoid having to switch to the next line with the idea that, potentially, the progression site is just a limited clone that is progressing despite the current systemic therapy.
 

Mark Klein. I find that to be a very attractive approach. I’m assuming you do that for any systemic therapy where people have maybe 1 or 2 sites and they do not have a big PSA jump. Do you have a number of sites that you’re willing to radiate? And then, when you do that, what radiation fractionation and dosing do you use? Is there any observational data behind that for efficacy?

Abhishek Solanki. It is a patient by patient decision. Some patients, if they have a very rapid pace of progression shortly after starting systemic therapy and metastases have grown in several areas, we think that perhaps this person may benefit less from aggressive local therapy. But if it’s somebody who has been on systemic therapy for a while and has up to 3 sites of disease growth, we consider SBRT for oligoprogressive disease. Typically, we’ll use SBRT, which delivers a high dose of radiation over 3 to 5 treatments. With SBRT you can give a higher biologic dose and use more sophisticated treatment machines and image guidance for treatments to focus the radiation on the tumor area and limit exposure to normal tissue structures.

In prostate cancer to the primary site, we will typically do around 35 to 40 Gy in 5 fractions. For metastases, it depends on the site. If it’s in the lung, typically we will do 3 to 5 treatments, giving approximately 50 to 60 Gy in that course. In the spine, we use lower doses near the spinal cord and the cauda equina, typically about 30 Gy in 3 fractions. In the liver, similar to the lung, we’ll typically do 50-54 Gy in 3-5 fractions. There aren’t a lot of high-level data guiding the optimal dose/fractionation to metastases, but these are the doses we’ll use for various malignancies.

Treatment Options for Patients With Adverse Events

Mark Klein. I was just reviewing the 2004 study that randomized patients to mitoxantrone or docetaxel for up to 10 cycles.^14,15 Who are good candidates for docetaxel after they have exhausted abiraterone and enzalutamide? How long do you hold to the 10-cycle rule, or do you go beyond that if they’re doing well? And if they’re not a good candidate, what are some options?

Julie Graff. The best candidates are those who are having a cancer-related AE, particularly pain, because docetaxel only improves survival over mitoxantrone by about 2.5 months. I don’t talk to patients about it as though it is a life extender, but it seems to help control pain—about 70% of patients benefited in terms of pain or some other cancer-related symptom.¹⁴

I have a lot of patients who say, “Never will I do chemotherapy.” I refer those patients to hospice, or if they’re appropriate for radium-223, I consider that. I typically give about 6 cycles of chemotherapy and then see how they’re doing. In some patients, the cancer just doesn’t respond to it.

I do tell patients about the papers that you mentioned, the 2 studies of docetaxel vs mitoxantrone where they use about 10 cycles, and some of my patients go all 10.^14,15 Sometimes we have to stop because of neuropathy or some other AE. I believe in taking breaks and that you can probably start it later.

Elizabeth Hansen. I agree, our practice is similar. A lot of our patients are not very interested in chemotherapy. You have to take into consideration their ECOG (Eastern Cooperative Oncology Group) status, their goals, and quality of life when talking to them about these medications. And a lot of them tend to choose more of a palliative route. Depending on their AEs and how things are going, we will dose reduce, hold treatment, or give treatment holidays.

Mark Klein. If patients are progressing on docetaxel, what are options that people would use? Radium-223 certainly is available for patients with nonvisceral metastases, as well as cabazitaxel, mitoxantrone, estramustine and other older drugs.

Julie Graff. We have some clinical trials for patients postdocetaxel. We have the TRITON2 and TRITON3 studies open at the VA. (NCT02952534 and NCT02975934, respectively) A lot of patients would get a biopsy, and we’d look for a BRCA 1 or 2 and ATM mutation. For those patients who don’t have those mutations—and maybe 80% of them don’t—we talk about radium-223 for the patients without visceral metastases and bone pain. I have had a fair number of patients go on cabazitaxel, but I have not used mitoxantrone since cabazitaxel came out. It’s not off the table, but it hasn’t shown improvement in survival.

Elizabeth Hansen. One of our challenges, because we’re an ambulatory care center, is that we are unable to give radium-223 in house, and these services have to be sent out to a non-VA facility. It is doable, but it takes more legwork and organization on our part.

Julie Graff. We have not had radium-223, although we’re working to get that online. And we are physically connected to Oregon Health Science University (OHSU), so we send our patients there for radium. It is a pain because the doctors at OHSU don’t have CPRS access. I’m often in the middle of making sure the complete blood counts (CBCs) are sent to OHSU and to get my patients their treatments.

Mark Klein. The Minneapolis VAMC has radium-223 on site, and we have used it for patients whose cancer has progressed while on docetaxel without visceral metastases. Katie, have you had an opportunity to coordinate that care for patients?

Kathleen Nelson. Radium is administered at our facility by one of our nuclear medicine physicians. A complete blood count is checked at least 3 days prior to the infusion date but no sooner than 6 days. Due to the cost of the material, ordering without knowing the patient’s counts are within a safe range to administer is prohibitive. This adds an additional burden of 2 visits (lab with return visit) to the patient. We have treated 12 patients. Four patients stopped treatment prior to completing the 6 planned treatments citing debilitating fatigue and/or nonresolution of symptoms as their reason to stop treatment. One patient died. The 7 remaining patients subjectively reported varying degrees of pain relief.

Elizabeth Hansen. Another thing to mention is the lack of a PSA response from radium-223 as well. Patients are generally very diligent about monitoring their PSA, so this can be a bit distressing.

Mark Klein. Julie, have you noticed a PSA flare with radium-223? I know it has been reported.

Julie Graff. I haven’t. But I put little stock in PSAs in these patients. I spend 20 minutes explaining to patients that the PSA is not helpful in determining whether or not the radium is working. I tell them that the bone marker alkaline phosphatase may decrease. And I think it’s important to note, too, that radium-223 is not a treatment we have on the shelf. We order it from Denver I believe. It is weight based, and it takes 5 days to get.

Clinical Trials

Mark Klein. That leads us into clinical trials. What is the role for precision oncology in prostate cancer right now, specifically looking at particular panels? One would be the DNA repair enzyme-based genes and/or also the AR variants and any other markers.

Elizabeth Hansen. The National Comprehensive Cancer Network came out with a statement recommending germ-line and somatic-mutation testing in all patients with metastatic prostate cancer. This highlights the need to offer patients the availability of clinical trials.

Julie Graff. I agree. We occasionally get to a place in the disease where patients are feeling fine, but we don’t have anything else to offer. The studies by Robinson¹⁶ and then Matteo¹⁷ showed that (a) these DNA repair defects are present in about a quarter of patients; and (b) that PARP inhibitors can help these patients. At least it has an anticancer effect.

What’s interesting is that we have TRITON2, and TRITON3, which are sponsored by Clovis,for patients with BRCA 1/2 and ATM mutations and using the PARP-inhibitor rucaparib. Based on the data we have available, we thought a quarter of patients would have the mutation in the tumor, but they’re finding that it is more like 10% to 15%. They are screening many patients but not finding it.

I agree that clinical trials are the way to go. I am hopeful that we’ll get more treatments based on molecular markers. The approval for pembrolizumab in any tumor type with microsatellite instability is interesting, but in prostate cancer, I believe that’s about 3%. I haven’t seen anyone qualify for pembrolizumab based on that. Another plug for clinical trials: Let’s learn more and offer our patients potentially beneficial treatments earlier.

Mark Klein. The first interim analysis from the TRITON2 study found about 12% of patients had alterations in BRCA 1/2. But in those that met the RECIST criteria, they were able to have evaluable disease via that standard with about a 44% response rate so far and a 51% PSA response rate. It is promising data, but it’s only 85 patients so far. We’ll know more because the TRITON2 study is of a more pretreated population than the TRITION3 study at this point. Are there any data on precision medicine and radiation in prostate cancer?

Abhishek Solanki. In the prostate cancer setting, there are not a lot of emerging data specifically looking at using precision oncology biomarkers to help guide decisions in radiation therapy. For example, genomic classifiers, like GenomeDx Decipher (Vancouver, BC) and Myriad Genetics Prolaris (Salt Lake City, UT) are increasingly being utilized in patients with localized disease. Decipher can help predict the risk of recurrence after radical prostatectomy. The difficulty is that there are limited data that show that by using these genomic classifiers, one can improve outcomes in patients over traditional clinical characteristics.

There are 2 trials currently ongoing through NRG Oncology that are using Decipher. The GU002 is a trial for patients who had a radical prostatectomy and had a postoperative PSA that never nadired below 0.2. These patients are randomized between salvage radiation with hormone therapy with or without docetaxel. This trial is collecting Decipher results for patients enrolled in the study. The GU006 is a trial for a slightly more favorable group of patients who do nadir but still have biochemical recurrence and relatively low PSAs. This trial randomizes between radiotherapy alone and radiotherapy and 6 months of apalutamide, stratifying patients based on Decipher results, specially differentiating between patients who have a luminal vs basal subtype of prostate cancer. There are data that suggest that patients who have a luminal subtype may benefit more from the combination of radiation and hormone therapy vs patients who have basal subtype.¹⁸ However this hasn’t been validated in a prospective setting, and that’s what this trial will hopefully do.

Immunotherapies

Mark Klein. Outside of prostate cancer, there has been a lot of research trying to determine how to improve PD-L1 expression. Where are immunotherapy trials moving? How radiation might play a role in conjunction with immunotherapy.

Julie Graff. Two phase 3 studies did not show statistically improved survival or statistically significant survival improvement on ipilimumab, an immunotherapy agent that targets CTLA4. Some early studies of the PD-1 drugs nivolumab and pembrolizumab did not show much response with monotherapy. Despite the negative phase 3 studies for ipilimumab, we periodically see exceptional responses.

In prostate cancer, enzalutamide is FDA approved. And there’s currently a phase 3 study of the PD-L1 inhibitor atezolizumab plus enzalutamide in patients who have progressed on abiraterone. That trial is fully accrued, but the results are not yet known. Soon a study will compare pembrolizumab plus enzalutamide vs enzalutamide alone. So the combinations are getting more interesting.

I just received a Prostate Cancer Foundation Challenge Award to open a VA-only study looking at fecal microbiota transplant from responders to nonresponders to see how manipulating host factors can increase potential responses to PD-1 inhibition.

Abhishek Solanki. The classic mechanism by which radiation therapy works is direct DNA damage and indirect DNA damage through hydroxyl radicals that leads to cytotoxicity. But preclinical and clinical data suggest that radiation therapy can augment the local and systemic immunotherapy response. The radiation oncologist’s dream is what is called the abscopal effect, which is the idea that when you treat one site of disease with radiation, it can induce a response at other sites that didn’t get radiation therapy through reactivation of the immune system. I like to think of the abscopal effect like bigfoot—it’s elusive. However, it seems that the setting it is most likely to happen in is in combination with immunotherapy.

One of the ways that radiation fails locally is that it can upregulate PD-1 expression, and as a result, you can have progression of the tumor because of local immune suppression. We know that T cells are important for the activity of radiation therapy. If you combine checkpoint inhibition with radiation therapy, you can not only have better local control in the area of the tumor, but perhaps you can release tumor antigens that will then induce a systemic response.

The other potential mechanism by which radiation may work synergistically with immunotherapy is as a debulking agent. There are some data that suggest that the ratio of T-cell reinvigoration to bulk of disease, or the volume of tumor burden, is important. That is, having T-cell reinvigoration may not be sufficient to have a response to immunotherapy in patients with a large burden of disease. By using radiation to debulk disease, perhaps you could help make checkpoint inhibition more effective. Ultimately, in the setting of prostate cancer, there are not a lot of data yet showing meaningful benefits with the combination of immunotherapy and radiotherapy, but there are trials that are ongoing that will educate on potential synergy.

Pharmacy

Julie Graff. Before we end I want to make sure that we applaud the amazing pharmacists and patient care navigation teams in the VA who do such a great job of getting veterans the appropriate treatment expeditiously and keeping them safe. It’s something that is truly unique to the VA. And I want to thank the people on this call who do this every day.

Elizabeth Hansen. Thank you Julie. Compared with working in the community, at the VA I’m honestly amazed by the ease of access to these medications for our patients. Being able to deliver medications sometimes the same day to the patient is just not something that happens in the community. It’s nice to see that our veterans are getting cared for in that manner.

Author disclosures
Dr. Solanki participated in advisory boards for Blue Earth Diagnostics’ fluciclovine PET and was previously paid as a consultant. Dr. Graff is a consultant for Sanofi (docetaxel) and Astellas (enzalutamide), and has received research funding (no personal funding)from Sanofi, Merck (pembrolizumab), Astellas, and Jannsen (abiraterone, apalutamide). The other authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the US Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

Sequencing Therapies

Mark Klein, MD. The last few years, there have been several new trials in prostate cancer for people in a metastatic setting or more advanced local setting, such as the STAMPEDE, LATITUDE, and CHAARTED trials.^1-4 In addition, recently a few trials have examined apalutamide and enzalutamide for people who have had PSA (prostate-specific antigen) levels rapidly rising within about 10 months or so. One of the questions that arises is, how do we wrap our heads around sequencing these therapies. Is there a sequence that we should be doing and thinking about upfront and how do the different trials compare?

Julie Graff, MD. It just got more complicated. There was news today (December 20, 2018) that using enzalutamide early on in newly diagnosed metastatic prostate cancer may have positive results. It is not yet approved by the US Food and Drug Administration (FDA), but for patients who present with metastatic prostate cancer, we may have 4 potential treatments. We could have androgen deprivation therapy (ADT) alone, ADT plus docetaxel, enzalutamide, or abiraterone.

When I see patients in this situation, I talk to them about their options, the pros and cons of each option, and try to cover all the trials that look at these combinations. It can be quite a long visit. I talk to the patient about who benefits most, whether it is patients with high-risk factors or high-volume cancers. Also, I talk with the patient about all the adverse effects (AEs), and I look at my patients’ comorbid conditions and come up with a plan.

I encourage any patient who has high-volume or high-risk disease to consider more than just ADT alone. For many patients, I have been using abiraterone plus ADT. I have a wonderful pharmacist. As a medical oncologist, I can’t do it on my own. I need someone to follow patients’ laboratory results and to be available for medication questions and complications.

Elizabeth Hansen, PharmD. With the increasing number of patients on oral antineoplastics, monitoring patients in the outpatient setting has become an increasing priority and one of my major roles as a pharmacist in the clinic at the Chalmers P. Wylie VA Ambulatory Care Center in Columbus, Ohio. This is especially important as some of these treatments require frequent laboratory monitoring, such as abiraterone with liver function tests every 2 weeks for the first 3 months of treatment and monthly thereafter. Without frequent-follow up it’s easy for these patients to get lost in the shuffle.

Abhishek Solanki, MD. You could argue that a fifth option is prostate-directed radiation for patients who have limited metastases based on the STAMPEDE trial, which we’ve started integrating into our practice at the Edward Hines, Jr. Veterans Affairs Hospital in Chicago, Illinois.⁴

Mark Klein. Do you have a feel for the data and using radiation in oligometastatic (≤ 5 metastatic tumors) disease in prostate cancer and how well that might work?

Abhishek Solanki. The best data we have are from the multi-arm, multistage STAMPEDE trial systemic therapies and local therapy in the setting of high-risk localized disease and metastatic disease.⁶ The most recent publication looked specifically at the population with newly diagnosed metastatic disease and compared standard ADT (and docetaxel in about 18% of the patients) with or without prostate-directed radiation therapy. There was no survival benefit with radiation in the overall population, but in the subgroup of patients with low metastatic burden, there was an 8% survival benefit at 3 years.

It’s difficult to know what to make of that information because, as we’ve discussed already, there are other systemic therapy options that are being used more and more upfront such as abiraterone. Can you see the same benefit of radiation in that setting? The flip side is that in this study, radiation just targeted the prostate; could survival be improved even more by targeting all sites of disease in patients with oligometastatic disease? These are still open questions in prostate cancer and there are clinical trials attempting to define the clinical benefit of radiation in the metastatic setting for patients with limited metastases.

Mark Klein. How do you select patients for radiation in this particular situation; How do you approach stratification when radiation is started upfront?

Abhishek Solanki. In the STAMPEDE trial, low metastatic burden was defined based on the definition in the CHAARTED trial, which was those patients who did not have ≥ 4 bone metastases with ≥ 1 outside the vertebral bodies or pelvis, and did not have visceral metastases.⁷ That’s tough, because this definition could be a patient with a solitary bone metastasis but also could include some patients who have involved nodes extending all the way up to the retroperitoneal nodes—that is a fairly heterogeneous population. What we have done at our institution is select patients who have 3 to 5 metastases, administer prostate radiation therapy, and add stereotactic body radiation therapy (SBRT) for the other sites of disease, invoking the oligometastasis approach.

We have been doing this more frequently in the last few months. Typically, we’ll do 3 to 5 fractions of SBRT to metastases. For the primary, if the patient chooses SBRT, we’ll take that approach. If the patient chooses a more standard fractionation, we’ll do 20 treatments, but from a logistic perspective, most patients would rather come in for 5 treatments than 20. We also typically would start these patients on systemic hormonal therapy.

Mark Klein. At that point, are they referred back to medical oncology for surveillance?

Abhishek Solanki. Yes, they are followed by medical oncology and radiation oncology, and typically would continue hormonal therapy.

Mark Klein. Julie, how have you thought about presenting the therapeutic options for those patients who would be either eligible for docetaxel with high-bulk disease or abiraterone? Do you find patients prefer one or the other?

Julie Graff. I try to be very open about all the possibilities, and I present both. I don’t just decide for the patient chemotherapy vs abiraterone, but after we talk about it, most of my patients do opt for the abiraterone. I had a patient referred from the community—we are seeing more and more of this because abiraterone is so expensive—whose ejection fraction was about 38%. I said to that patient, “we could do chemotherapy, but we shouldn’t do abiraterone.” But usually it’s not that clear-cut.

Elizabeth Hansen. There was also an update from the STAMPEDE trial published recently comparing upfront abiraterone and prednisone to docetaxel (18 weeks) in advanced or metastatic prostate cancer. Results from this trial indicated a nearly identical overall survival (OS) (hazard ratio [HR] = 1.16; 95% CI, 0.82-1.65; P = .40). However, the failure-free survival (HR = 0.51; 95% CI, 0.39-0.67; P < .001) and progression-free survival (PFS) (HR= 0.65; 95% CI, 0.0.48-0.88; P = .005) favored abiraterone.^8,9 The authors argue that while there was no change in OS, this trial demonstrates an important difference in the pattern of treatment failure.

Julie, do you think there will be any change in the treatment paradigm between docetaxel and abiraterone with this new update?

Julie Graff. I wasn’t that impressed by that study. I do not see it as practice changing, and it makes sense to me that the PFS is different in the 2 arms because we give chemotherapy and take a break vs giving abiraterone indefinitely. For me, there’s not really a shift.

Patients With Rising PSAs

Mark Klein. Let’s discuss the data from the recent studies on enzalutamide and apalutamide for the patients with fast-rising PSAs. In your discussions with other prostate researchers, will this become a standard part of practice or not?

Julie Graff. I was one of the authors on the SPARTAN apalutamide study.¹⁰ For a long time, we have had patients without metastatic disease but with a PSA relapse after surgery or radiation; and the PSA levels climb when the cancer becomes resistant to ADT. We haven’t had many options in that setting except to use bicalutamide and some older androgen receptor (AR) antagonists. We used to use estrogen and ketoconazole as well.

But now 2 studies have come out looking at a primary endpoint of metastases-free survival. Patients whose PSA was doubling every 10 months or shorter were randomized to either apalutamide (SPARTAN¹⁰) or enzalutamide (PROSPER¹¹), both second-generation AR antagonists. There was a placebo control arm in each of the studies. Both studies found that adding the second-generation AR targeting agent delayed the time to metastatic disease by about 2 years. There is not any signal yet for statistically significant OS benefit, so it is not entirely clear if you could wait for the first metastasis to develop and then give 1 of these treatments and have the same OS benefit.

At the VA Portland Health Care System (VAPORHCS), it took a while to make these drugs available. My fellows were excited to give these drugs right away, but I often counsel patients that we don’t know if the second-generation AR targeting agents will improve survival. They almost certainly will bring down PSAs, which helps with peace of mind, but anything we add to the ADT can cause more AEs.

I have been cautious with second-generation AR antagonists because patients, when they take one of these drugs, are going to be on it for a long time. The FDA has approved those 2 drugs regardless of PSA doubling time, but I would not give it for a PSA doubling time > 10 months. In my practice about a quarter of patients who would qualify for apalutamide or enzalutamide are actually taking one, and the others are monitored closely with computed tomography (CT) and bone scans. When the disease becomes metastatic, then we start those drugs.

Mark Klein. Why 10 months, why not 6 months, a year, or 18 months? Is there reasoning behind that?

Julie Graff. There was a publication by Matthew Smith showing that the PSA doubling time was predictive of the development of metastatic disease and cancer death or prostate cancer death, and that 10 months seemed to be the cutoff between when the prostate cancer was going to become deadly vs not.¹² If you actually look at the trial data, I think the PSA doubling time was between 3 and 4 months for the participants, so pretty short.

Adverse Effects

Mark Klein. What are the AEs people are seeing from using apalutamide, enzalutamide, and abiraterone? What are they seeing in their practice vs what is in the studies? When I have had to stop people on abiraterone or drop down the dose, almost always it has been for fatigue. We check liver function tests (LFTs) repeatedly, but I can’t remember ever having to drop down the dose or take it away even for that reason.

Elizabeth Hansen. The toxicities of these 3 agents are very different. In my practice I have seen a few patients develop hepatotoxicity with abiraterone, and I think this reflects the known incidence of transaminitis (grade 3/4) seen in clinical trials, reported at 6%. Generally, we’ve been able to restart treatment by withholding abiraterone until liver function returns to baseline and then subsequently dose reducing. Like Julie mentioned, abiraterone should be used with caution and/or avoided in patients with serious cardiac disease, recent myocardial infarction, or heart failure. I also always check blood pressure history, to ensure it is well controlled prior to initiation, and order a home blood pressure cuff for monitoring. With enzalutamide one of the main concerns is fatigue, which occurred in > 10% of patients in clinical trials. In my experience this has been dose limiting and can be managed with dose reductions. Seizures also occurred in 0.4% of patients on enzalutamide, so I always ask about seizure history and screen the medication list for concomitant medications that may lower the seizure threshold or other risk factors such as brain metastasis. Last, enzalutamide is a strong CYP3A4 inducer, so there is a strong possibility for drug interactions with other medications, and it is associated with increased cardiac events. With apalutamide you have the cardiac concerns, thyroid dysfunction, fracture risk, and drug interactions to worry about as well. To be honest, we have not used this agent yet at my practice.

Mark Klein. At the Minneapolis VA Health Care System (MVAHCS) when apalutamide first came out, for the PSA rapid doubling, there had already been an abstract presenting the enzalutamide data. We have chosen to recommend enzalutamide as our choice for the people with PSA doubling based on the cost. It’s significantly cheaper for the VA. Between the 2 papers there is very little difference in the efficacy data. I’m wondering what other sites have done with regard to that specific point at their VAs?

Elizabeth Hansen. In Columbus, we prefer to use either abiraterone and enzalutamide because they’re essentially cost neutral. However, this may change with generic abiraterone coming to market. Apalutamide is really cost prohibitive currently.

Julie Graff. I agree.

Patient Education

Mark Klein. At MVAHCS, the navigators handle a lot of upfront education. We have 3 navigators, including Kathleen Nelson who is on this roundtable. She works with patients and provides much of the patient education. How have you handled education for patients?

Kathleen Nelson. For the most part, our pharmacists do the drug-specific education for the oral agents, and the nurse navigators provide more generic education. We did a trial for patients on IV therapies. We learned that patients really don’t report in much detail, but if you call and ask them specific questions, then you can tease out some more detail.

Elizabeth Hansen. It is interesting that every site is different. One of my main roles is oral antineoplastic monitoring, which includes many patients on enzalutamide or abiraterone. At least initially with these patients, I try to follow them closely—abiraterone more so than enzalutamide. I typically call every 2 to 4 weeks, in between clinic visits, to follow up the laboratory tests and manage the AEs. I always try to ask direct and open-ended questions: How often are you checking your blood pressure? What is your current weight? How has your energy level changed since therapy initiation?

The VA telehealth system is amazing. For patients who need to monitor blood pressure regularly, it’s really nice for them to have those numbers come directly back to me in CPRS (Computerized Patient Record System). That has worked wonders for some of our patients to get them through therapy.

Mark Klein. What do you tend to use when the prostate cancer is progressing for a patient? And how do you determine that progression? Some studies will use PSA rise only as a marker for progression. Other studies have not used PSA rise as the only marker for progression and oftentimes require some sort of bone scan criteria or CT imaging criteria for progression.

Julie Graff. We have a limited number of treatment options. Providers typically use enzalutamide or abiraterone as there is a high degree of resistance between the 2. Then there is chemotherapy and then radium, which quite a few people don’t qualify for. We need to be very thoughtful when we change treatments. I look at the 3 factors of biochemical progression or response—PSA, radiographic progression, and clinical progression. If I don’t see 2 out of 3, I typically don’t change treatments. Then after enzalutamide or abiraterone, I wait until there are cancer-related symptoms before I consider chemotherapy and closely monitor my patients.

Imaging Modalities

Abhishek Solanki. Over the last few years the Hines VA Hospital has used fluciclovine positron emission tomography (PET), which is one of the novel imaging modalities for prostate cancer. Really the 2 novel imaging modalities that have gained the most excitement are prostate-specific membrane antigen (PSMA) PET and fluciclovine PET. Fluciclovine PET is based on a synthetic amino acid that’s taken up in multiple tissues, including prostate cancer. It has changed our practice in the localized setting for patients who have developed recurrence after radiation or radical prostatectomy. We have incorporated the scan into our workup of patients with recurrent disease, which can give us some more information at lower PSAs than historically we could get with CT, bone scan, or magnetic resonance imaging.

Our medical oncologists have started using it more and more as well. We are getting a lot of patients who have a negative CT or bone scan but have a positive fluciclovine PET. There are a few different disease settings where that becomes relevant. In patients who develop biochemical recurrence after radiation or salvage radiation after radical, we are finding that a lot of these patients who have no CT or bone scan findings of disease ultimately are found to have a PET-positive lesion. Sometimes it’s difficult to know how best to help patients with PET-only disease. Should you target the disease with an oligometastasis approach or just pursue systemic therapy or surveillance? It is challenging but more and more we are moving toward metastasis-directed therapy. There are multiple randomized trials in progress testing whether metastasis-directed therapy to the PET areas of recurrence can improve outcomes or delay systemic ADT. The STOMP trial randomized surveillance vs SBRT or surgery for patients with oligometastatic disease that showed improvement in biochemical control and ADT-free survival.¹³ However this was a small trial that tried to identify a signal. More definitive trials are necessary.

The other setting where we have found novel PET imaging to be helpful is in patients who have become castration resistant but don’t have clear metastases on conventional imaging. We’re identifying more patients who have only a few sites of progression, and we’ll pursue metastasis-directed therapy to those areas to try to get more mileage out of the systemic therapy that the patient is currently on and to try to avoid having to switch to the next line with the idea that, potentially, the progression site is just a limited clone that is progressing despite the current systemic therapy.
 

Mark Klein. I find that to be a very attractive approach. I’m assuming you do that for any systemic therapy where people have maybe 1 or 2 sites and they do not have a big PSA jump. Do you have a number of sites that you’re willing to radiate? And then, when you do that, what radiation fractionation and dosing do you use? Is there any observational data behind that for efficacy?

Abhishek Solanki. It is a patient by patient decision. Some patients, if they have a very rapid pace of progression shortly after starting systemic therapy and metastases have grown in several areas, we think that perhaps this person may benefit less from aggressive local therapy. But if it’s somebody who has been on systemic therapy for a while and has up to 3 sites of disease growth, we consider SBRT for oligoprogressive disease. Typically, we’ll use SBRT, which delivers a high dose of radiation over 3 to 5 treatments. With SBRT you can give a higher biologic dose and use more sophisticated treatment machines and image guidance for treatments to focus the radiation on the tumor area and limit exposure to normal tissue structures.

In prostate cancer to the primary site, we will typically do around 35 to 40 Gy in 5 fractions. For metastases, it depends on the site. If it’s in the lung, typically we will do 3 to 5 treatments, giving approximately 50 to 60 Gy in that course. In the spine, we use lower doses near the spinal cord and the cauda equina, typically about 30 Gy in 3 fractions. In the liver, similar to the lung, we’ll typically do 50-54 Gy in 3-5 fractions. There aren’t a lot of high-level data guiding the optimal dose/fractionation to metastases, but these are the doses we’ll use for various malignancies.

Treatment Options for Patients With Adverse Events

Mark Klein. I was just reviewing the 2004 study that randomized patients to mitoxantrone or docetaxel for up to 10 cycles.^14,15 Who are good candidates for docetaxel after they have exhausted abiraterone and enzalutamide? How long do you hold to the 10-cycle rule, or do you go beyond that if they’re doing well? And if they’re not a good candidate, what are some options?

Julie Graff. The best candidates are those who are having a cancer-related AE, particularly pain, because docetaxel only improves survival over mitoxantrone by about 2.5 months. I don’t talk to patients about it as though it is a life extender, but it seems to help control pain—about 70% of patients benefited in terms of pain or some other cancer-related symptom.¹⁴

I have a lot of patients who say, “Never will I do chemotherapy.” I refer those patients to hospice, or if they’re appropriate for radium-223, I consider that. I typically give about 6 cycles of chemotherapy and then see how they’re doing. In some patients, the cancer just doesn’t respond to it.

I do tell patients about the papers that you mentioned, the 2 studies of docetaxel vs mitoxantrone where they use about 10 cycles, and some of my patients go all 10.^14,15 Sometimes we have to stop because of neuropathy or some other AE. I believe in taking breaks and that you can probably start it later.

Elizabeth Hansen. I agree, our practice is similar. A lot of our patients are not very interested in chemotherapy. You have to take into consideration their ECOG (Eastern Cooperative Oncology Group) status, their goals, and quality of life when talking to them about these medications. And a lot of them tend to choose more of a palliative route. Depending on their AEs and how things are going, we will dose reduce, hold treatment, or give treatment holidays.

Mark Klein. If patients are progressing on docetaxel, what are options that people would use? Radium-223 certainly is available for patients with nonvisceral metastases, as well as cabazitaxel, mitoxantrone, estramustine and other older drugs.

Julie Graff. We have some clinical trials for patients postdocetaxel. We have the TRITON2 and TRITON3 studies open at the VA. (NCT02952534 and NCT02975934, respectively) A lot of patients would get a biopsy, and we’d look for a BRCA 1 or 2 and ATM mutation. For those patients who don’t have those mutations—and maybe 80% of them don’t—we talk about radium-223 for the patients without visceral metastases and bone pain. I have had a fair number of patients go on cabazitaxel, but I have not used mitoxantrone since cabazitaxel came out. It’s not off the table, but it hasn’t shown improvement in survival.

Elizabeth Hansen. One of our challenges, because we’re an ambulatory care center, is that we are unable to give radium-223 in house, and these services have to be sent out to a non-VA facility. It is doable, but it takes more legwork and organization on our part.

Julie Graff. We have not had radium-223, although we’re working to get that online. And we are physically connected to Oregon Health Science University (OHSU), so we send our patients there for radium. It is a pain because the doctors at OHSU don’t have CPRS access. I’m often in the middle of making sure the complete blood counts (CBCs) are sent to OHSU and to get my patients their treatments.

Mark Klein. The Minneapolis VAMC has radium-223 on site, and we have used it for patients whose cancer has progressed while on docetaxel without visceral metastases. Katie, have you had an opportunity to coordinate that care for patients?

Kathleen Nelson. Radium is administered at our facility by one of our nuclear medicine physicians. A complete blood count is checked at least 3 days prior to the infusion date but no sooner than 6 days. Due to the cost of the material, ordering without knowing the patient’s counts are within a safe range to administer is prohibitive. This adds an additional burden of 2 visits (lab with return visit) to the patient. We have treated 12 patients. Four patients stopped treatment prior to completing the 6 planned treatments citing debilitating fatigue and/or nonresolution of symptoms as their reason to stop treatment. One patient died. The 7 remaining patients subjectively reported varying degrees of pain relief.

Elizabeth Hansen. Another thing to mention is the lack of a PSA response from radium-223 as well. Patients are generally very diligent about monitoring their PSA, so this can be a bit distressing.

Mark Klein. Julie, have you noticed a PSA flare with radium-223? I know it has been reported.

Julie Graff. I haven’t. But I put little stock in PSAs in these patients. I spend 20 minutes explaining to patients that the PSA is not helpful in determining whether or not the radium is working. I tell them that the bone marker alkaline phosphatase may decrease. And I think it’s important to note, too, that radium-223 is not a treatment we have on the shelf. We order it from Denver I believe. It is weight based, and it takes 5 days to get.

Clinical Trials

Mark Klein. That leads us into clinical trials. What is the role for precision oncology in prostate cancer right now, specifically looking at particular panels? One would be the DNA repair enzyme-based genes and/or also the AR variants and any other markers.

Elizabeth Hansen. The National Comprehensive Cancer Network came out with a statement recommending germ-line and somatic-mutation testing in all patients with metastatic prostate cancer. This highlights the need to offer patients the availability of clinical trials.

Julie Graff. I agree. We occasionally get to a place in the disease where patients are feeling fine, but we don’t have anything else to offer. The studies by Robinson¹⁶ and then Matteo¹⁷ showed that (a) these DNA repair defects are present in about a quarter of patients; and (b) that PARP inhibitors can help these patients. At least it has an anticancer effect.

What’s interesting is that we have TRITON2, and TRITON3, which are sponsored by Clovis,for patients with BRCA 1/2 and ATM mutations and using the PARP-inhibitor rucaparib. Based on the data we have available, we thought a quarter of patients would have the mutation in the tumor, but they’re finding that it is more like 10% to 15%. They are screening many patients but not finding it.

I agree that clinical trials are the way to go. I am hopeful that we’ll get more treatments based on molecular markers. The approval for pembrolizumab in any tumor type with microsatellite instability is interesting, but in prostate cancer, I believe that’s about 3%. I haven’t seen anyone qualify for pembrolizumab based on that. Another plug for clinical trials: Let’s learn more and offer our patients potentially beneficial treatments earlier.

Mark Klein. The first interim analysis from the TRITON2 study found about 12% of patients had alterations in BRCA 1/2. But in those that met the RECIST criteria, they were able to have evaluable disease via that standard with about a 44% response rate so far and a 51% PSA response rate. It is promising data, but it’s only 85 patients so far. We’ll know more because the TRITON2 study is of a more pretreated population than the TRITION3 study at this point. Are there any data on precision medicine and radiation in prostate cancer?

Abhishek Solanki. In the prostate cancer setting, there are not a lot of emerging data specifically looking at using precision oncology biomarkers to help guide decisions in radiation therapy. For example, genomic classifiers, like GenomeDx Decipher (Vancouver, BC) and Myriad Genetics Prolaris (Salt Lake City, UT) are increasingly being utilized in patients with localized disease. Decipher can help predict the risk of recurrence after radical prostatectomy. The difficulty is that there are limited data that show that by using these genomic classifiers, one can improve outcomes in patients over traditional clinical characteristics.

There are 2 trials currently ongoing through NRG Oncology that are using Decipher. The GU002 is a trial for patients who had a radical prostatectomy and had a postoperative PSA that never nadired below 0.2. These patients are randomized between salvage radiation with hormone therapy with or without docetaxel. This trial is collecting Decipher results for patients enrolled in the study. The GU006 is a trial for a slightly more favorable group of patients who do nadir but still have biochemical recurrence and relatively low PSAs. This trial randomizes between radiotherapy alone and radiotherapy and 6 months of apalutamide, stratifying patients based on Decipher results, specially differentiating between patients who have a luminal vs basal subtype of prostate cancer. There are data that suggest that patients who have a luminal subtype may benefit more from the combination of radiation and hormone therapy vs patients who have basal subtype.¹⁸ However this hasn’t been validated in a prospective setting, and that’s what this trial will hopefully do.

Immunotherapies

Mark Klein. Outside of prostate cancer, there has been a lot of research trying to determine how to improve PD-L1 expression. Where are immunotherapy trials moving? How radiation might play a role in conjunction with immunotherapy.

Julie Graff. Two phase 3 studies did not show statistically improved survival or statistically significant survival improvement on ipilimumab, an immunotherapy agent that targets CTLA4. Some early studies of the PD-1 drugs nivolumab and pembrolizumab did not show much response with monotherapy. Despite the negative phase 3 studies for ipilimumab, we periodically see exceptional responses.

In prostate cancer, enzalutamide is FDA approved. And there’s currently a phase 3 study of the PD-L1 inhibitor atezolizumab plus enzalutamide in patients who have progressed on abiraterone. That trial is fully accrued, but the results are not yet known. Soon a study will compare pembrolizumab plus enzalutamide vs enzalutamide alone. So the combinations are getting more interesting.

I just received a Prostate Cancer Foundation Challenge Award to open a VA-only study looking at fecal microbiota transplant from responders to nonresponders to see how manipulating host factors can increase potential responses to PD-1 inhibition.

Abhishek Solanki. The classic mechanism by which radiation therapy works is direct DNA damage and indirect DNA damage through hydroxyl radicals that leads to cytotoxicity. But preclinical and clinical data suggest that radiation therapy can augment the local and systemic immunotherapy response. The radiation oncologist’s dream is what is called the abscopal effect, which is the idea that when you treat one site of disease with radiation, it can induce a response at other sites that didn’t get radiation therapy through reactivation of the immune system. I like to think of the abscopal effect like bigfoot—it’s elusive. However, it seems that the setting it is most likely to happen in is in combination with immunotherapy.

One of the ways that radiation fails locally is that it can upregulate PD-1 expression, and as a result, you can have progression of the tumor because of local immune suppression. We know that T cells are important for the activity of radiation therapy. If you combine checkpoint inhibition with radiation therapy, you can not only have better local control in the area of the tumor, but perhaps you can release tumor antigens that will then induce a systemic response.

The other potential mechanism by which radiation may work synergistically with immunotherapy is as a debulking agent. There are some data that suggest that the ratio of T-cell reinvigoration to bulk of disease, or the volume of tumor burden, is important. That is, having T-cell reinvigoration may not be sufficient to have a response to immunotherapy in patients with a large burden of disease. By using radiation to debulk disease, perhaps you could help make checkpoint inhibition more effective. Ultimately, in the setting of prostate cancer, there are not a lot of data yet showing meaningful benefits with the combination of immunotherapy and radiotherapy, but there are trials that are ongoing that will educate on potential synergy.

Pharmacy

Julie Graff. Before we end I want to make sure that we applaud the amazing pharmacists and patient care navigation teams in the VA who do such a great job of getting veterans the appropriate treatment expeditiously and keeping them safe. It’s something that is truly unique to the VA. And I want to thank the people on this call who do this every day.

Elizabeth Hansen. Thank you Julie. Compared with working in the community, at the VA I’m honestly amazed by the ease of access to these medications for our patients. Being able to deliver medications sometimes the same day to the patient is just not something that happens in the community. It’s nice to see that our veterans are getting cared for in that manner.

Author disclosures
Dr. Solanki participated in advisory boards for Blue Earth Diagnostics’ fluciclovine PET and was previously paid as a consultant. Dr. Graff is a consultant for Sanofi (docetaxel) and Astellas (enzalutamide), and has received research funding (no personal funding)from Sanofi, Merck (pembrolizumab), Astellas, and Jannsen (abiraterone, apalutamide). The other authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the US Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

The general public may have been led to believe that by decoding genes into their constituent parts, clinicians can prevent or predict serious illnesses and personalize treatment. While this may be true in some areas of medicine, such as oncology, using a pharmacogenetic testing-based “lookup table” to prescribe psychiatric medications is disturbing. This practice could lead to incorrect prescriptions, as well as a lack of follow-up or appropriate dosage titration or medication switching. These problems could put a patient’s life at risk and, consequently, bring the field of psychiatry into disrepute.

In the last few years, using pharmacogenetics to predict or prevent illness and personalize treatment has become very attractive. A 2019 meta-analysis of 5 randomized controlled trials examined the use of pharmacogenetic-guided decision support tools for major depressive disorder (MDD). Researchers randomized 1,737 participants with MDD to either pharmacogenetic-guided decision support tools or treatment as usual.¹ Patients were assessed using the Hamilton Depression Rating Scale–17 three times over 8 weeks. Compared with those who received treatment as usual, those who were managed using pharmacogenetic-guided decision support tools were more likely to achieve remission from depressive symptoms (relative risk = 1.71; 95% CI, 1.17 to 2.48; P = .005). However, these results are controversial because the included studies were industry-funded, and proprietary algorithms were used to interpret the results. (Editor's note: For more information about this study and pharma­cogenetic testing, see “Pharmacogenomics testing: What the FDA says,” Savvy Psychopharmacology, Current Psych­­iatry. April 2019, p. 29-33.)

In a policy statement on the use of pharmacogenetic testing in psychiatry, the International Society of Psychiatric Genetics (ISPG) explained that such testing should be viewed as a decision support tool to assist in implementing good clinical care, rather than as an alternative to standard protocols.² Furthermore, the ISPG stated that “common genetic variants are not sufficient to cause psychiatric disorders such as depression, bipolar disorder, substance dependence, or schizophrenia.”²

Some manufacturers have claimed that their pharmacogenetic tests can provide information on how a patient will respond to medications for treating depression and other conditions, and when a clinician can or should change a patient’s medication. However, the relationship between DNA variations and the effectiveness of antidepressant medications has not been established, and basing clinical decisions on the results of these tests may lead to inappropriate medication changes.

Pharmacogenetic tests are being advertised to both clinicians and patients, but the FDA has not approved the use of any test for providing information on a patient’s ability to respond to any specific medication.³ Therefore, psychiatrists should discuss the use of pharmacogenetic testing with their patients, and advise patients to avoid stopping or changing their medications based on the results of any pharmacogenetic test. Clinicians should not change a patient’s medication regimen solely based on the results of pharmacogenetic testing. These tests are not supported by scientific or clinical evidence, and using these tests for clinical decisions may put the patient at risk for potentially serious health consequences.

Aneela Jafri, MD, MS
Research Volunteer
Ocean Medical Center
Nutley, New Jersey

Ramon Solhkhah, MD
Founding Chair and Professor
Department of Psychiatry and Behavioral Health
Hackensack Meridian School of Medicine at Seton Hall University
Nutley, New Jersey
Chair
Department of Psychiatry
Jersey Shore University Medical Center
Neptune, New Jersey
Residency Training Director
General Psychiatry
Ocean Medical Center
Brick, New Jersey

Stacy Doumas, MD
Vice Chair
Associate Professor
Department of Psychiatry and Behavioral Health
Hackensack Meridian School of Medicine at Seton Hall University
Nutley, New Jersey
Vice Chair for Education & Research
Residency Training Director
General Psychiatry
Jersey Shore University Medical Center Neptune, New Jersey

Saba Afzal, MD
Assistant Professor
Department of Psychiatry and Behavioral Health
Hackensack Meridian School of Medicine at Seton Hall University
Nutley, New Jersey
Associate Residency Training Director General Psychiatry
Ocean Medical Center
Brick, New Jersey

Disclosures: The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

The general public may have been led to believe that by decoding genes into their constituent parts, clinicians can prevent or predict serious illnesses and personalize treatment. While this may be true in some areas of medicine, such as oncology, using a pharmacogenetic testing-based “lookup table” to prescribe psychiatric medications is disturbing. This practice could lead to incorrect prescriptions, as well as a lack of follow-up or appropriate dosage titration or medication switching. These problems could put a patient’s life at risk and, consequently, bring the field of psychiatry into disrepute.

In the last few years, using pharmacogenetics to predict or prevent illness and personalize treatment has become very attractive. A 2019 meta-analysis of 5 randomized controlled trials examined the use of pharmacogenetic-guided decision support tools for major depressive disorder (MDD). Researchers randomized 1,737 participants with MDD to either pharmacogenetic-guided decision support tools or treatment as usual.¹ Patients were assessed using the Hamilton Depression Rating Scale–17 three times over 8 weeks. Compared with those who received treatment as usual, those who were managed using pharmacogenetic-guided decision support tools were more likely to achieve remission from depressive symptoms (relative risk = 1.71; 95% CI, 1.17 to 2.48; P = .005). However, these results are controversial because the included studies were industry-funded, and proprietary algorithms were used to interpret the results. (Editor's note: For more information about this study and pharma­cogenetic testing, see “Pharmacogenomics testing: What the FDA says,” Savvy Psychopharmacology, Current Psych­­iatry. April 2019, p. 29-33.)

In a policy statement on the use of pharmacogenetic testing in psychiatry, the International Society of Psychiatric Genetics (ISPG) explained that such testing should be viewed as a decision support tool to assist in implementing good clinical care, rather than as an alternative to standard protocols.² Furthermore, the ISPG stated that “common genetic variants are not sufficient to cause psychiatric disorders such as depression, bipolar disorder, substance dependence, or schizophrenia.”²

Some manufacturers have claimed that their pharmacogenetic tests can provide information on how a patient will respond to medications for treating depression and other conditions, and when a clinician can or should change a patient’s medication. However, the relationship between DNA variations and the effectiveness of antidepressant medications has not been established, and basing clinical decisions on the results of these tests may lead to inappropriate medication changes.

Pharmacogenetic tests are being advertised to both clinicians and patients, but the FDA has not approved the use of any test for providing information on a patient’s ability to respond to any specific medication.³ Therefore, psychiatrists should discuss the use of pharmacogenetic testing with their patients, and advise patients to avoid stopping or changing their medications based on the results of any pharmacogenetic test. Clinicians should not change a patient’s medication regimen solely based on the results of pharmacogenetic testing. These tests are not supported by scientific or clinical evidence, and using these tests for clinical decisions may put the patient at risk for potentially serious health consequences.

Aneela Jafri, MD, MS
Research Volunteer
Ocean Medical Center
Nutley, New Jersey

Ramon Solhkhah, MD
Founding Chair and Professor
Department of Psychiatry and Behavioral Health
Hackensack Meridian School of Medicine at Seton Hall University
Nutley, New Jersey
Chair
Department of Psychiatry
Jersey Shore University Medical Center
Neptune, New Jersey
Residency Training Director
General Psychiatry
Ocean Medical Center
Brick, New Jersey

Stacy Doumas, MD
Vice Chair
Associate Professor
Department of Psychiatry and Behavioral Health
Hackensack Meridian School of Medicine at Seton Hall University
Nutley, New Jersey
Vice Chair for Education & Research
Residency Training Director
General Psychiatry
Jersey Shore University Medical Center Neptune, New Jersey

Saba Afzal, MD
Assistant Professor
Department of Psychiatry and Behavioral Health
Hackensack Meridian School of Medicine at Seton Hall University
Nutley, New Jersey
Associate Residency Training Director General Psychiatry
Ocean Medical Center
Brick, New Jersey

Disclosures: The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

The general public may have been led to believe that by decoding genes into their constituent parts, clinicians can prevent or predict serious illnesses and personalize treatment. While this may be true in some areas of medicine, such as oncology, using a pharmacogenetic testing-based “lookup table” to prescribe psychiatric medications is disturbing. This practice could lead to incorrect prescriptions, as well as a lack of follow-up or appropriate dosage titration or medication switching. These problems could put a patient’s life at risk and, consequently, bring the field of psychiatry into disrepute.

In the last few years, using pharmacogenetics to predict or prevent illness and personalize treatment has become very attractive. A 2019 meta-analysis of 5 randomized controlled trials examined the use of pharmacogenetic-guided decision support tools for major depressive disorder (MDD). Researchers randomized 1,737 participants with MDD to either pharmacogenetic-guided decision support tools or treatment as usual.¹ Patients were assessed using the Hamilton Depression Rating Scale–17 three times over 8 weeks. Compared with those who received treatment as usual, those who were managed using pharmacogenetic-guided decision support tools were more likely to achieve remission from depressive symptoms (relative risk = 1.71; 95% CI, 1.17 to 2.48; P = .005). However, these results are controversial because the included studies were industry-funded, and proprietary algorithms were used to interpret the results. (Editor's note: For more information about this study and pharma­cogenetic testing, see “Pharmacogenomics testing: What the FDA says,” Savvy Psychopharmacology, Current Psych­­iatry. April 2019, p. 29-33.)

In a policy statement on the use of pharmacogenetic testing in psychiatry, the International Society of Psychiatric Genetics (ISPG) explained that such testing should be viewed as a decision support tool to assist in implementing good clinical care, rather than as an alternative to standard protocols.² Furthermore, the ISPG stated that “common genetic variants are not sufficient to cause psychiatric disorders such as depression, bipolar disorder, substance dependence, or schizophrenia.”²

Some manufacturers have claimed that their pharmacogenetic tests can provide information on how a patient will respond to medications for treating depression and other conditions, and when a clinician can or should change a patient’s medication. However, the relationship between DNA variations and the effectiveness of antidepressant medications has not been established, and basing clinical decisions on the results of these tests may lead to inappropriate medication changes.

Pharmacogenetic tests are being advertised to both clinicians and patients, but the FDA has not approved the use of any test for providing information on a patient’s ability to respond to any specific medication.³ Therefore, psychiatrists should discuss the use of pharmacogenetic testing with their patients, and advise patients to avoid stopping or changing their medications based on the results of any pharmacogenetic test. Clinicians should not change a patient’s medication regimen solely based on the results of pharmacogenetic testing. These tests are not supported by scientific or clinical evidence, and using these tests for clinical decisions may put the patient at risk for potentially serious health consequences.

Aneela Jafri, MD, MS
Research Volunteer
Ocean Medical Center
Nutley, New Jersey

Ramon Solhkhah, MD
Founding Chair and Professor
Department of Psychiatry and Behavioral Health
Hackensack Meridian School of Medicine at Seton Hall University
Nutley, New Jersey
Chair
Department of Psychiatry
Jersey Shore University Medical Center
Neptune, New Jersey
Residency Training Director
General Psychiatry
Ocean Medical Center
Brick, New Jersey

Stacy Doumas, MD
Vice Chair
Associate Professor
Department of Psychiatry and Behavioral Health
Hackensack Meridian School of Medicine at Seton Hall University
Nutley, New Jersey
Vice Chair for Education & Research
Residency Training Director
General Psychiatry
Jersey Shore University Medical Center Neptune, New Jersey

Saba Afzal, MD
Assistant Professor
Department of Psychiatry and Behavioral Health
Hackensack Meridian School of Medicine at Seton Hall University
Nutley, New Jersey
Associate Residency Training Director General Psychiatry
Ocean Medical Center
Brick, New Jersey

Disclosures: The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

One of the most malignant threats that is adversely impacting physicians is the insidious metastasis of the term “provider” within the national health care system over the past 2 to 3 decades.

This demeaning adjective is outrageously inappropriate and beneath the stature of medical doctors (MDs) who sacrificed 12 to 15 years of their lives in college, medical schools, residency programs, and post-residency fellowships to become physicians, specialists, and subspecialists. It is distressing to see hospitals, clinics, pharmacies, insurance corporations, and managed care companies refer to psychiatrists and other physicians as “providers.” It is time to fight back and restore our noble medical identity, which society has always respected and appreciated.

Our unique professional identify is at stake. We do not want to be lumped with nonphysicians as if we are interchangeable parts of a health care system or cogs in a wheel. No other mental health professional has the extensive training, scientific knowledge, clinical expertise, research accomplishments, and teaching/supervisory abilities that physicians have. We strongly uphold the sacred tenet of the physician-patient relationship, and adamantly reject its corruption into a provider-consumer transaction.

Even plumbers and electricians are not referred to as “providers.” Lawyers are not called legal aid providers. Teachers are not called knowledge providers, and administrators and CEOs are not called management providers. So why should physicians in any specialty, including psychiatry, obsequiously accept the denigration of their esteemed medical identify into the vague, amorphous ipseity of a “provider”? Family physicians, internists, and pediatricians used to be called primary care physicians, but have been reduced to primary care providers, which is insulting and degrading to these highly trained MD specialists.

The corruption and debasement of the professional identify of physicians and the propagation of the usage of the belittling term “provider” can be traced back to 3 entities:

1. The Nazi Third Reich. This is the most evil origin of the term “provider,” inflicted on Jewish physicians as part of the despicable persecution of German Jews in the 1930s. The Nazis decided to deprive pediatricians of being called physicians (“Arzt” in German) and forcefully relabeled them as “behandlers” or “providers,” thus erasing their noble medical identity.¹ In 1933, all Jewish pediatricians were expelled or forced to resign from the German Society of Pediatrics and were no longer allowed to be called doctors. This deliberate and systematic humiliation of pediatric clinicians and scientists was followed by deporting the lowly “providers” to concentration camps. So why perpetuate this pernicious Nazi terminology?

2. The Federal Government. The term “provider” was introduced and propagated in Public Law 93-641 titled “The National Health Planning and Resource Development Act of 1974.” In that document, patients were referred to as “consumers” and physicians as “providers” (this term was used 19 times in that law). At that time, the civil service employees who drafted the law that marginalized physicians by using generic, nonmedical nomenclature may not have realized the dire consequences of relabeling physicians as “providers.”

Continue to: Insurance companies, managed care companies, and consolidated health systems...

3. Insurance companies, managed care companies, and consolidated health systems have jubilantly adopted the term “provider” because they can equate physicians with less expensive, nonphysician clinicians (physician assistants, nurse practitioners, and certified registered nurse anesthetists), especially when physicians across several specialties (particularly psychiatry) are in short supply. None of these clinicians deserve to be labeled “providers,” either.

To understand why the term “provider” was used instead of “clinicians” or “clinical practitioner,” one must recognize the “businessification” of medicine and the commoditization of clinical care in our country. In some ways, health care has adopted a model similar to a fast-food joint, where workers provide customers with a hamburger. The question here is why did the 1.1 million physicians in the United States not halt this terminology shift before it spread and permeated the national health care system? Physicians who graduate from medical schools (not “provider” schools!) must vigorously and loudly fight back and put this wicked genie back in its bottle. This is feasible only if the American Medical Association (which would never conceive of itself as the “American Provider Association”), along with all 48 specialty organizations (Table), including the American Psychiatric Association (APA), unite and demand that physicians be called medical doctors or physicians, or by a term that reflects their specialty (orthopedists, psychiatrists, oncologists, gastroenterologists, anesthesiologists, cardiologists, etc.). This is an urgent issue to prevent the dissolution of our professional identity and its highly regarded societal image. It is a travesty that we physicians have allowed it to go on unopposed and to become entrenched in the dumbed-down jargon of health care. Physicians tend to avoid confrontation and adversarial stances, but we must unite and demand a return to the traditional nomenclature of medicine.

Much debate has emerged lately about an epidemic of “burnout” among physicians. Proposed causes include the savage increase in the amount of paperwork at the expense of patient care, the sense of helplessness that pre-authorization has inflicted on physicians’ decision-making, and the tyranny of relative value units (RVUs) as a benchmark for physician performance, as if healing patients is like manufacturing widgets. However, the blow to the self-esteem of physicians by being called “providers” daily is certainly another major factor contributing to burnout. It is perfectly legitimate for physicians to expect recognition for their long, rigorous, and uniquely advanced medical training, instead of being lumped together with less qualified professionals as anonymous “providers” in the name of politically correct pseudo-equality of all clinical practitioners. Let the administrators stop and contemplate whether tertiary or quaternary care for the most complex and severely ill patients in medical, surgical, or psychiatric intensive care units can operate without highly specialized physicians.

I urge APA leadership to take a visible and strong stand to rid psychiatrists of this assault on our medical identity. As I mentioned in my January 2020 editorial,² it is vital that the name of our national psychiatric organization (APA) be modified to the American Psychiatric Physicians Association, to remind all health care systems, as well as patients, the public, and the media, of our medical identity as physicians before we specialized in psychiatry.

Continue to: Patients, not clients

We should also emphasize that our suffering and medically ill patients with serious neuropsychiatric disorders such as schizophrenia, bipolar disorder, depression, panic disorder, or obsessive-compulsive disorder are patients, not clients. The terminology used in community mental health centers around the country almost universally includes “providers” and “clients.” This de-medicalization of psychiatrists and our patients must be corrected and reversed so that the public understands that treating mental illness is not a business transaction between a “provider” and a “client.” Using the correct terminology may help generate sympathy and compassion towards patients with serious psychiatric illnesses, just as it does for patients with cancer, heart disease, or stroke. The term “client” will never evoke the public sympathy and support that our patients truly deserve.

Let’s keep this issue alive and translate our demands into actions, both locally and nationally. Psychiatrists and physicians of all other specialties must stand up for their rights and inform their systems of care that they must be called by their legitimate and lawful name: physicians or medical doctors (never “providers”). This is an issue that unites all 1.1 million of us. The US health care system would collapse without us, and asking that we be called exactly what our medical license displays is our right and our professional identity.

One of the most malignant threats that is adversely impacting physicians is the insidious metastasis of the term “provider” within the national health care system over the past 2 to 3 decades.

This demeaning adjective is outrageously inappropriate and beneath the stature of medical doctors (MDs) who sacrificed 12 to 15 years of their lives in college, medical schools, residency programs, and post-residency fellowships to become physicians, specialists, and subspecialists. It is distressing to see hospitals, clinics, pharmacies, insurance corporations, and managed care companies refer to psychiatrists and other physicians as “providers.” It is time to fight back and restore our noble medical identity, which society has always respected and appreciated.

Our unique professional identify is at stake. We do not want to be lumped with nonphysicians as if we are interchangeable parts of a health care system or cogs in a wheel. No other mental health professional has the extensive training, scientific knowledge, clinical expertise, research accomplishments, and teaching/supervisory abilities that physicians have. We strongly uphold the sacred tenet of the physician-patient relationship, and adamantly reject its corruption into a provider-consumer transaction.

Even plumbers and electricians are not referred to as “providers.” Lawyers are not called legal aid providers. Teachers are not called knowledge providers, and administrators and CEOs are not called management providers. So why should physicians in any specialty, including psychiatry, obsequiously accept the denigration of their esteemed medical identify into the vague, amorphous ipseity of a “provider”? Family physicians, internists, and pediatricians used to be called primary care physicians, but have been reduced to primary care providers, which is insulting and degrading to these highly trained MD specialists.

The corruption and debasement of the professional identify of physicians and the propagation of the usage of the belittling term “provider” can be traced back to 3 entities:

1. The Nazi Third Reich. This is the most evil origin of the term “provider,” inflicted on Jewish physicians as part of the despicable persecution of German Jews in the 1930s. The Nazis decided to deprive pediatricians of being called physicians (“Arzt” in German) and forcefully relabeled them as “behandlers” or “providers,” thus erasing their noble medical identity.¹ In 1933, all Jewish pediatricians were expelled or forced to resign from the German Society of Pediatrics and were no longer allowed to be called doctors. This deliberate and systematic humiliation of pediatric clinicians and scientists was followed by deporting the lowly “providers” to concentration camps. So why perpetuate this pernicious Nazi terminology?

2. The Federal Government. The term “provider” was introduced and propagated in Public Law 93-641 titled “The National Health Planning and Resource Development Act of 1974.” In that document, patients were referred to as “consumers” and physicians as “providers” (this term was used 19 times in that law). At that time, the civil service employees who drafted the law that marginalized physicians by using generic, nonmedical nomenclature may not have realized the dire consequences of relabeling physicians as “providers.”

Continue to: Insurance companies, managed care companies, and consolidated health systems...

3. Insurance companies, managed care companies, and consolidated health systems have jubilantly adopted the term “provider” because they can equate physicians with less expensive, nonphysician clinicians (physician assistants, nurse practitioners, and certified registered nurse anesthetists), especially when physicians across several specialties (particularly psychiatry) are in short supply. None of these clinicians deserve to be labeled “providers,” either.

To understand why the term “provider” was used instead of “clinicians” or “clinical practitioner,” one must recognize the “businessification” of medicine and the commoditization of clinical care in our country. In some ways, health care has adopted a model similar to a fast-food joint, where workers provide customers with a hamburger. The question here is why did the 1.1 million physicians in the United States not halt this terminology shift before it spread and permeated the national health care system? Physicians who graduate from medical schools (not “provider” schools!) must vigorously and loudly fight back and put this wicked genie back in its bottle. This is feasible only if the American Medical Association (which would never conceive of itself as the “American Provider Association”), along with all 48 specialty organizations (Table), including the American Psychiatric Association (APA), unite and demand that physicians be called medical doctors or physicians, or by a term that reflects their specialty (orthopedists, psychiatrists, oncologists, gastroenterologists, anesthesiologists, cardiologists, etc.). This is an urgent issue to prevent the dissolution of our professional identity and its highly regarded societal image. It is a travesty that we physicians have allowed it to go on unopposed and to become entrenched in the dumbed-down jargon of health care. Physicians tend to avoid confrontation and adversarial stances, but we must unite and demand a return to the traditional nomenclature of medicine.

Much debate has emerged lately about an epidemic of “burnout” among physicians. Proposed causes include the savage increase in the amount of paperwork at the expense of patient care, the sense of helplessness that pre-authorization has inflicted on physicians’ decision-making, and the tyranny of relative value units (RVUs) as a benchmark for physician performance, as if healing patients is like manufacturing widgets. However, the blow to the self-esteem of physicians by being called “providers” daily is certainly another major factor contributing to burnout. It is perfectly legitimate for physicians to expect recognition for their long, rigorous, and uniquely advanced medical training, instead of being lumped together with less qualified professionals as anonymous “providers” in the name of politically correct pseudo-equality of all clinical practitioners. Let the administrators stop and contemplate whether tertiary or quaternary care for the most complex and severely ill patients in medical, surgical, or psychiatric intensive care units can operate without highly specialized physicians.

I urge APA leadership to take a visible and strong stand to rid psychiatrists of this assault on our medical identity. As I mentioned in my January 2020 editorial,² it is vital that the name of our national psychiatric organization (APA) be modified to the American Psychiatric Physicians Association, to remind all health care systems, as well as patients, the public, and the media, of our medical identity as physicians before we specialized in psychiatry.

Continue to: Patients, not clients

We should also emphasize that our suffering and medically ill patients with serious neuropsychiatric disorders such as schizophrenia, bipolar disorder, depression, panic disorder, or obsessive-compulsive disorder are patients, not clients. The terminology used in community mental health centers around the country almost universally includes “providers” and “clients.” This de-medicalization of psychiatrists and our patients must be corrected and reversed so that the public understands that treating mental illness is not a business transaction between a “provider” and a “client.” Using the correct terminology may help generate sympathy and compassion towards patients with serious psychiatric illnesses, just as it does for patients with cancer, heart disease, or stroke. The term “client” will never evoke the public sympathy and support that our patients truly deserve.

Let’s keep this issue alive and translate our demands into actions, both locally and nationally. Psychiatrists and physicians of all other specialties must stand up for their rights and inform their systems of care that they must be called by their legitimate and lawful name: physicians or medical doctors (never “providers”). This is an issue that unites all 1.1 million of us. The US health care system would collapse without us, and asking that we be called exactly what our medical license displays is our right and our professional identity.

One of the most malignant threats that is adversely impacting physicians is the insidious metastasis of the term “provider” within the national health care system over the past 2 to 3 decades.

This demeaning adjective is outrageously inappropriate and beneath the stature of medical doctors (MDs) who sacrificed 12 to 15 years of their lives in college, medical schools, residency programs, and post-residency fellowships to become physicians, specialists, and subspecialists. It is distressing to see hospitals, clinics, pharmacies, insurance corporations, and managed care companies refer to psychiatrists and other physicians as “providers.” It is time to fight back and restore our noble medical identity, which society has always respected and appreciated.

Our unique professional identify is at stake. We do not want to be lumped with nonphysicians as if we are interchangeable parts of a health care system or cogs in a wheel. No other mental health professional has the extensive training, scientific knowledge, clinical expertise, research accomplishments, and teaching/supervisory abilities that physicians have. We strongly uphold the sacred tenet of the physician-patient relationship, and adamantly reject its corruption into a provider-consumer transaction.

Even plumbers and electricians are not referred to as “providers.” Lawyers are not called legal aid providers. Teachers are not called knowledge providers, and administrators and CEOs are not called management providers. So why should physicians in any specialty, including psychiatry, obsequiously accept the denigration of their esteemed medical identify into the vague, amorphous ipseity of a “provider”? Family physicians, internists, and pediatricians used to be called primary care physicians, but have been reduced to primary care providers, which is insulting and degrading to these highly trained MD specialists.

The corruption and debasement of the professional identify of physicians and the propagation of the usage of the belittling term “provider” can be traced back to 3 entities:

1. The Nazi Third Reich. This is the most evil origin of the term “provider,” inflicted on Jewish physicians as part of the despicable persecution of German Jews in the 1930s. The Nazis decided to deprive pediatricians of being called physicians (“Arzt” in German) and forcefully relabeled them as “behandlers” or “providers,” thus erasing their noble medical identity.¹ In 1933, all Jewish pediatricians were expelled or forced to resign from the German Society of Pediatrics and were no longer allowed to be called doctors. This deliberate and systematic humiliation of pediatric clinicians and scientists was followed by deporting the lowly “providers” to concentration camps. So why perpetuate this pernicious Nazi terminology?

2. The Federal Government. The term “provider” was introduced and propagated in Public Law 93-641 titled “The National Health Planning and Resource Development Act of 1974.” In that document, patients were referred to as “consumers” and physicians as “providers” (this term was used 19 times in that law). At that time, the civil service employees who drafted the law that marginalized physicians by using generic, nonmedical nomenclature may not have realized the dire consequences of relabeling physicians as “providers.”

Continue to: Insurance companies, managed care companies, and consolidated health systems...

3. Insurance companies, managed care companies, and consolidated health systems have jubilantly adopted the term “provider” because they can equate physicians with less expensive, nonphysician clinicians (physician assistants, nurse practitioners, and certified registered nurse anesthetists), especially when physicians across several specialties (particularly psychiatry) are in short supply. None of these clinicians deserve to be labeled “providers,” either.

To understand why the term “provider” was used instead of “clinicians” or “clinical practitioner,” one must recognize the “businessification” of medicine and the commoditization of clinical care in our country. In some ways, health care has adopted a model similar to a fast-food joint, where workers provide customers with a hamburger. The question here is why did the 1.1 million physicians in the United States not halt this terminology shift before it spread and permeated the national health care system? Physicians who graduate from medical schools (not “provider” schools!) must vigorously and loudly fight back and put this wicked genie back in its bottle. This is feasible only if the American Medical Association (which would never conceive of itself as the “American Provider Association”), along with all 48 specialty organizations (Table), including the American Psychiatric Association (APA), unite and demand that physicians be called medical doctors or physicians, or by a term that reflects their specialty (orthopedists, psychiatrists, oncologists, gastroenterologists, anesthesiologists, cardiologists, etc.). This is an urgent issue to prevent the dissolution of our professional identity and its highly regarded societal image. It is a travesty that we physicians have allowed it to go on unopposed and to become entrenched in the dumbed-down jargon of health care. Physicians tend to avoid confrontation and adversarial stances, but we must unite and demand a return to the traditional nomenclature of medicine.

Much debate has emerged lately about an epidemic of “burnout” among physicians. Proposed causes include the savage increase in the amount of paperwork at the expense of patient care, the sense of helplessness that pre-authorization has inflicted on physicians’ decision-making, and the tyranny of relative value units (RVUs) as a benchmark for physician performance, as if healing patients is like manufacturing widgets. However, the blow to the self-esteem of physicians by being called “providers” daily is certainly another major factor contributing to burnout. It is perfectly legitimate for physicians to expect recognition for their long, rigorous, and uniquely advanced medical training, instead of being lumped together with less qualified professionals as anonymous “providers” in the name of politically correct pseudo-equality of all clinical practitioners. Let the administrators stop and contemplate whether tertiary or quaternary care for the most complex and severely ill patients in medical, surgical, or psychiatric intensive care units can operate without highly specialized physicians.

I urge APA leadership to take a visible and strong stand to rid psychiatrists of this assault on our medical identity. As I mentioned in my January 2020 editorial,² it is vital that the name of our national psychiatric organization (APA) be modified to the American Psychiatric Physicians Association, to remind all health care systems, as well as patients, the public, and the media, of our medical identity as physicians before we specialized in psychiatry.

Continue to: Patients, not clients

We should also emphasize that our suffering and medically ill patients with serious neuropsychiatric disorders such as schizophrenia, bipolar disorder, depression, panic disorder, or obsessive-compulsive disorder are patients, not clients. The terminology used in community mental health centers around the country almost universally includes “providers” and “clients.” This de-medicalization of psychiatrists and our patients must be corrected and reversed so that the public understands that treating mental illness is not a business transaction between a “provider” and a “client.” Using the correct terminology may help generate sympathy and compassion towards patients with serious psychiatric illnesses, just as it does for patients with cancer, heart disease, or stroke. The term “client” will never evoke the public sympathy and support that our patients truly deserve.

Let’s keep this issue alive and translate our demands into actions, both locally and nationally. Psychiatrists and physicians of all other specialties must stand up for their rights and inform their systems of care that they must be called by their legitimate and lawful name: physicians or medical doctors (never “providers”). This is an issue that unites all 1.1 million of us. The US health care system would collapse without us, and asking that we be called exactly what our medical license displays is our right and our professional identity.

A number of years ago, a patient I was treating mentioned that she was not eating tomatoes. There had been stories in the news about people contracting bacterial infections from tomatoes, but I paused for a moment, then asked her: “Have there been any contaminated tomatoes here in Maryland?” There had not been and I was still happily eating salsa, but my patient thought about this differently: If disease-causing tomatoes were to come to our state, someone would be the first person to become ill. She did not want to take any risks. My patient, however, was a heavy smoker and already grappling with health issues that were caused by smoking, so I found her choice of what she should worry about and how it influenced her behavior to be perplexing. I realize it’s not the same; nicotine is an addiction, while tomatoes remain a choice for most of us, and it’s common for people to worry about very unlikely events even when we are surrounded by very real and statistically more probable threats to our well-being.

Today’s news reports are filled with stories about 2019 Novel Coronavirus (2019-nCoV), an illness that started in Wuhan, China; as of Jan. 31, 2020, there were 9,776 confirmed cases and 213 deaths. There have been an additional 118 cases reported outside of mainland China, including 6 in the United States, and no one outside of China has died.

The response to the virus has been remarkable: Wuhan, a city of more than 11 million inhabitants, is on lockdown, as are 15 other cities in China; 46 million people have been affected, the largest quarantine in human history. Travel is restricted in parts of China, airports all over the world are screening those who fly in from Wuhan, foreign governments are bringing their citizens home from Wuhan, and even Starbucks has temporarily closed half its stores in China. The economics of containing this virus are astounding.

In the meantime, the Centers for Disease Control and Prevention reports that, as of the week of Jan. 25, there have been 19 million cases of the flu in the United States. Of those stricken, 180,000 people have been hospitalized and 10,000 have died, including 68 pediatric patients. No cities are on lockdown, public transportation runs as usual, airports don’t screen passengers for flu symptoms, and Starbucks continues to serve vanilla lattes to any willing customer. Anxiety about illness is not new; we’ve seen it with SARS, Ebola, measles, and even around Chipotle’s food poisoning cases – to name just a few recent scares. We have also seen a lot of media on vaping-related deaths, and as of early January 2020, vaping-related illnesses affected 2,602 people with 59 deaths. It has been a topic of discussion among legislators, with an emphasis on either outlawing the flavoring that might appeal to younger people or simply outlawing e-cigarettes. No one, however, is talking about outlawing regular cigarettes, despite the fact that many people have switched from cigarettes to vaping products as a way to quit smoking. So, while vaping has caused 59 deaths since 2018, cigarettes are responsible for 480,000 fatalities a year in the United States and smokers live, on average, 10 years less than nonsmokers.

So what fuels anxiety about the latest health scare, and why aren’t we more anxious about the more common causes of premature mortality? Certainly, the newness and the unknown are factors in the coronavirus scare. It’s not certain how this illness was introduced into the human population, although one theory is that it started with the consumption of bats who carry the virus. It’s spreading fast, and in some people, it has been lethal. The incubation period is not known, or whether it is contagious before symptoms appear. Coronavirus is getting a lot of public health attention and the World Health Organization just announced that the virus is a public health emergency of international concern. On the televised news on Jan. 29, 2020, coronavirus was the top story in the United States, even though an impeachment trial is in progress for our country’s president.

The public health response of locking down cities may help contain the outbreak and prevent a global epidemic, although millions of people had already left Wuhan, so the heavy-handed attempt to prevent spread of the virus may well be too late. In the case of the Ebola virus – a much more lethal disease that was also thought to be introduced by bats – public health measures certainly curtailed global spread, and the epidemic of 2014-2016 was limited to 28,600 cases and 11,325 deaths, nearly all of them in West Africa.

Most of the things that cause people to die are not new and are not topics the media chooses to sensationalize. Dissemination of news has changed over the decades, with so much more of it, instant reports on social media, and competition for viewers that leads journalists to pull at our emotions. We might worry about getting food poisoning from romaine lettuce – if that is what the news is focusing on – but we don’t worry when we enter our cars, keep firearms in our homes, or light up cigarettes. And while we may, or may not, get flu shots and avoid those who have the flu, how and where we position both our anxiety and our resources does not always make sense. Certainly some people are predisposed to worry about both common and uncommon dangers, while others seem never to worry and engage in acts that many of us would consider dangerous. If we are looking for logic, it may be hard to find – there are those who would happily go bungee jumping but wouldn’t dream of leaving the house out without hand sanitizer.

The repercussions from this massive response to the Wuhan coronavirus are significant. For the millions of people on lockdown in China, each day gets emotionally harder; some may begin to have issues procuring food, and the financial losses for the economy will be significant. It’s not really possible to know yet if this response is warranted; we do know that infectious diseases can kill millions. The AIDS pandemic has taken the lives of 36 million people since 1981, and the influenza pandemic of 1918 resulted in an estimated 20 million to 50 million deaths after infecting 500 million people. Still, one might wonder if other, more mundane causes of morbidity and mortality – the ones that no longer garner our dread or make it to the front pages – might also be worthy of more hype and resources.

Dr. Miller is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins, both in Baltimore.

A number of years ago, a patient I was treating mentioned that she was not eating tomatoes. There had been stories in the news about people contracting bacterial infections from tomatoes, but I paused for a moment, then asked her: “Have there been any contaminated tomatoes here in Maryland?” There had not been and I was still happily eating salsa, but my patient thought about this differently: If disease-causing tomatoes were to come to our state, someone would be the first person to become ill. She did not want to take any risks. My patient, however, was a heavy smoker and already grappling with health issues that were caused by smoking, so I found her choice of what she should worry about and how it influenced her behavior to be perplexing. I realize it’s not the same; nicotine is an addiction, while tomatoes remain a choice for most of us, and it’s common for people to worry about very unlikely events even when we are surrounded by very real and statistically more probable threats to our well-being.

Today’s news reports are filled with stories about 2019 Novel Coronavirus (2019-nCoV), an illness that started in Wuhan, China; as of Jan. 31, 2020, there were 9,776 confirmed cases and 213 deaths. There have been an additional 118 cases reported outside of mainland China, including 6 in the United States, and no one outside of China has died.

The response to the virus has been remarkable: Wuhan, a city of more than 11 million inhabitants, is on lockdown, as are 15 other cities in China; 46 million people have been affected, the largest quarantine in human history. Travel is restricted in parts of China, airports all over the world are screening those who fly in from Wuhan, foreign governments are bringing their citizens home from Wuhan, and even Starbucks has temporarily closed half its stores in China. The economics of containing this virus are astounding.

In the meantime, the Centers for Disease Control and Prevention reports that, as of the week of Jan. 25, there have been 19 million cases of the flu in the United States. Of those stricken, 180,000 people have been hospitalized and 10,000 have died, including 68 pediatric patients. No cities are on lockdown, public transportation runs as usual, airports don’t screen passengers for flu symptoms, and Starbucks continues to serve vanilla lattes to any willing customer. Anxiety about illness is not new; we’ve seen it with SARS, Ebola, measles, and even around Chipotle’s food poisoning cases – to name just a few recent scares. We have also seen a lot of media on vaping-related deaths, and as of early January 2020, vaping-related illnesses affected 2,602 people with 59 deaths. It has been a topic of discussion among legislators, with an emphasis on either outlawing the flavoring that might appeal to younger people or simply outlawing e-cigarettes. No one, however, is talking about outlawing regular cigarettes, despite the fact that many people have switched from cigarettes to vaping products as a way to quit smoking. So, while vaping has caused 59 deaths since 2018, cigarettes are responsible for 480,000 fatalities a year in the United States and smokers live, on average, 10 years less than nonsmokers.

So what fuels anxiety about the latest health scare, and why aren’t we more anxious about the more common causes of premature mortality? Certainly, the newness and the unknown are factors in the coronavirus scare. It’s not certain how this illness was introduced into the human population, although one theory is that it started with the consumption of bats who carry the virus. It’s spreading fast, and in some people, it has been lethal. The incubation period is not known, or whether it is contagious before symptoms appear. Coronavirus is getting a lot of public health attention and the World Health Organization just announced that the virus is a public health emergency of international concern. On the televised news on Jan. 29, 2020, coronavirus was the top story in the United States, even though an impeachment trial is in progress for our country’s president.

The public health response of locking down cities may help contain the outbreak and prevent a global epidemic, although millions of people had already left Wuhan, so the heavy-handed attempt to prevent spread of the virus may well be too late. In the case of the Ebola virus – a much more lethal disease that was also thought to be introduced by bats – public health measures certainly curtailed global spread, and the epidemic of 2014-2016 was limited to 28,600 cases and 11,325 deaths, nearly all of them in West Africa.

Most of the things that cause people to die are not new and are not topics the media chooses to sensationalize. Dissemination of news has changed over the decades, with so much more of it, instant reports on social media, and competition for viewers that leads journalists to pull at our emotions. We might worry about getting food poisoning from romaine lettuce – if that is what the news is focusing on – but we don’t worry when we enter our cars, keep firearms in our homes, or light up cigarettes. And while we may, or may not, get flu shots and avoid those who have the flu, how and where we position both our anxiety and our resources does not always make sense. Certainly some people are predisposed to worry about both common and uncommon dangers, while others seem never to worry and engage in acts that many of us would consider dangerous. If we are looking for logic, it may be hard to find – there are those who would happily go bungee jumping but wouldn’t dream of leaving the house out without hand sanitizer.

The repercussions from this massive response to the Wuhan coronavirus are significant. For the millions of people on lockdown in China, each day gets emotionally harder; some may begin to have issues procuring food, and the financial losses for the economy will be significant. It’s not really possible to know yet if this response is warranted; we do know that infectious diseases can kill millions. The AIDS pandemic has taken the lives of 36 million people since 1981, and the influenza pandemic of 1918 resulted in an estimated 20 million to 50 million deaths after infecting 500 million people. Still, one might wonder if other, more mundane causes of morbidity and mortality – the ones that no longer garner our dread or make it to the front pages – might also be worthy of more hype and resources.

Dr. Miller is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins, both in Baltimore.

A number of years ago, a patient I was treating mentioned that she was not eating tomatoes. There had been stories in the news about people contracting bacterial infections from tomatoes, but I paused for a moment, then asked her: “Have there been any contaminated tomatoes here in Maryland?” There had not been and I was still happily eating salsa, but my patient thought about this differently: If disease-causing tomatoes were to come to our state, someone would be the first person to become ill. She did not want to take any risks. My patient, however, was a heavy smoker and already grappling with health issues that were caused by smoking, so I found her choice of what she should worry about and how it influenced her behavior to be perplexing. I realize it’s not the same; nicotine is an addiction, while tomatoes remain a choice for most of us, and it’s common for people to worry about very unlikely events even when we are surrounded by very real and statistically more probable threats to our well-being.

Today’s news reports are filled with stories about 2019 Novel Coronavirus (2019-nCoV), an illness that started in Wuhan, China; as of Jan. 31, 2020, there were 9,776 confirmed cases and 213 deaths. There have been an additional 118 cases reported outside of mainland China, including 6 in the United States, and no one outside of China has died.

The response to the virus has been remarkable: Wuhan, a city of more than 11 million inhabitants, is on lockdown, as are 15 other cities in China; 46 million people have been affected, the largest quarantine in human history. Travel is restricted in parts of China, airports all over the world are screening those who fly in from Wuhan, foreign governments are bringing their citizens home from Wuhan, and even Starbucks has temporarily closed half its stores in China. The economics of containing this virus are astounding.

In the meantime, the Centers for Disease Control and Prevention reports that, as of the week of Jan. 25, there have been 19 million cases of the flu in the United States. Of those stricken, 180,000 people have been hospitalized and 10,000 have died, including 68 pediatric patients. No cities are on lockdown, public transportation runs as usual, airports don’t screen passengers for flu symptoms, and Starbucks continues to serve vanilla lattes to any willing customer. Anxiety about illness is not new; we’ve seen it with SARS, Ebola, measles, and even around Chipotle’s food poisoning cases – to name just a few recent scares. We have also seen a lot of media on vaping-related deaths, and as of early January 2020, vaping-related illnesses affected 2,602 people with 59 deaths. It has been a topic of discussion among legislators, with an emphasis on either outlawing the flavoring that might appeal to younger people or simply outlawing e-cigarettes. No one, however, is talking about outlawing regular cigarettes, despite the fact that many people have switched from cigarettes to vaping products as a way to quit smoking. So, while vaping has caused 59 deaths since 2018, cigarettes are responsible for 480,000 fatalities a year in the United States and smokers live, on average, 10 years less than nonsmokers.

So what fuels anxiety about the latest health scare, and why aren’t we more anxious about the more common causes of premature mortality? Certainly, the newness and the unknown are factors in the coronavirus scare. It’s not certain how this illness was introduced into the human population, although one theory is that it started with the consumption of bats who carry the virus. It’s spreading fast, and in some people, it has been lethal. The incubation period is not known, or whether it is contagious before symptoms appear. Coronavirus is getting a lot of public health attention and the World Health Organization just announced that the virus is a public health emergency of international concern. On the televised news on Jan. 29, 2020, coronavirus was the top story in the United States, even though an impeachment trial is in progress for our country’s president.

The public health response of locking down cities may help contain the outbreak and prevent a global epidemic, although millions of people had already left Wuhan, so the heavy-handed attempt to prevent spread of the virus may well be too late. In the case of the Ebola virus – a much more lethal disease that was also thought to be introduced by bats – public health measures certainly curtailed global spread, and the epidemic of 2014-2016 was limited to 28,600 cases and 11,325 deaths, nearly all of them in West Africa.

Most of the things that cause people to die are not new and are not topics the media chooses to sensationalize. Dissemination of news has changed over the decades, with so much more of it, instant reports on social media, and competition for viewers that leads journalists to pull at our emotions. We might worry about getting food poisoning from romaine lettuce – if that is what the news is focusing on – but we don’t worry when we enter our cars, keep firearms in our homes, or light up cigarettes. And while we may, or may not, get flu shots and avoid those who have the flu, how and where we position both our anxiety and our resources does not always make sense. Certainly some people are predisposed to worry about both common and uncommon dangers, while others seem never to worry and engage in acts that many of us would consider dangerous. If we are looking for logic, it may be hard to find – there are those who would happily go bungee jumping but wouldn’t dream of leaving the house out without hand sanitizer.

The repercussions from this massive response to the Wuhan coronavirus are significant. For the millions of people on lockdown in China, each day gets emotionally harder; some may begin to have issues procuring food, and the financial losses for the economy will be significant. It’s not really possible to know yet if this response is warranted; we do know that infectious diseases can kill millions. The AIDS pandemic has taken the lives of 36 million people since 1981, and the influenza pandemic of 1918 resulted in an estimated 20 million to 50 million deaths after infecting 500 million people. Still, one might wonder if other, more mundane causes of morbidity and mortality – the ones that no longer garner our dread or make it to the front pages – might also be worthy of more hype and resources.

Dr. Miller is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins, both in Baltimore.

Diabetes is a complex disease with a range of nuanced therapy options and a plethora of risk factors that could significantly affect patient quality of life and long-term outcomes. From the outset, after diagnosis, a selected regimen has to be meticulously tailored to a patient’s clinical needs and monitored over time, and many other nonclinical variables, such as patient preference, social history, access to care, and support systems, as well as the cost of the drugs and its impact on the patient, must also be considered.

The increase in the incidence of youth-onset diabetes means that more young adults are making the transition from pediatric to adult care, and careful care coordination is paramount at the handover point to ensure that a full and complete account of the history gets transferred to the adult-care provider.

So how do you distill the information from all those records (on paper and online) that you’ve accumulated during the time you’ve been treating a young adult who is now transitioning to adult care?
 

Transition summary

One resource that can facilitate this handover is the transition summary. It effectively consolidates and packages the aforementioned aspects of care and patient history so that the adult-care provider does not have to collect the patient’s history from the start. The transition summary should not be confused with the discharge or medical summary, which focuses only on the preceding clinical care.

It is important to stress at this stage that collaboration between the pediatric- and adult-care providers is crucial to the success of such a summary, from its creation, to its implementation, and through the subsequent and inevitable revisions and updates.
 

Benefits all around

After we introduced the transition summary at my institution, we found that the average initial patient visit with the new adult-care provider decreased by 12 minutes (with a range of 6-19 min). The adult-care providers welcomed receiving such detailed, important patient information packaged in a concise and readily accessible format. It helped them identify the preceding care team members, which facilitated continuity of care, and it also helped them forge a better therapeutic relationship with the patient earlier on in their engagement.

We also learned that patients were more comfortable with the transition, and the referring providers were relieved and reassured that their patients would continue to receive personalized care with the new adult-care provider.

At a personal level, I found I was less stressed as I could spend better-quality clinical time with patients. And I got to eliminate those unwieldy stacks of medical records since getting buy-in from divisional and IT leadership enabled us to automate the entire process of information transfer.

It is important to note that the patient has to consent to release of medical records to other institutions.
 

Setting up the summary

At our clinic, I started out by adapting the transition summary from guidelines provided by the Endocrine Society to make a template. Then, in collaboration with my pediatric colleagues, I removed and added information so that the revised document would contain information that is vitally important and not readily available in the chart and would be feasible to fill out. For example, we included details such as the patient’s psychosocial history, an estimation of the patient barriers to diabetes management, family relationship issues, and the patient’s reasons for not adopting advanced diabetes technology (see accompanying example of a transition summary) .

I kept the summary brief, at two pages, and piloted it with referring providers who were interested in using the summary and with related supporting services. I also sought buy-in from my institution. This meant that I needed pediatric and adult divisional leadership support, which offered me information technology, resources, and expertise to automate the summary within the electronic health record. Once I had feedback from would-be users, we revised and updated the summary. We set up training for staff, including pediatric providers, nurse practitioners, social workers, and nurses who could fill out the summary, and ultimately succeeded in making it mandatory that the adult-care provider receive a summary before scheduling or seeing the transfer patient.

I started out with a paper version, and once we’d refined the questions, we incorporated it into the electronic medical record.

The information we use in our summary is grouped under the following headings:

• Reason for transition.
• Diabetes type.
• Degree of diabetes control.
• Type of insulin therapy and supplies.
• Current and former insulin regimen: reasons for discontinuation of any therapies or reluctance to start any therapies.
• Diabetes health maintenance.
• Social history and support, including living situation, main social support network, child protective services involvement.
• Other pertinent medical surgical history, including psychiatric disease.

Tips and takeaways

Top of the list of takeaways is that you should make the final document work for you, your colleagues, and ultimately, your patients – customize it as you see fit, but be sure to keep it short and easy to fill out. Make a note as you start using it in practice of what you think might be missing from the chart and whether updates are needed. If you can, it’s a great idea to fold the transfer summary into the electronic medical record, though it’s not imperative. Care coordination is key to successful transfer of patients, whether from pediatric to adult care or hospital to home. A small change to work flow can result in a huge change in patient and provider satisfaction, as well as a reduction in visit times.
 

Dr. Agarwal is director of the Supporting Emerging Adults With Diabetes (SEAD) program at Montefiore Medical Center and assistant professor of medicine at Albert Einstein College of Medicine, New York. She reports no disclosures or financial conflicts of interest. Write to her at [email protected].

Diabetes is a complex disease with a range of nuanced therapy options and a plethora of risk factors that could significantly affect patient quality of life and long-term outcomes. From the outset, after diagnosis, a selected regimen has to be meticulously tailored to a patient’s clinical needs and monitored over time, and many other nonclinical variables, such as patient preference, social history, access to care, and support systems, as well as the cost of the drugs and its impact on the patient, must also be considered.

The increase in the incidence of youth-onset diabetes means that more young adults are making the transition from pediatric to adult care, and careful care coordination is paramount at the handover point to ensure that a full and complete account of the history gets transferred to the adult-care provider.

So how do you distill the information from all those records (on paper and online) that you’ve accumulated during the time you’ve been treating a young adult who is now transitioning to adult care?
 

Transition summary

One resource that can facilitate this handover is the transition summary. It effectively consolidates and packages the aforementioned aspects of care and patient history so that the adult-care provider does not have to collect the patient’s history from the start. The transition summary should not be confused with the discharge or medical summary, which focuses only on the preceding clinical care.

It is important to stress at this stage that collaboration between the pediatric- and adult-care providers is crucial to the success of such a summary, from its creation, to its implementation, and through the subsequent and inevitable revisions and updates.
 

Benefits all around

After we introduced the transition summary at my institution, we found that the average initial patient visit with the new adult-care provider decreased by 12 minutes (with a range of 6-19 min). The adult-care providers welcomed receiving such detailed, important patient information packaged in a concise and readily accessible format. It helped them identify the preceding care team members, which facilitated continuity of care, and it also helped them forge a better therapeutic relationship with the patient earlier on in their engagement.

We also learned that patients were more comfortable with the transition, and the referring providers were relieved and reassured that their patients would continue to receive personalized care with the new adult-care provider.

At a personal level, I found I was less stressed as I could spend better-quality clinical time with patients. And I got to eliminate those unwieldy stacks of medical records since getting buy-in from divisional and IT leadership enabled us to automate the entire process of information transfer.

It is important to note that the patient has to consent to release of medical records to other institutions.
 

Setting up the summary

At our clinic, I started out by adapting the transition summary from guidelines provided by the Endocrine Society to make a template. Then, in collaboration with my pediatric colleagues, I removed and added information so that the revised document would contain information that is vitally important and not readily available in the chart and would be feasible to fill out. For example, we included details such as the patient’s psychosocial history, an estimation of the patient barriers to diabetes management, family relationship issues, and the patient’s reasons for not adopting advanced diabetes technology (see accompanying example of a transition summary) .

I kept the summary brief, at two pages, and piloted it with referring providers who were interested in using the summary and with related supporting services. I also sought buy-in from my institution. This meant that I needed pediatric and adult divisional leadership support, which offered me information technology, resources, and expertise to automate the summary within the electronic health record. Once I had feedback from would-be users, we revised and updated the summary. We set up training for staff, including pediatric providers, nurse practitioners, social workers, and nurses who could fill out the summary, and ultimately succeeded in making it mandatory that the adult-care provider receive a summary before scheduling or seeing the transfer patient.

I started out with a paper version, and once we’d refined the questions, we incorporated it into the electronic medical record.

The information we use in our summary is grouped under the following headings:

• Reason for transition.
• Diabetes type.
• Degree of diabetes control.
• Type of insulin therapy and supplies.
• Current and former insulin regimen: reasons for discontinuation of any therapies or reluctance to start any therapies.
• Diabetes health maintenance.
• Social history and support, including living situation, main social support network, child protective services involvement.
• Other pertinent medical surgical history, including psychiatric disease.

Tips and takeaways

Top of the list of takeaways is that you should make the final document work for you, your colleagues, and ultimately, your patients – customize it as you see fit, but be sure to keep it short and easy to fill out. Make a note as you start using it in practice of what you think might be missing from the chart and whether updates are needed. If you can, it’s a great idea to fold the transfer summary into the electronic medical record, though it’s not imperative. Care coordination is key to successful transfer of patients, whether from pediatric to adult care or hospital to home. A small change to work flow can result in a huge change in patient and provider satisfaction, as well as a reduction in visit times.
 

Dr. Agarwal is director of the Supporting Emerging Adults With Diabetes (SEAD) program at Montefiore Medical Center and assistant professor of medicine at Albert Einstein College of Medicine, New York. She reports no disclosures or financial conflicts of interest. Write to her at [email protected].

Diabetes is a complex disease with a range of nuanced therapy options and a plethora of risk factors that could significantly affect patient quality of life and long-term outcomes. From the outset, after diagnosis, a selected regimen has to be meticulously tailored to a patient’s clinical needs and monitored over time, and many other nonclinical variables, such as patient preference, social history, access to care, and support systems, as well as the cost of the drugs and its impact on the patient, must also be considered.

The increase in the incidence of youth-onset diabetes means that more young adults are making the transition from pediatric to adult care, and careful care coordination is paramount at the handover point to ensure that a full and complete account of the history gets transferred to the adult-care provider.

So how do you distill the information from all those records (on paper and online) that you’ve accumulated during the time you’ve been treating a young adult who is now transitioning to adult care?
 

Transition summary

One resource that can facilitate this handover is the transition summary. It effectively consolidates and packages the aforementioned aspects of care and patient history so that the adult-care provider does not have to collect the patient’s history from the start. The transition summary should not be confused with the discharge or medical summary, which focuses only on the preceding clinical care.

It is important to stress at this stage that collaboration between the pediatric- and adult-care providers is crucial to the success of such a summary, from its creation, to its implementation, and through the subsequent and inevitable revisions and updates.
 

Benefits all around

After we introduced the transition summary at my institution, we found that the average initial patient visit with the new adult-care provider decreased by 12 minutes (with a range of 6-19 min). The adult-care providers welcomed receiving such detailed, important patient information packaged in a concise and readily accessible format. It helped them identify the preceding care team members, which facilitated continuity of care, and it also helped them forge a better therapeutic relationship with the patient earlier on in their engagement.

We also learned that patients were more comfortable with the transition, and the referring providers were relieved and reassured that their patients would continue to receive personalized care with the new adult-care provider.

At a personal level, I found I was less stressed as I could spend better-quality clinical time with patients. And I got to eliminate those unwieldy stacks of medical records since getting buy-in from divisional and IT leadership enabled us to automate the entire process of information transfer.

It is important to note that the patient has to consent to release of medical records to other institutions.
 

Setting up the summary

At our clinic, I started out by adapting the transition summary from guidelines provided by the Endocrine Society to make a template. Then, in collaboration with my pediatric colleagues, I removed and added information so that the revised document would contain information that is vitally important and not readily available in the chart and would be feasible to fill out. For example, we included details such as the patient’s psychosocial history, an estimation of the patient barriers to diabetes management, family relationship issues, and the patient’s reasons for not adopting advanced diabetes technology (see accompanying example of a transition summary) .

I kept the summary brief, at two pages, and piloted it with referring providers who were interested in using the summary and with related supporting services. I also sought buy-in from my institution. This meant that I needed pediatric and adult divisional leadership support, which offered me information technology, resources, and expertise to automate the summary within the electronic health record. Once I had feedback from would-be users, we revised and updated the summary. We set up training for staff, including pediatric providers, nurse practitioners, social workers, and nurses who could fill out the summary, and ultimately succeeded in making it mandatory that the adult-care provider receive a summary before scheduling or seeing the transfer patient.

I started out with a paper version, and once we’d refined the questions, we incorporated it into the electronic medical record.

The information we use in our summary is grouped under the following headings:

• Reason for transition.
• Diabetes type.
• Degree of diabetes control.
• Type of insulin therapy and supplies.
• Current and former insulin regimen: reasons for discontinuation of any therapies or reluctance to start any therapies.
• Diabetes health maintenance.
• Social history and support, including living situation, main social support network, child protective services involvement.
• Other pertinent medical surgical history, including psychiatric disease.

Tips and takeaways

Top of the list of takeaways is that you should make the final document work for you, your colleagues, and ultimately, your patients – customize it as you see fit, but be sure to keep it short and easy to fill out. Make a note as you start using it in practice of what you think might be missing from the chart and whether updates are needed. If you can, it’s a great idea to fold the transfer summary into the electronic medical record, though it’s not imperative. Care coordination is key to successful transfer of patients, whether from pediatric to adult care or hospital to home. A small change to work flow can result in a huge change in patient and provider satisfaction, as well as a reduction in visit times.
 

Dr. Agarwal is director of the Supporting Emerging Adults With Diabetes (SEAD) program at Montefiore Medical Center and assistant professor of medicine at Albert Einstein College of Medicine, New York. She reports no disclosures or financial conflicts of interest. Write to her at [email protected].

The 2019 Novel Coronavirus (2019-nCoV) outbreak has unfolded so rapidly that many clinicians are scrambling to stay on top of it. Here are the answers to some frequently asked questions about how to prepare your clinic to respond to this outbreak.

Keep in mind that the outbreak is moving rapidly. Though scientific and epidemiologic knowledge has increased at unprecedented speed, there is much we don’t know, and some of what we think we know will change. Follow the links for the most up-to-date information.

What should our clinic do first?

Plan ahead with the following:

• Develop a plan for office staff to take travel histories from anyone with a respiratory illness and provide training for those who need it. Travel history at present should include asking about travel to China in the past 14 days, specifically Wuhan city or Hubei province.
• Review up-to-date infection control practices with all office staff and provide training for those who need it.
• Take an inventory of supplies of personal protective equipment (PPE), such as gowns, gloves, masks, eye protection, and N95 respirators or powered air-purifying respirators (PAPRs), and order items that are missing or low in stock.
• Fit-test users of N95 masks for maximal effectiveness.
• Plan where a potential patient would be isolated while obtaining expert advice.
• Know whom to contact at the state or local health department if you have a patient with the appropriate travel history.

The Centers for Disease Control and Prevention has prepared a toolkit to help frontline health care professionals prepare for this virus. Providers need to stay up to date on the latest recommendations, as the situation is changing rapidly.

When should I suspect 2019-nCoV illness, and what should I do?

Take the following steps to assess the concern and respond:

• If a patient with respiratory illness has traveled to China in the past 14 days, immediately put a mask on the patient and move the individual to a private room. Use a negative-pressure room if available.
• Put on appropriate PPE (including gloves, gown, eye protection, and mask) for contact, droplet, and airborne precautions. CDC recommends an N95 respirator mask if available, although we don’t know yet if there is true airborne spread.
• Obtain an accurate travel history, including dates and cities. (Tip: Get the correct spelling, as the English spelling of cities in China can cause confusion.)
• If the patient meets the current CDC definition of “person under investigation” or PUI, or if you need guidance on how to proceed, notify infection control (if you are in a facility that has it) and call your state or local health department immediately.
• Contact public health authorities who can help decide whether the patient should be admitted to airborne isolation or monitored at home with appropriate precautions.

What is the definition of a PUI?

The current definition of a PUI is a person who has fever and symptoms of a respiratory infection (cough, shortness of breath) AND who has EITHER been in Wuhan city or Hubei province in the past 14 days OR had close contact with a person either under investigation for 2019-nCoV infection or with confirmed infection. The definition of a PUI will change over time, so check this link.

How can I test for 2019-nCoV?

As of Jan. 30, 2020, testing is by polymerase chain reaction (PCR) and is available in the United States only through the CDC in Atlanta. Testing should soon be available in state health department laboratories. If public health authorities decide that your patient should be tested, they will instruct you on which samples to obtain.

The full sequence of 2019-nCoV has been shared, so some reference laboratories may develop and validate tests, ideally with assistance from CDC. If testing becomes available, make certain that it is a reputable lab that has carefully validated the test.

Should I test for other viruses?

Because the symptoms of 2019-nCoV infection overlap with those of influenza and other respiratory viruses, PCR testing for other viruses should be considered if it will change management (i.e., change the decision to provide influenza antivirals). Use appropriate PPE while collecting specimens, including eye protection. If 2019-nCoV is a consideration, you may want to send the specimen to a hospital lab for testing, where the sample will be processed under a biosafety hood, rather than doing point-of-care testing in the office.

How dangerous is 2019-nCoV?

The current estimated mortality rate is 2%-3%. That is probably an overestimate, as those with severe disease and those who die are more likely to be tested and reported early in an epidemic.

Our current knowledge is based on preliminary reports from hospitalized patients and will probably change. From the speed of spread and a single family cluster, it seems likely that there are milder cases and perhaps asymptomatic infection.

What else do I need to know about coronaviruses?

Coronaviruses are a large and diverse group of viruses, many of which are animal viruses. Before the discovery of the 2019-nCoV, six coronaviruses were known to infect humans. Four of these (HKU1, NL63, OC43, and 229E) predominantly caused mild to moderate upper respiratory illness, and they are thought to be responsible for 10%-30% of colds. They occasionally cause viral pneumonia and can be detected by some commercial multiplex panels.

Two other coronaviruses have caused outbreaks of severe respiratory illness in people: SARS, which emerged in Southern China in 2002, and MERS in the Middle East, in 2012. Unlike SARS, sporadic cases of MERS continue to occur.

The current outbreak is caused by 2019-nCoV, a previously unknown beta coronavirus. It is most closely related (~96%) to a bat virus and shares about 80% sequence homology with SARS CoV.

Andrew T. Pavia, MD, is the George and Esther Gross Presidential Professor and chief of the division of pediatric infectious disease in the department of pediatrics at the University of Utah, Salt Lake City. He is also director of hospital epidemiology and associate director of antimicrobial stewardship at Primary Children’s Hospital, Salt Lake City. Dr. Pavia has disclosed that he has served as a consultant for Genentech, Merck, and Seqirus and that he has served as associate editor for The Sanford Guide.

This article first appeared on Medscape.com.

The 2019 Novel Coronavirus (2019-nCoV) outbreak has unfolded so rapidly that many clinicians are scrambling to stay on top of it. Here are the answers to some frequently asked questions about how to prepare your clinic to respond to this outbreak.

Keep in mind that the outbreak is moving rapidly. Though scientific and epidemiologic knowledge has increased at unprecedented speed, there is much we don’t know, and some of what we think we know will change. Follow the links for the most up-to-date information.

What should our clinic do first?

Plan ahead with the following:

• Develop a plan for office staff to take travel histories from anyone with a respiratory illness and provide training for those who need it. Travel history at present should include asking about travel to China in the past 14 days, specifically Wuhan city or Hubei province.
• Review up-to-date infection control practices with all office staff and provide training for those who need it.
• Take an inventory of supplies of personal protective equipment (PPE), such as gowns, gloves, masks, eye protection, and N95 respirators or powered air-purifying respirators (PAPRs), and order items that are missing or low in stock.
• Fit-test users of N95 masks for maximal effectiveness.
• Plan where a potential patient would be isolated while obtaining expert advice.
• Know whom to contact at the state or local health department if you have a patient with the appropriate travel history.

The Centers for Disease Control and Prevention has prepared a toolkit to help frontline health care professionals prepare for this virus. Providers need to stay up to date on the latest recommendations, as the situation is changing rapidly.

When should I suspect 2019-nCoV illness, and what should I do?

Take the following steps to assess the concern and respond:

• If a patient with respiratory illness has traveled to China in the past 14 days, immediately put a mask on the patient and move the individual to a private room. Use a negative-pressure room if available.
• Put on appropriate PPE (including gloves, gown, eye protection, and mask) for contact, droplet, and airborne precautions. CDC recommends an N95 respirator mask if available, although we don’t know yet if there is true airborne spread.
• Obtain an accurate travel history, including dates and cities. (Tip: Get the correct spelling, as the English spelling of cities in China can cause confusion.)
• If the patient meets the current CDC definition of “person under investigation” or PUI, or if you need guidance on how to proceed, notify infection control (if you are in a facility that has it) and call your state or local health department immediately.
• Contact public health authorities who can help decide whether the patient should be admitted to airborne isolation or monitored at home with appropriate precautions.

What is the definition of a PUI?

The current definition of a PUI is a person who has fever and symptoms of a respiratory infection (cough, shortness of breath) AND who has EITHER been in Wuhan city or Hubei province in the past 14 days OR had close contact with a person either under investigation for 2019-nCoV infection or with confirmed infection. The definition of a PUI will change over time, so check this link.

How can I test for 2019-nCoV?

As of Jan. 30, 2020, testing is by polymerase chain reaction (PCR) and is available in the United States only through the CDC in Atlanta. Testing should soon be available in state health department laboratories. If public health authorities decide that your patient should be tested, they will instruct you on which samples to obtain.

The full sequence of 2019-nCoV has been shared, so some reference laboratories may develop and validate tests, ideally with assistance from CDC. If testing becomes available, make certain that it is a reputable lab that has carefully validated the test.

Should I test for other viruses?

Because the symptoms of 2019-nCoV infection overlap with those of influenza and other respiratory viruses, PCR testing for other viruses should be considered if it will change management (i.e., change the decision to provide influenza antivirals). Use appropriate PPE while collecting specimens, including eye protection. If 2019-nCoV is a consideration, you may want to send the specimen to a hospital lab for testing, where the sample will be processed under a biosafety hood, rather than doing point-of-care testing in the office.

How dangerous is 2019-nCoV?

The current estimated mortality rate is 2%-3%. That is probably an overestimate, as those with severe disease and those who die are more likely to be tested and reported early in an epidemic.

Our current knowledge is based on preliminary reports from hospitalized patients and will probably change. From the speed of spread and a single family cluster, it seems likely that there are milder cases and perhaps asymptomatic infection.

What else do I need to know about coronaviruses?

Coronaviruses are a large and diverse group of viruses, many of which are animal viruses. Before the discovery of the 2019-nCoV, six coronaviruses were known to infect humans. Four of these (HKU1, NL63, OC43, and 229E) predominantly caused mild to moderate upper respiratory illness, and they are thought to be responsible for 10%-30% of colds. They occasionally cause viral pneumonia and can be detected by some commercial multiplex panels.

Two other coronaviruses have caused outbreaks of severe respiratory illness in people: SARS, which emerged in Southern China in 2002, and MERS in the Middle East, in 2012. Unlike SARS, sporadic cases of MERS continue to occur.

The current outbreak is caused by 2019-nCoV, a previously unknown beta coronavirus. It is most closely related (~96%) to a bat virus and shares about 80% sequence homology with SARS CoV.

Andrew T. Pavia, MD, is the George and Esther Gross Presidential Professor and chief of the division of pediatric infectious disease in the department of pediatrics at the University of Utah, Salt Lake City. He is also director of hospital epidemiology and associate director of antimicrobial stewardship at Primary Children’s Hospital, Salt Lake City. Dr. Pavia has disclosed that he has served as a consultant for Genentech, Merck, and Seqirus and that he has served as associate editor for The Sanford Guide.

This article first appeared on Medscape.com.

The 2019 Novel Coronavirus (2019-nCoV) outbreak has unfolded so rapidly that many clinicians are scrambling to stay on top of it. Here are the answers to some frequently asked questions about how to prepare your clinic to respond to this outbreak.

Keep in mind that the outbreak is moving rapidly. Though scientific and epidemiologic knowledge has increased at unprecedented speed, there is much we don’t know, and some of what we think we know will change. Follow the links for the most up-to-date information.

What should our clinic do first?

Plan ahead with the following:

• Develop a plan for office staff to take travel histories from anyone with a respiratory illness and provide training for those who need it. Travel history at present should include asking about travel to China in the past 14 days, specifically Wuhan city or Hubei province.
• Review up-to-date infection control practices with all office staff and provide training for those who need it.
• Take an inventory of supplies of personal protective equipment (PPE), such as gowns, gloves, masks, eye protection, and N95 respirators or powered air-purifying respirators (PAPRs), and order items that are missing or low in stock.
• Fit-test users of N95 masks for maximal effectiveness.
• Plan where a potential patient would be isolated while obtaining expert advice.
• Know whom to contact at the state or local health department if you have a patient with the appropriate travel history.

The Centers for Disease Control and Prevention has prepared a toolkit to help frontline health care professionals prepare for this virus. Providers need to stay up to date on the latest recommendations, as the situation is changing rapidly.

When should I suspect 2019-nCoV illness, and what should I do?

Take the following steps to assess the concern and respond:

• If a patient with respiratory illness has traveled to China in the past 14 days, immediately put a mask on the patient and move the individual to a private room. Use a negative-pressure room if available.
• Put on appropriate PPE (including gloves, gown, eye protection, and mask) for contact, droplet, and airborne precautions. CDC recommends an N95 respirator mask if available, although we don’t know yet if there is true airborne spread.
• Obtain an accurate travel history, including dates and cities. (Tip: Get the correct spelling, as the English spelling of cities in China can cause confusion.)
• If the patient meets the current CDC definition of “person under investigation” or PUI, or if you need guidance on how to proceed, notify infection control (if you are in a facility that has it) and call your state or local health department immediately.
• Contact public health authorities who can help decide whether the patient should be admitted to airborne isolation or monitored at home with appropriate precautions.

What is the definition of a PUI?

The current definition of a PUI is a person who has fever and symptoms of a respiratory infection (cough, shortness of breath) AND who has EITHER been in Wuhan city or Hubei province in the past 14 days OR had close contact with a person either under investigation for 2019-nCoV infection or with confirmed infection. The definition of a PUI will change over time, so check this link.

How can I test for 2019-nCoV?

As of Jan. 30, 2020, testing is by polymerase chain reaction (PCR) and is available in the United States only through the CDC in Atlanta. Testing should soon be available in state health department laboratories. If public health authorities decide that your patient should be tested, they will instruct you on which samples to obtain.

The full sequence of 2019-nCoV has been shared, so some reference laboratories may develop and validate tests, ideally with assistance from CDC. If testing becomes available, make certain that it is a reputable lab that has carefully validated the test.

Should I test for other viruses?

Because the symptoms of 2019-nCoV infection overlap with those of influenza and other respiratory viruses, PCR testing for other viruses should be considered if it will change management (i.e., change the decision to provide influenza antivirals). Use appropriate PPE while collecting specimens, including eye protection. If 2019-nCoV is a consideration, you may want to send the specimen to a hospital lab for testing, where the sample will be processed under a biosafety hood, rather than doing point-of-care testing in the office.

How dangerous is 2019-nCoV?

The current estimated mortality rate is 2%-3%. That is probably an overestimate, as those with severe disease and those who die are more likely to be tested and reported early in an epidemic.

Our current knowledge is based on preliminary reports from hospitalized patients and will probably change. From the speed of spread and a single family cluster, it seems likely that there are milder cases and perhaps asymptomatic infection.

What else do I need to know about coronaviruses?

Coronaviruses are a large and diverse group of viruses, many of which are animal viruses. Before the discovery of the 2019-nCoV, six coronaviruses were known to infect humans. Four of these (HKU1, NL63, OC43, and 229E) predominantly caused mild to moderate upper respiratory illness, and they are thought to be responsible for 10%-30% of colds. They occasionally cause viral pneumonia and can be detected by some commercial multiplex panels.

Two other coronaviruses have caused outbreaks of severe respiratory illness in people: SARS, which emerged in Southern China in 2002, and MERS in the Middle East, in 2012. Unlike SARS, sporadic cases of MERS continue to occur.

The current outbreak is caused by 2019-nCoV, a previously unknown beta coronavirus. It is most closely related (~96%) to a bat virus and shares about 80% sequence homology with SARS CoV.

Andrew T. Pavia, MD, is the George and Esther Gross Presidential Professor and chief of the division of pediatric infectious disease in the department of pediatrics at the University of Utah, Salt Lake City. He is also director of hospital epidemiology and associate director of antimicrobial stewardship at Primary Children’s Hospital, Salt Lake City. Dr. Pavia has disclosed that he has served as a consultant for Genentech, Merck, and Seqirus and that he has served as associate editor for The Sanford Guide.

This article first appeared on Medscape.com.

Traditionally, U.S. health care has operated under a fee-for-service payment model, in which health care providers (such as physicians, hospitals, and health care systems) receive a fee for services such as office visits, hospital stays, procedures, and tests. However, reimbursement discussions are increasingly moving from fee-for-service to value-based, in which payments are tied to managing population health and total cost of care.

Because these changes will impact the entire system all the way down to individual providers, in the upcoming Population Management article series in The Hospitalist, we will discuss the nuances and implications that physicians, executives, and hospitals should be aware of. In this first article, we will examine the impetus for the shift toward population management and introduce common terminology to lay the foundation for the future content.
 

The traditional model: Fee for service

Under the traditional fee-for-service payment system, health care providers are paid per unit of service. For example, hospitals receive diagnosis-related group (DRG) payments for inpatient stays, and physicians are paid per patient visit. The more services that hospitals or physicians provide, the more money both get paid, without financial consequences for quality outcomes or total cost of care. Total cost of care includes clinic visits, outpatient procedures and tests, hospital and ED visits, home health, skilled nursing facilities, durable medical equipment, and sometimes drugs during an episode of care (for example, a hospital stay plus 90 days after discharge) or over a period of time (for example, a month or a year).

As a result of the fee-for-service payment system, the United States spends more money on health care than other wealthy countries, yet it lags behind other countries on many quality measures, such as disease burden, overall mortality, premature death, and preventable death.^1,2

In 2007, the Institute for Healthcare Improvement (IHI) developed the Triple Aim framework that focused on the following:

• Improving the patient experience of care (including quality and satisfaction).
• Improving the health of populations.
• Reducing per capita cost of care.

Both public payers like Medicare and Medicaid, as well as private payers, embraced the Triple Aim to reform how health care is delivered and paid for. As such, health care delivery focus and financial incentives are shifting from managing discrete patient encounters for acute illness to managing population health and total cost of care.
 

A new approach: Population management

Before diving into population management, it is important to first understand the terms “population” and “population health.” A population can be defined geographically or may include employees of an organization, members of a health plan, or patients receiving care from a specific physician group or health care system. David A. Kindig, MD, PhD, professor emeritus of population health sciences at the University of Wisconsin–Madison, defined population health as “the health outcomes of a group of individuals, including the distribution of such outcomes within the group.”³ Dr. Kindig noted that population health outcomes have many determinants, such as the following:⁴

• Health care (access, cost, quantity, and quality of health care services).
• Individual behavior (including diet, exercise, and substance abuse).
• Genetics.
• The social environment (education, income, occupation, class, and social support).
• Physical environment (air and water quality, lead exposure, and the design of neighborhoods).

IHI operationally defines population health by measures such as life expectancy, mortality rates, health and functional status, the incidence and/or prevalence of chronic disease, and behavioral and physiological factors such as smoking, physical activity, diet, blood pressure, body mass index, and cholesterol.⁵

On the other hand, population management is primarily concerned with health care determinants of health and, according to IHI, should be clearly distinguished from population health, which focuses on the broader determinants of health.⁵

According to Ron Greeno, MD, MHM, one of the founding members and a past-president of the Society of Hospital Medicine, population management is a “global approach of caring for an entire patient population to deliver safe and equitable care and to more intelligently allocate resources to keep people well.”

Population management requires understanding the patient population, which includes risk stratification and redesigning and delivering services that are guided by integrated clinical and administrative data and enabled by information technology.
 

Cost-sharing payment models

The cornerstone of population management is provider accountability for the cost of care, which can be accomplished through shared-risk models or population-based payments. Let’s take a closer look at each.

Under shared-risk models, providers receive payment based on their performance against cost targets. The goal is to generate cost savings by improving care coordination, engaging patients in shared decision making based on their health goals, and reducing utilization of care that provides little to no value for patients (for example, preventable hospital admissions or unnecessary imaging or procedures).

Cost targets and actual spending are reconciled retrospectively. If providers beat cost targets, they are eligible to keep a share of generated savings based on their performance on selected quality measures. However, if providers’ actual spending exceeds cost targets, they will compensate payers for a portion of the losses. Under one-sided risk models, providers are eligible for shared savings but not financially responsible for losses. Under two-sided risk models, providers are accountable for both savings and losses.

With prospective population-based payments, also known as capitation, providers receive in advance a fixed amount of money per patient per unit of time (for example, per month) that creates a budget to cover the cost of agreed-upon health care services. The prospective payments are risk adjusted and typically tied to performance on selected quality, effectiveness, and patient experience measures.

Professional services capitation arrangements between physician groups and payers cover the cost of physician services including primary care, specialty care, and related laboratory and radiology services. Under global capitation or global payment arrangements, health care systems receive payments that cover the total cost of care for the patient population for a defined period.

Population-based payments create incentives to provide high-quality and efficient care within a set budget.⁶ If actual cost of delivering services to the defined patient population comes under the budget, the providers will realize savings, but otherwise will encounter losses.
 

What is next?

Now that we have explained the impetus for population management and the terminology, in the next article in this series we will discuss the current state of population management. We will also delve into a hospitalist’s role and participation so you can be aware of impending changes and ensure you are set up for success, no matter how the payment models evolve.
 

Dr. Farah is a hospitalist, physician adviser, and Lean Six Sigma Black Belt. She is a performance improvement consultant based in Corvallis, Ore., and a member of The Hospitalist’s editorial advisory board.

References

1. Source: https://www.healthsystemtracker.org/chart-collection/health-spending-u-s-compare-countries/#item-start

2. Source: https://www.healthsystemtracker.org/brief/on-several-indicators-of-healthcare-quality the-u-s-falls-short/

3. Kindig D, Asada Y, Booske B. (2008). A Population Health Framework for Setting National and State Health Goals. JAMA, 299, 2081-2083.

4. Source: https://improvingpopulationhealth.typepad.com/blog/what-are-health-factorsdeterminants.html

5. Source: http://www.ihi.org/communities/blogs/population-health-population-management-terminology-in-us-health-care

6. Source: http://hcp-lan.org/workproducts/apm-refresh-whitepaper-final.pdf

Traditionally, U.S. health care has operated under a fee-for-service payment model, in which health care providers (such as physicians, hospitals, and health care systems) receive a fee for services such as office visits, hospital stays, procedures, and tests. However, reimbursement discussions are increasingly moving from fee-for-service to value-based, in which payments are tied to managing population health and total cost of care.

Because these changes will impact the entire system all the way down to individual providers, in the upcoming Population Management article series in The Hospitalist, we will discuss the nuances and implications that physicians, executives, and hospitals should be aware of. In this first article, we will examine the impetus for the shift toward population management and introduce common terminology to lay the foundation for the future content.
 

The traditional model: Fee for service

Under the traditional fee-for-service payment system, health care providers are paid per unit of service. For example, hospitals receive diagnosis-related group (DRG) payments for inpatient stays, and physicians are paid per patient visit. The more services that hospitals or physicians provide, the more money both get paid, without financial consequences for quality outcomes or total cost of care. Total cost of care includes clinic visits, outpatient procedures and tests, hospital and ED visits, home health, skilled nursing facilities, durable medical equipment, and sometimes drugs during an episode of care (for example, a hospital stay plus 90 days after discharge) or over a period of time (for example, a month or a year).

As a result of the fee-for-service payment system, the United States spends more money on health care than other wealthy countries, yet it lags behind other countries on many quality measures, such as disease burden, overall mortality, premature death, and preventable death.^1,2

In 2007, the Institute for Healthcare Improvement (IHI) developed the Triple Aim framework that focused on the following:

• Improving the patient experience of care (including quality and satisfaction).
• Improving the health of populations.
• Reducing per capita cost of care.

Both public payers like Medicare and Medicaid, as well as private payers, embraced the Triple Aim to reform how health care is delivered and paid for. As such, health care delivery focus and financial incentives are shifting from managing discrete patient encounters for acute illness to managing population health and total cost of care.
 

A new approach: Population management

Before diving into population management, it is important to first understand the terms “population” and “population health.” A population can be defined geographically or may include employees of an organization, members of a health plan, or patients receiving care from a specific physician group or health care system. David A. Kindig, MD, PhD, professor emeritus of population health sciences at the University of Wisconsin–Madison, defined population health as “the health outcomes of a group of individuals, including the distribution of such outcomes within the group.”³ Dr. Kindig noted that population health outcomes have many determinants, such as the following:⁴

• Health care (access, cost, quantity, and quality of health care services).
• Individual behavior (including diet, exercise, and substance abuse).
• Genetics.
• The social environment (education, income, occupation, class, and social support).
• Physical environment (air and water quality, lead exposure, and the design of neighborhoods).

IHI operationally defines population health by measures such as life expectancy, mortality rates, health and functional status, the incidence and/or prevalence of chronic disease, and behavioral and physiological factors such as smoking, physical activity, diet, blood pressure, body mass index, and cholesterol.⁵

On the other hand, population management is primarily concerned with health care determinants of health and, according to IHI, should be clearly distinguished from population health, which focuses on the broader determinants of health.⁵

According to Ron Greeno, MD, MHM, one of the founding members and a past-president of the Society of Hospital Medicine, population management is a “global approach of caring for an entire patient population to deliver safe and equitable care and to more intelligently allocate resources to keep people well.”

Population management requires understanding the patient population, which includes risk stratification and redesigning and delivering services that are guided by integrated clinical and administrative data and enabled by information technology.
 

Cost-sharing payment models

The cornerstone of population management is provider accountability for the cost of care, which can be accomplished through shared-risk models or population-based payments. Let’s take a closer look at each.

Under shared-risk models, providers receive payment based on their performance against cost targets. The goal is to generate cost savings by improving care coordination, engaging patients in shared decision making based on their health goals, and reducing utilization of care that provides little to no value for patients (for example, preventable hospital admissions or unnecessary imaging or procedures).

Cost targets and actual spending are reconciled retrospectively. If providers beat cost targets, they are eligible to keep a share of generated savings based on their performance on selected quality measures. However, if providers’ actual spending exceeds cost targets, they will compensate payers for a portion of the losses. Under one-sided risk models, providers are eligible for shared savings but not financially responsible for losses. Under two-sided risk models, providers are accountable for both savings and losses.

With prospective population-based payments, also known as capitation, providers receive in advance a fixed amount of money per patient per unit of time (for example, per month) that creates a budget to cover the cost of agreed-upon health care services. The prospective payments are risk adjusted and typically tied to performance on selected quality, effectiveness, and patient experience measures.

Professional services capitation arrangements between physician groups and payers cover the cost of physician services including primary care, specialty care, and related laboratory and radiology services. Under global capitation or global payment arrangements, health care systems receive payments that cover the total cost of care for the patient population for a defined period.

Population-based payments create incentives to provide high-quality and efficient care within a set budget.⁶ If actual cost of delivering services to the defined patient population comes under the budget, the providers will realize savings, but otherwise will encounter losses.
 

What is next?

Now that we have explained the impetus for population management and the terminology, in the next article in this series we will discuss the current state of population management. We will also delve into a hospitalist’s role and participation so you can be aware of impending changes and ensure you are set up for success, no matter how the payment models evolve.
 

Dr. Farah is a hospitalist, physician adviser, and Lean Six Sigma Black Belt. She is a performance improvement consultant based in Corvallis, Ore., and a member of The Hospitalist’s editorial advisory board.

References

1. Source: https://www.healthsystemtracker.org/chart-collection/health-spending-u-s-compare-countries/#item-start

2. Source: https://www.healthsystemtracker.org/brief/on-several-indicators-of-healthcare-quality the-u-s-falls-short/

3. Kindig D, Asada Y, Booske B. (2008). A Population Health Framework for Setting National and State Health Goals. JAMA, 299, 2081-2083.

4. Source: https://improvingpopulationhealth.typepad.com/blog/what-are-health-factorsdeterminants.html

5. Source: http://www.ihi.org/communities/blogs/population-health-population-management-terminology-in-us-health-care

6. Source: http://hcp-lan.org/workproducts/apm-refresh-whitepaper-final.pdf

Traditionally, U.S. health care has operated under a fee-for-service payment model, in which health care providers (such as physicians, hospitals, and health care systems) receive a fee for services such as office visits, hospital stays, procedures, and tests. However, reimbursement discussions are increasingly moving from fee-for-service to value-based, in which payments are tied to managing population health and total cost of care.

Because these changes will impact the entire system all the way down to individual providers, in the upcoming Population Management article series in The Hospitalist, we will discuss the nuances and implications that physicians, executives, and hospitals should be aware of. In this first article, we will examine the impetus for the shift toward population management and introduce common terminology to lay the foundation for the future content.
 

The traditional model: Fee for service

Under the traditional fee-for-service payment system, health care providers are paid per unit of service. For example, hospitals receive diagnosis-related group (DRG) payments for inpatient stays, and physicians are paid per patient visit. The more services that hospitals or physicians provide, the more money both get paid, without financial consequences for quality outcomes or total cost of care. Total cost of care includes clinic visits, outpatient procedures and tests, hospital and ED visits, home health, skilled nursing facilities, durable medical equipment, and sometimes drugs during an episode of care (for example, a hospital stay plus 90 days after discharge) or over a period of time (for example, a month or a year).

As a result of the fee-for-service payment system, the United States spends more money on health care than other wealthy countries, yet it lags behind other countries on many quality measures, such as disease burden, overall mortality, premature death, and preventable death.^1,2

In 2007, the Institute for Healthcare Improvement (IHI) developed the Triple Aim framework that focused on the following:

• Improving the patient experience of care (including quality and satisfaction).
• Improving the health of populations.
• Reducing per capita cost of care.

Both public payers like Medicare and Medicaid, as well as private payers, embraced the Triple Aim to reform how health care is delivered and paid for. As such, health care delivery focus and financial incentives are shifting from managing discrete patient encounters for acute illness to managing population health and total cost of care.
 

A new approach: Population management

Before diving into population management, it is important to first understand the terms “population” and “population health.” A population can be defined geographically or may include employees of an organization, members of a health plan, or patients receiving care from a specific physician group or health care system. David A. Kindig, MD, PhD, professor emeritus of population health sciences at the University of Wisconsin–Madison, defined population health as “the health outcomes of a group of individuals, including the distribution of such outcomes within the group.”³ Dr. Kindig noted that population health outcomes have many determinants, such as the following:⁴

• Health care (access, cost, quantity, and quality of health care services).
• Individual behavior (including diet, exercise, and substance abuse).
• Genetics.
• The social environment (education, income, occupation, class, and social support).
• Physical environment (air and water quality, lead exposure, and the design of neighborhoods).

IHI operationally defines population health by measures such as life expectancy, mortality rates, health and functional status, the incidence and/or prevalence of chronic disease, and behavioral and physiological factors such as smoking, physical activity, diet, blood pressure, body mass index, and cholesterol.⁵

On the other hand, population management is primarily concerned with health care determinants of health and, according to IHI, should be clearly distinguished from population health, which focuses on the broader determinants of health.⁵

According to Ron Greeno, MD, MHM, one of the founding members and a past-president of the Society of Hospital Medicine, population management is a “global approach of caring for an entire patient population to deliver safe and equitable care and to more intelligently allocate resources to keep people well.”

Population management requires understanding the patient population, which includes risk stratification and redesigning and delivering services that are guided by integrated clinical and administrative data and enabled by information technology.
 

Cost-sharing payment models

The cornerstone of population management is provider accountability for the cost of care, which can be accomplished through shared-risk models or population-based payments. Let’s take a closer look at each.

Under shared-risk models, providers receive payment based on their performance against cost targets. The goal is to generate cost savings by improving care coordination, engaging patients in shared decision making based on their health goals, and reducing utilization of care that provides little to no value for patients (for example, preventable hospital admissions or unnecessary imaging or procedures).

Cost targets and actual spending are reconciled retrospectively. If providers beat cost targets, they are eligible to keep a share of generated savings based on their performance on selected quality measures. However, if providers’ actual spending exceeds cost targets, they will compensate payers for a portion of the losses. Under one-sided risk models, providers are eligible for shared savings but not financially responsible for losses. Under two-sided risk models, providers are accountable for both savings and losses.

With prospective population-based payments, also known as capitation, providers receive in advance a fixed amount of money per patient per unit of time (for example, per month) that creates a budget to cover the cost of agreed-upon health care services. The prospective payments are risk adjusted and typically tied to performance on selected quality, effectiveness, and patient experience measures.

Professional services capitation arrangements between physician groups and payers cover the cost of physician services including primary care, specialty care, and related laboratory and radiology services. Under global capitation or global payment arrangements, health care systems receive payments that cover the total cost of care for the patient population for a defined period.

Population-based payments create incentives to provide high-quality and efficient care within a set budget.⁶ If actual cost of delivering services to the defined patient population comes under the budget, the providers will realize savings, but otherwise will encounter losses.
 

What is next?

Now that we have explained the impetus for population management and the terminology, in the next article in this series we will discuss the current state of population management. We will also delve into a hospitalist’s role and participation so you can be aware of impending changes and ensure you are set up for success, no matter how the payment models evolve.
 

Dr. Farah is a hospitalist, physician adviser, and Lean Six Sigma Black Belt. She is a performance improvement consultant based in Corvallis, Ore., and a member of The Hospitalist’s editorial advisory board.

References

1. Source: https://www.healthsystemtracker.org/chart-collection/health-spending-u-s-compare-countries/#item-start

2. Source: https://www.healthsystemtracker.org/brief/on-several-indicators-of-healthcare-quality the-u-s-falls-short/

3. Kindig D, Asada Y, Booske B. (2008). A Population Health Framework for Setting National and State Health Goals. JAMA, 299, 2081-2083.

4. Source: https://improvingpopulationhealth.typepad.com/blog/what-are-health-factorsdeterminants.html

5. Source: http://www.ihi.org/communities/blogs/population-health-population-management-terminology-in-us-health-care

6. Source: http://hcp-lan.org/workproducts/apm-refresh-whitepaper-final.pdf