Federal Practitioner

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series by this news organization that tells these stories.

It was my first night off after 12 days. It was a Friday night, and I went to a bar in Naples to get a beer with some friends. As it turned out, it wasn’t a night off after all.

As soon as we got inside, we heard over the speaker that they needed medical personnel and to please go to the left side of the bar. I thought it would be syncope or something like that.

I went over there and saw a woman holding up a man. He was basically leaning all over her. The light was low, and the music was pounding. I started to assess him and tried to get him to answer me. No response. I checked for pulses — nothing.

Now, I’m in a bar, right? It’s a cardiac arrest. The first thing you think is overdose or alcohol. I asked the woman if the man was doing any drugs. She said she didn’t know. Turns out they were both employees. He was a bouncer and a DJ.

The woman helped me lower him to the floor. I checked again for a pulse. Still nothing. I said, “Call 911,” and started compressions.

The difficult part was the place was completely dark. I knew where his body was on the floor. I could see his chest. But I couldn’t see his face at all.

It was also extremely loud with the music thumping. After a while, they finally shut it off.

Pretty soon, the security personnel from the bar brought me an automated external defibrillator, and it showed the man was having V-fib arrest. I shocked him. Still no pulse. I continued with cardiopulmonary resuscitation (CPR).

I hadn’t noticed, but lots of people were crowding around us. Somebody came up and said, “He’s my friend. He has a 9-year-old daughter. He can’t die. Let me help with the compressions.” I was like, “Go for it.”

The guy started kind of pushing on the man’s abdomen. He had no idea how to do compressions. I said, “Okay, let me take over again.”

Out of the crowd, nobody else volunteered to help. No one asked me, “Hey, what can I do?” Meanwhile, I found out later that someone was filming the whole thing on their phone.

But what the guy said about the man’s young daughter stayed in my brain. I thought, we need to keep going.

I did more compressions and shocked him again. Still no pulse. At that point, the police and emergency medical services showed up. They checked, nothing had changed, so they got him into the ambulance.

I asked one of the paramedics, “Where are you taking him? I can call ahead.”

But he said, “That’s HIPAA. We can’t tell you.” They also wouldn’t let me go with him in the ambulance.

“I have an active Florida license, and I work in the ICU [intensive care unit],” I said.

“No, we need to follow our protocol,” he replied.

I understood that, but I just wanted to help.

It was around 10:30 PM by then, and I was drenched in sweat. I had to go home. The first thing I did after taking a shower was open the computer and check my system. I needed to find out what happened to the guy.

I was looking for admissions, and I didn’t see him. I called the main hospital downtown and the one in North Naples. I couldn’t find him anywhere. I stayed up until almost 1:00 AM checking for his name. At that point I thought, okay, maybe he died.

The next night, Saturday, I was home and got a call from one of my colleagues. “Hey, were you in a bar yesterday? Did you do CPR on somebody?”

“How did you know?” I said.

He said the paramedics had described me — “a tall doctor with glasses who was a nice guy.” It was funny that he knew that was me.

He told me, “The guy’s alive. He’s sick and needs to be put on dialysis, but he’s alive.”

Apparently, the guy had gone to the emergency department at North Naples, and the doctors in the emergency room (ER) worked on him for over an hour. They did continuous CPR and shocked him for close to 40 minutes. They finally got his pulse back, and after that, he was transferred to the main hospital ICU. They didn’t admit him at the ER, which was why I couldn’t find his name.

On Sunday, I was checking my patients’ charts for the ICU that coming week. And there he was. I saw his name and the documentation by the ED that CPR was provided by a critical care doctor in the field. He was still alive. That gave me so much joy.

So, the man I had helped became my patient. When I saw him on Monday, he was intubated and needed dialysis. I finally saw his face and thought, Oh, so that’s what you look like. I hadn’t realized he was only 39 years old.

When he was awake, I explained to him I was the doctor that provided CPR at the bar. He was very grateful, but of course, he didn’t remember anything.

Eventually, I met his daughter, and she just said, “Thank you for allowing me to have my dad.”

The funny part is that he broke his leg. Well, that’s not funny, but no one had any idea how it happened. That was his only complaint. He was asking me, “Doctor, how did you break my leg?”

“Hey, I have no idea how you broke your leg,” I replied. “I was trying to save your life.”

He was in the hospital for almost a month but made a full recovery. The amazing part: After all the evaluations, he has no neurological deficits. He’s back to a normal life now.

They never found a cause for the cardiac arrest. I mean, he had an ejection fraction of 10%. All my money was on something drug related, but that wasn’t the case. They’d done a cardiac cut, and there was no obstruction. They couldn’t find a reason.

We’ve become friends. He still works as a DJ at the bar. He changed his name to “DJ the Survivor” or something like that.

Sometimes, he’ll text me: “Doctor, what are you doing? You want to come down to the bar?”

I’m like, “No. I don’t.”

It’s been more than a year, but I remember every detail. When you go into medicine, you dream that one day you’ll be able to say, “I saved somebody.”

He texted me a year later and told me he’s celebrating two birthdays now. He said, “I’m turning 1 year old today!”

I think about the value of life. How we can take it for granted. We think, I’m young, nothing is going to happen to me. But this guy was 39. He went to work and died that night.

I was able to help bring him back. That makes me thankful for every day.

Jose Valle Giler, MD, is a pulmonary, critical care, and sleep medicine physician at NCH Healthcare System in Naples, Florida.

A version of this article appeared on Medscape.com .

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series by this news organization that tells these stories.

It was my first night off after 12 days. It was a Friday night, and I went to a bar in Naples to get a beer with some friends. As it turned out, it wasn’t a night off after all.

As soon as we got inside, we heard over the speaker that they needed medical personnel and to please go to the left side of the bar. I thought it would be syncope or something like that.

I went over there and saw a woman holding up a man. He was basically leaning all over her. The light was low, and the music was pounding. I started to assess him and tried to get him to answer me. No response. I checked for pulses — nothing.

Now, I’m in a bar, right? It’s a cardiac arrest. The first thing you think is overdose or alcohol. I asked the woman if the man was doing any drugs. She said she didn’t know. Turns out they were both employees. He was a bouncer and a DJ.

The woman helped me lower him to the floor. I checked again for a pulse. Still nothing. I said, “Call 911,” and started compressions.

The difficult part was the place was completely dark. I knew where his body was on the floor. I could see his chest. But I couldn’t see his face at all.

It was also extremely loud with the music thumping. After a while, they finally shut it off.

Pretty soon, the security personnel from the bar brought me an automated external defibrillator, and it showed the man was having V-fib arrest. I shocked him. Still no pulse. I continued with cardiopulmonary resuscitation (CPR).

I hadn’t noticed, but lots of people were crowding around us. Somebody came up and said, “He’s my friend. He has a 9-year-old daughter. He can’t die. Let me help with the compressions.” I was like, “Go for it.”

The guy started kind of pushing on the man’s abdomen. He had no idea how to do compressions. I said, “Okay, let me take over again.”

Out of the crowd, nobody else volunteered to help. No one asked me, “Hey, what can I do?” Meanwhile, I found out later that someone was filming the whole thing on their phone.

But what the guy said about the man’s young daughter stayed in my brain. I thought, we need to keep going.

I did more compressions and shocked him again. Still no pulse. At that point, the police and emergency medical services showed up. They checked, nothing had changed, so they got him into the ambulance.

I asked one of the paramedics, “Where are you taking him? I can call ahead.”

But he said, “That’s HIPAA. We can’t tell you.” They also wouldn’t let me go with him in the ambulance.

“I have an active Florida license, and I work in the ICU [intensive care unit],” I said.

“No, we need to follow our protocol,” he replied.

I understood that, but I just wanted to help.

It was around 10:30 PM by then, and I was drenched in sweat. I had to go home. The first thing I did after taking a shower was open the computer and check my system. I needed to find out what happened to the guy.

I was looking for admissions, and I didn’t see him. I called the main hospital downtown and the one in North Naples. I couldn’t find him anywhere. I stayed up until almost 1:00 AM checking for his name. At that point I thought, okay, maybe he died.

The next night, Saturday, I was home and got a call from one of my colleagues. “Hey, were you in a bar yesterday? Did you do CPR on somebody?”

“How did you know?” I said.

He said the paramedics had described me — “a tall doctor with glasses who was a nice guy.” It was funny that he knew that was me.

He told me, “The guy’s alive. He’s sick and needs to be put on dialysis, but he’s alive.”

Apparently, the guy had gone to the emergency department at North Naples, and the doctors in the emergency room (ER) worked on him for over an hour. They did continuous CPR and shocked him for close to 40 minutes. They finally got his pulse back, and after that, he was transferred to the main hospital ICU. They didn’t admit him at the ER, which was why I couldn’t find his name.

On Sunday, I was checking my patients’ charts for the ICU that coming week. And there he was. I saw his name and the documentation by the ED that CPR was provided by a critical care doctor in the field. He was still alive. That gave me so much joy.

So, the man I had helped became my patient. When I saw him on Monday, he was intubated and needed dialysis. I finally saw his face and thought, Oh, so that’s what you look like. I hadn’t realized he was only 39 years old.

When he was awake, I explained to him I was the doctor that provided CPR at the bar. He was very grateful, but of course, he didn’t remember anything.

Eventually, I met his daughter, and she just said, “Thank you for allowing me to have my dad.”

The funny part is that he broke his leg. Well, that’s not funny, but no one had any idea how it happened. That was his only complaint. He was asking me, “Doctor, how did you break my leg?”

“Hey, I have no idea how you broke your leg,” I replied. “I was trying to save your life.”

He was in the hospital for almost a month but made a full recovery. The amazing part: After all the evaluations, he has no neurological deficits. He’s back to a normal life now.

They never found a cause for the cardiac arrest. I mean, he had an ejection fraction of 10%. All my money was on something drug related, but that wasn’t the case. They’d done a cardiac cut, and there was no obstruction. They couldn’t find a reason.

We’ve become friends. He still works as a DJ at the bar. He changed his name to “DJ the Survivor” or something like that.

Sometimes, he’ll text me: “Doctor, what are you doing? You want to come down to the bar?”

I’m like, “No. I don’t.”

It’s been more than a year, but I remember every detail. When you go into medicine, you dream that one day you’ll be able to say, “I saved somebody.”

He texted me a year later and told me he’s celebrating two birthdays now. He said, “I’m turning 1 year old today!”

I think about the value of life. How we can take it for granted. We think, I’m young, nothing is going to happen to me. But this guy was 39. He went to work and died that night.

I was able to help bring him back. That makes me thankful for every day.

Jose Valle Giler, MD, is a pulmonary, critical care, and sleep medicine physician at NCH Healthcare System in Naples, Florida.

A version of this article appeared on Medscape.com .

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series by this news organization that tells these stories.

It was my first night off after 12 days. It was a Friday night, and I went to a bar in Naples to get a beer with some friends. As it turned out, it wasn’t a night off after all.

As soon as we got inside, we heard over the speaker that they needed medical personnel and to please go to the left side of the bar. I thought it would be syncope or something like that.

I went over there and saw a woman holding up a man. He was basically leaning all over her. The light was low, and the music was pounding. I started to assess him and tried to get him to answer me. No response. I checked for pulses — nothing.

Now, I’m in a bar, right? It’s a cardiac arrest. The first thing you think is overdose or alcohol. I asked the woman if the man was doing any drugs. She said she didn’t know. Turns out they were both employees. He was a bouncer and a DJ.

The woman helped me lower him to the floor. I checked again for a pulse. Still nothing. I said, “Call 911,” and started compressions.

The difficult part was the place was completely dark. I knew where his body was on the floor. I could see his chest. But I couldn’t see his face at all.

It was also extremely loud with the music thumping. After a while, they finally shut it off.

Pretty soon, the security personnel from the bar brought me an automated external defibrillator, and it showed the man was having V-fib arrest. I shocked him. Still no pulse. I continued with cardiopulmonary resuscitation (CPR).

I hadn’t noticed, but lots of people were crowding around us. Somebody came up and said, “He’s my friend. He has a 9-year-old daughter. He can’t die. Let me help with the compressions.” I was like, “Go for it.”

The guy started kind of pushing on the man’s abdomen. He had no idea how to do compressions. I said, “Okay, let me take over again.”

Out of the crowd, nobody else volunteered to help. No one asked me, “Hey, what can I do?” Meanwhile, I found out later that someone was filming the whole thing on their phone.

But what the guy said about the man’s young daughter stayed in my brain. I thought, we need to keep going.

I did more compressions and shocked him again. Still no pulse. At that point, the police and emergency medical services showed up. They checked, nothing had changed, so they got him into the ambulance.

I asked one of the paramedics, “Where are you taking him? I can call ahead.”

But he said, “That’s HIPAA. We can’t tell you.” They also wouldn’t let me go with him in the ambulance.

“I have an active Florida license, and I work in the ICU [intensive care unit],” I said.

“No, we need to follow our protocol,” he replied.

I understood that, but I just wanted to help.

It was around 10:30 PM by then, and I was drenched in sweat. I had to go home. The first thing I did after taking a shower was open the computer and check my system. I needed to find out what happened to the guy.

I was looking for admissions, and I didn’t see him. I called the main hospital downtown and the one in North Naples. I couldn’t find him anywhere. I stayed up until almost 1:00 AM checking for his name. At that point I thought, okay, maybe he died.

The next night, Saturday, I was home and got a call from one of my colleagues. “Hey, were you in a bar yesterday? Did you do CPR on somebody?”

“How did you know?” I said.

He said the paramedics had described me — “a tall doctor with glasses who was a nice guy.” It was funny that he knew that was me.

He told me, “The guy’s alive. He’s sick and needs to be put on dialysis, but he’s alive.”

Apparently, the guy had gone to the emergency department at North Naples, and the doctors in the emergency room (ER) worked on him for over an hour. They did continuous CPR and shocked him for close to 40 minutes. They finally got his pulse back, and after that, he was transferred to the main hospital ICU. They didn’t admit him at the ER, which was why I couldn’t find his name.

On Sunday, I was checking my patients’ charts for the ICU that coming week. And there he was. I saw his name and the documentation by the ED that CPR was provided by a critical care doctor in the field. He was still alive. That gave me so much joy.

So, the man I had helped became my patient. When I saw him on Monday, he was intubated and needed dialysis. I finally saw his face and thought, Oh, so that’s what you look like. I hadn’t realized he was only 39 years old.

When he was awake, I explained to him I was the doctor that provided CPR at the bar. He was very grateful, but of course, he didn’t remember anything.

Eventually, I met his daughter, and she just said, “Thank you for allowing me to have my dad.”

The funny part is that he broke his leg. Well, that’s not funny, but no one had any idea how it happened. That was his only complaint. He was asking me, “Doctor, how did you break my leg?”

“Hey, I have no idea how you broke your leg,” I replied. “I was trying to save your life.”

He was in the hospital for almost a month but made a full recovery. The amazing part: After all the evaluations, he has no neurological deficits. He’s back to a normal life now.

They never found a cause for the cardiac arrest. I mean, he had an ejection fraction of 10%. All my money was on something drug related, but that wasn’t the case. They’d done a cardiac cut, and there was no obstruction. They couldn’t find a reason.

We’ve become friends. He still works as a DJ at the bar. He changed his name to “DJ the Survivor” or something like that.

Sometimes, he’ll text me: “Doctor, what are you doing? You want to come down to the bar?”

I’m like, “No. I don’t.”

It’s been more than a year, but I remember every detail. When you go into medicine, you dream that one day you’ll be able to say, “I saved somebody.”

He texted me a year later and told me he’s celebrating two birthdays now. He said, “I’m turning 1 year old today!”

I think about the value of life. How we can take it for granted. We think, I’m young, nothing is going to happen to me. But this guy was 39. He went to work and died that night.

I was able to help bring him back. That makes me thankful for every day.

Jose Valle Giler, MD, is a pulmonary, critical care, and sleep medicine physician at NCH Healthcare System in Naples, Florida.

A version of this article appeared on Medscape.com .

Physicians who misuse the “copy-and-paste” feature in patients’ electronic health records (EHRs) can face serious consequences, including lost hospital privileges, fines, and malpractice lawsuits.

In California, a locum tenens physician lost her hospital privileges after repeatedly violating the copy-and-paste policy developed at Santa Rosa Memorial Hospital, Santa Rosa, California.

“Her use of copy and paste impaired continuity of care,” said Alvin Gore, MD, who was involved in the case as the hospital’s director of utilization management.

Dr. Gore said the hospital warned the doctor, but she did not change her behavior. He did not identify the physician, citing confidentiality. The case occurred more than 5 years ago. Since then, several physicians have been called onto the carpet for violations of the policy, but no one else has lost privileges, Dr. Gore said.

Copy-paste practices can save doctors’ time when dealing with cumbersome EHR systems, but they also can lead to redundant, outdated, or inconsistent information that can compromise patient care, experts said.

“EHRs are imperfect, time consuming, and somewhat rigid,” said Robert A. Dowling, MD, a practice management consultant for large medical groups. “If physicians can’t easily figure out a complex system, they’re likely to use a workaround like copy and paste.”

Copy-and-paste abuse has also led to fines. A six-member cardiology group in Somerville, New Jersey, paid a $422,000 fine to the federal government to settle copy-and-paste charges, following an investigation by the Office of the Inspector General of the Department of Health and Human Services, according to the Report on Medicare Compliance.

This big settlement, announced in 2016, is a rare case in which physicians were charged with copy-and-paste fraud — intentionally using it to enhance reimbursement.

More commonly, Medicare contractors identify physicians who unintentionally received overpayments through sloppy copy-and-paste practices, according to a coding and documentation auditor who worked for 10 years at a Medicare contractor in Pennsylvania.

Such cases are frequent and are handled confidentially, said the auditor, who asked not to be identified. Practices must return the overpayment, and the physicians involved are “contacted and educated,” she said.

Copy and paste can also show up in malpractice lawsuits. In a 2012 survey, 53% of professional liability carriers said they had handled an EHR-related malpractice claim, and 71% of those claims included copy-and-paste use.

One such case, described by CRICO, a malpractice carrier based in Massachusetts, took place in 2012-2013. “A patient developed amiodarone toxicity because the patient›s history and medications were copied from a previous note that did not document that the patient was already on the medication,» CRICO stated.

“If you do face a malpractice claim, copying and pasting the same note repeatedly makes you look clinically inattentive, even if the copy/pasted material is unrelated to the adverse event,” CRICO officials noted in a report.
 

The Push to Use Copy and Paste

Copy and paste is a great time-saver. One study linked its use to lower burnout rates. However, it can easily introduce errors into the medical record. “This can be a huge problem,” Dr. Dowling said. “If, for example, you copy forward a previous note that said the patient had blood in their urine ‘6 days ago,’ it is immediately inaccurate.”

Practices can control use of copy and paste through coding clerks who read the medical records and then educate doctors when problems crop up.

The Pennsylvania auditor, who now works for a large group practice, said the group has very few copy-and-paste problems because of her role. “Not charting responsibly rarely happens because I work very closely with the doctors,” she said.

Dr. Dowling, however, reports that many physicians continue to overuse copy and paste. He points to a 2022 study which found that, on average, half the clinical note at one health system had been copied and pasted.

One solution might be to sanction physicians for overusing copy and paste, just as they’re sometimes penalized for not completing their notes on time with a reduction in income or possible termination.

Practices could periodically audit medical records for excessive copy-paste use. EHR systems like Epic’s can indicate how much of a doctor’s note has been copied. But Dr. Dowling doesn’t know of any practices that do this.

“There is little appetite to introduce a new enforcement activity for physicians,” he said. “Physicians would see it just as a way to make their lives more difficult than they already are.”
 

Monitoring in Hospitals and Health Systems

Some hospitals and health systems have gone as far as disabling copy-and-paste function in their EHR systems. However, enterprising physicians have found ways around these blocks.

Some institutions have also introduced formal policies, directing doctors on how they can copy and paste, including Banner Health in Arizona, Northwell Health in New York, UConn Health in Connecticut, University of Maryland Medical System, and University of Toledo in Ohio.

Definitions of what is not acceptable vary, but most of these policies oppose copying someone else’s notes and direct physicians to indicate the origin of pasted material.

Santa Rosa Memorial’s policy is quite specific. It still allows some copy and paste but stipulates that it cannot be used for the chief complaint, the review of systems, the physical examination, and the assessment and plan in the medical record, except when the information can’t be obtained directly from the patient. Also, physicians must summarize test results and provide references to other providers’ notes.

Dr. Gore said he and a physician educator who works with physicians on clinical documentation proposed the policy about a decade ago. When physicians on staff were asked to comment, some said they would be opposed to a complete ban, but they generally agreed that copy and paste was a serious problem that needed to be addressed, he said.

The hospital could have simply adopted guidelines, as opposed to rules with consequences, but “we wanted our policy to have teeth,” Dr. Gore said.

When violators are identified, Dr. Gore says he meets with them confidentially and educates them on proper use of copy and paste. Sometimes, the department head is brought in. Some physicians go on to violate the policy again and have to attend another meeting, he said, but aside from the one case, no one else has been disciplined.

It’s unclear how many physicians have faced consequences for misusing copy-paste features — such data aren’t tracked, and sanctions are likely to be handled confidentially, as a personnel matter.

Geisinger Health in Pennsylvania regularly monitors copy-and-paste usage and makes it part of physicians’ professional evaluations, according to a 2022 presentation by a Geisinger official.

Meanwhile, even when systems don’t have specific policies, they may still discipline physicians when copy and paste leads to errors. Scott MacDonald, MD, chief medical information officer at UC Davis Health in Sacramento, California, told this news organization that copy-and-paste abuse has come up a few times over the years in investigations of clinical errors.
 

Holding Physicians Accountable

Physicians can be held accountable for copy and paste by Medicare contractors and in malpractice lawsuits, but the most obvious way is at their place of work: A practice, hospital, or health system.

One physician has lost staff privileges, but more typically, coding clerks or colleagues talk to offending physicians and try to educate them on proper use of copy and paste.

Educational outreach, however, is often ineffective, said Robert Hirschtick, MD, a retired teaching physician at Northwestern University Feinberg School of Medicine, Chicago, Illinois. “The physician may be directed to take an online course,” he said. “When they take the course, the goal is to get it done with, rather than to learn something new.”

Dr. Hirschtick’s articles on copy and paste, including one titled, “Sloppy and Paste,” have put him at the front lines of the debate. “This is an ethical issue,” he said in an interview. He agrees that some forms of copy and paste are permissible, but in many cases, “it is intellectually dishonest and potentially even plagiarism,” he said.

Dr. Hirschtick argues that copy-and-paste policies need more teeth. “Tying violations to compensation would be quite effective,” he said. “Even if physicians were rarely penalized, just knowing that it could happen to you might be enough. But I haven’t heard of anyone doing this.”

A version of this article appeared on Medscape.com.

Physicians who misuse the “copy-and-paste” feature in patients’ electronic health records (EHRs) can face serious consequences, including lost hospital privileges, fines, and malpractice lawsuits.

In California, a locum tenens physician lost her hospital privileges after repeatedly violating the copy-and-paste policy developed at Santa Rosa Memorial Hospital, Santa Rosa, California.

“Her use of copy and paste impaired continuity of care,” said Alvin Gore, MD, who was involved in the case as the hospital’s director of utilization management.

Dr. Gore said the hospital warned the doctor, but she did not change her behavior. He did not identify the physician, citing confidentiality. The case occurred more than 5 years ago. Since then, several physicians have been called onto the carpet for violations of the policy, but no one else has lost privileges, Dr. Gore said.

Copy-paste practices can save doctors’ time when dealing with cumbersome EHR systems, but they also can lead to redundant, outdated, or inconsistent information that can compromise patient care, experts said.

“EHRs are imperfect, time consuming, and somewhat rigid,” said Robert A. Dowling, MD, a practice management consultant for large medical groups. “If physicians can’t easily figure out a complex system, they’re likely to use a workaround like copy and paste.”

Copy-and-paste abuse has also led to fines. A six-member cardiology group in Somerville, New Jersey, paid a $422,000 fine to the federal government to settle copy-and-paste charges, following an investigation by the Office of the Inspector General of the Department of Health and Human Services, according to the Report on Medicare Compliance.

This big settlement, announced in 2016, is a rare case in which physicians were charged with copy-and-paste fraud — intentionally using it to enhance reimbursement.

More commonly, Medicare contractors identify physicians who unintentionally received overpayments through sloppy copy-and-paste practices, according to a coding and documentation auditor who worked for 10 years at a Medicare contractor in Pennsylvania.

Such cases are frequent and are handled confidentially, said the auditor, who asked not to be identified. Practices must return the overpayment, and the physicians involved are “contacted and educated,” she said.

Copy and paste can also show up in malpractice lawsuits. In a 2012 survey, 53% of professional liability carriers said they had handled an EHR-related malpractice claim, and 71% of those claims included copy-and-paste use.

One such case, described by CRICO, a malpractice carrier based in Massachusetts, took place in 2012-2013. “A patient developed amiodarone toxicity because the patient›s history and medications were copied from a previous note that did not document that the patient was already on the medication,» CRICO stated.

“If you do face a malpractice claim, copying and pasting the same note repeatedly makes you look clinically inattentive, even if the copy/pasted material is unrelated to the adverse event,” CRICO officials noted in a report.
 

The Push to Use Copy and Paste

Copy and paste is a great time-saver. One study linked its use to lower burnout rates. However, it can easily introduce errors into the medical record. “This can be a huge problem,” Dr. Dowling said. “If, for example, you copy forward a previous note that said the patient had blood in their urine ‘6 days ago,’ it is immediately inaccurate.”

Practices can control use of copy and paste through coding clerks who read the medical records and then educate doctors when problems crop up.

The Pennsylvania auditor, who now works for a large group practice, said the group has very few copy-and-paste problems because of her role. “Not charting responsibly rarely happens because I work very closely with the doctors,” she said.

Dr. Dowling, however, reports that many physicians continue to overuse copy and paste. He points to a 2022 study which found that, on average, half the clinical note at one health system had been copied and pasted.

One solution might be to sanction physicians for overusing copy and paste, just as they’re sometimes penalized for not completing their notes on time with a reduction in income or possible termination.

Practices could periodically audit medical records for excessive copy-paste use. EHR systems like Epic’s can indicate how much of a doctor’s note has been copied. But Dr. Dowling doesn’t know of any practices that do this.

“There is little appetite to introduce a new enforcement activity for physicians,” he said. “Physicians would see it just as a way to make their lives more difficult than they already are.”
 

Monitoring in Hospitals and Health Systems

Some hospitals and health systems have gone as far as disabling copy-and-paste function in their EHR systems. However, enterprising physicians have found ways around these blocks.

Some institutions have also introduced formal policies, directing doctors on how they can copy and paste, including Banner Health in Arizona, Northwell Health in New York, UConn Health in Connecticut, University of Maryland Medical System, and University of Toledo in Ohio.

Definitions of what is not acceptable vary, but most of these policies oppose copying someone else’s notes and direct physicians to indicate the origin of pasted material.

Santa Rosa Memorial’s policy is quite specific. It still allows some copy and paste but stipulates that it cannot be used for the chief complaint, the review of systems, the physical examination, and the assessment and plan in the medical record, except when the information can’t be obtained directly from the patient. Also, physicians must summarize test results and provide references to other providers’ notes.

Dr. Gore said he and a physician educator who works with physicians on clinical documentation proposed the policy about a decade ago. When physicians on staff were asked to comment, some said they would be opposed to a complete ban, but they generally agreed that copy and paste was a serious problem that needed to be addressed, he said.

The hospital could have simply adopted guidelines, as opposed to rules with consequences, but “we wanted our policy to have teeth,” Dr. Gore said.

When violators are identified, Dr. Gore says he meets with them confidentially and educates them on proper use of copy and paste. Sometimes, the department head is brought in. Some physicians go on to violate the policy again and have to attend another meeting, he said, but aside from the one case, no one else has been disciplined.

It’s unclear how many physicians have faced consequences for misusing copy-paste features — such data aren’t tracked, and sanctions are likely to be handled confidentially, as a personnel matter.

Geisinger Health in Pennsylvania regularly monitors copy-and-paste usage and makes it part of physicians’ professional evaluations, according to a 2022 presentation by a Geisinger official.

Meanwhile, even when systems don’t have specific policies, they may still discipline physicians when copy and paste leads to errors. Scott MacDonald, MD, chief medical information officer at UC Davis Health in Sacramento, California, told this news organization that copy-and-paste abuse has come up a few times over the years in investigations of clinical errors.
 

Holding Physicians Accountable

Physicians can be held accountable for copy and paste by Medicare contractors and in malpractice lawsuits, but the most obvious way is at their place of work: A practice, hospital, or health system.

One physician has lost staff privileges, but more typically, coding clerks or colleagues talk to offending physicians and try to educate them on proper use of copy and paste.

Educational outreach, however, is often ineffective, said Robert Hirschtick, MD, a retired teaching physician at Northwestern University Feinberg School of Medicine, Chicago, Illinois. “The physician may be directed to take an online course,” he said. “When they take the course, the goal is to get it done with, rather than to learn something new.”

Dr. Hirschtick’s articles on copy and paste, including one titled, “Sloppy and Paste,” have put him at the front lines of the debate. “This is an ethical issue,” he said in an interview. He agrees that some forms of copy and paste are permissible, but in many cases, “it is intellectually dishonest and potentially even plagiarism,” he said.

Dr. Hirschtick argues that copy-and-paste policies need more teeth. “Tying violations to compensation would be quite effective,” he said. “Even if physicians were rarely penalized, just knowing that it could happen to you might be enough. But I haven’t heard of anyone doing this.”

A version of this article appeared on Medscape.com.

Physicians who misuse the “copy-and-paste” feature in patients’ electronic health records (EHRs) can face serious consequences, including lost hospital privileges, fines, and malpractice lawsuits.

In California, a locum tenens physician lost her hospital privileges after repeatedly violating the copy-and-paste policy developed at Santa Rosa Memorial Hospital, Santa Rosa, California.

“Her use of copy and paste impaired continuity of care,” said Alvin Gore, MD, who was involved in the case as the hospital’s director of utilization management.

Dr. Gore said the hospital warned the doctor, but she did not change her behavior. He did not identify the physician, citing confidentiality. The case occurred more than 5 years ago. Since then, several physicians have been called onto the carpet for violations of the policy, but no one else has lost privileges, Dr. Gore said.

Copy-paste practices can save doctors’ time when dealing with cumbersome EHR systems, but they also can lead to redundant, outdated, or inconsistent information that can compromise patient care, experts said.

“EHRs are imperfect, time consuming, and somewhat rigid,” said Robert A. Dowling, MD, a practice management consultant for large medical groups. “If physicians can’t easily figure out a complex system, they’re likely to use a workaround like copy and paste.”

Copy-and-paste abuse has also led to fines. A six-member cardiology group in Somerville, New Jersey, paid a $422,000 fine to the federal government to settle copy-and-paste charges, following an investigation by the Office of the Inspector General of the Department of Health and Human Services, according to the Report on Medicare Compliance.

This big settlement, announced in 2016, is a rare case in which physicians were charged with copy-and-paste fraud — intentionally using it to enhance reimbursement.

More commonly, Medicare contractors identify physicians who unintentionally received overpayments through sloppy copy-and-paste practices, according to a coding and documentation auditor who worked for 10 years at a Medicare contractor in Pennsylvania.

Such cases are frequent and are handled confidentially, said the auditor, who asked not to be identified. Practices must return the overpayment, and the physicians involved are “contacted and educated,” she said.

Copy and paste can also show up in malpractice lawsuits. In a 2012 survey, 53% of professional liability carriers said they had handled an EHR-related malpractice claim, and 71% of those claims included copy-and-paste use.

One such case, described by CRICO, a malpractice carrier based in Massachusetts, took place in 2012-2013. “A patient developed amiodarone toxicity because the patient›s history and medications were copied from a previous note that did not document that the patient was already on the medication,» CRICO stated.

“If you do face a malpractice claim, copying and pasting the same note repeatedly makes you look clinically inattentive, even if the copy/pasted material is unrelated to the adverse event,” CRICO officials noted in a report.
 

The Push to Use Copy and Paste

Copy and paste is a great time-saver. One study linked its use to lower burnout rates. However, it can easily introduce errors into the medical record. “This can be a huge problem,” Dr. Dowling said. “If, for example, you copy forward a previous note that said the patient had blood in their urine ‘6 days ago,’ it is immediately inaccurate.”

Practices can control use of copy and paste through coding clerks who read the medical records and then educate doctors when problems crop up.

The Pennsylvania auditor, who now works for a large group practice, said the group has very few copy-and-paste problems because of her role. “Not charting responsibly rarely happens because I work very closely with the doctors,” she said.

Dr. Dowling, however, reports that many physicians continue to overuse copy and paste. He points to a 2022 study which found that, on average, half the clinical note at one health system had been copied and pasted.

One solution might be to sanction physicians for overusing copy and paste, just as they’re sometimes penalized for not completing their notes on time with a reduction in income or possible termination.

Practices could periodically audit medical records for excessive copy-paste use. EHR systems like Epic’s can indicate how much of a doctor’s note has been copied. But Dr. Dowling doesn’t know of any practices that do this.

“There is little appetite to introduce a new enforcement activity for physicians,” he said. “Physicians would see it just as a way to make their lives more difficult than they already are.”
 

Monitoring in Hospitals and Health Systems

Some hospitals and health systems have gone as far as disabling copy-and-paste function in their EHR systems. However, enterprising physicians have found ways around these blocks.

Some institutions have also introduced formal policies, directing doctors on how they can copy and paste, including Banner Health in Arizona, Northwell Health in New York, UConn Health in Connecticut, University of Maryland Medical System, and University of Toledo in Ohio.

Definitions of what is not acceptable vary, but most of these policies oppose copying someone else’s notes and direct physicians to indicate the origin of pasted material.

Santa Rosa Memorial’s policy is quite specific. It still allows some copy and paste but stipulates that it cannot be used for the chief complaint, the review of systems, the physical examination, and the assessment and plan in the medical record, except when the information can’t be obtained directly from the patient. Also, physicians must summarize test results and provide references to other providers’ notes.

Dr. Gore said he and a physician educator who works with physicians on clinical documentation proposed the policy about a decade ago. When physicians on staff were asked to comment, some said they would be opposed to a complete ban, but they generally agreed that copy and paste was a serious problem that needed to be addressed, he said.

The hospital could have simply adopted guidelines, as opposed to rules with consequences, but “we wanted our policy to have teeth,” Dr. Gore said.

When violators are identified, Dr. Gore says he meets with them confidentially and educates them on proper use of copy and paste. Sometimes, the department head is brought in. Some physicians go on to violate the policy again and have to attend another meeting, he said, but aside from the one case, no one else has been disciplined.

It’s unclear how many physicians have faced consequences for misusing copy-paste features — such data aren’t tracked, and sanctions are likely to be handled confidentially, as a personnel matter.

Geisinger Health in Pennsylvania regularly monitors copy-and-paste usage and makes it part of physicians’ professional evaluations, according to a 2022 presentation by a Geisinger official.

Meanwhile, even when systems don’t have specific policies, they may still discipline physicians when copy and paste leads to errors. Scott MacDonald, MD, chief medical information officer at UC Davis Health in Sacramento, California, told this news organization that copy-and-paste abuse has come up a few times over the years in investigations of clinical errors.
 

Holding Physicians Accountable

Physicians can be held accountable for copy and paste by Medicare contractors and in malpractice lawsuits, but the most obvious way is at their place of work: A practice, hospital, or health system.

One physician has lost staff privileges, but more typically, coding clerks or colleagues talk to offending physicians and try to educate them on proper use of copy and paste.

Educational outreach, however, is often ineffective, said Robert Hirschtick, MD, a retired teaching physician at Northwestern University Feinberg School of Medicine, Chicago, Illinois. “The physician may be directed to take an online course,” he said. “When they take the course, the goal is to get it done with, rather than to learn something new.”

Dr. Hirschtick’s articles on copy and paste, including one titled, “Sloppy and Paste,” have put him at the front lines of the debate. “This is an ethical issue,” he said in an interview. He agrees that some forms of copy and paste are permissible, but in many cases, “it is intellectually dishonest and potentially even plagiarism,” he said.

Dr. Hirschtick argues that copy-and-paste policies need more teeth. “Tying violations to compensation would be quite effective,” he said. “Even if physicians were rarely penalized, just knowing that it could happen to you might be enough. But I haven’t heard of anyone doing this.”

A version of this article appeared on Medscape.com.

SAN DIEGO — A liquid biopsy assay that combines a microRNA signature and a well-known biomarker for pancreatic cancer has demonstrated an accuracy of 97% for detecting stage I/II pancreatic ductal adenocarcinoma, the most common type of pancreatic cancer.

It is quite encouraging to know we have a blood test that could potentially find this disease early, said Ajay Goel, PhD, a molecular diagnostics specialist at City of Hope in Duarte, California, who presented the findings at the annual meeting of the American Association for Cancer Research (AACR).

Dr. Goel and colleagues developed a signature for pancreatic cancer based on microRNAs identified in the exomes shed from pancreatic cancers and cell-free DNA markers found in the blood of patients with the disease.

Their initial assay tested blood samples for this signature in a training cohort of 252 people in Japan, approximately 60% of whom had pancreatic cancer. The rest were healthy controls. The assay was then tested in validation cohorts of 400 subjects, half with pancreatic cancer and half controls, in China and South Korea.

In both the initial and validation tests, the microRNA assay had an accuracy of about 90% for stage I/II pancreatic cancer, already far better than commercially available assays.

In an additional validation cohort in the United States with 139 patients with pancreatic cancer and 193 controls at six centers across the country, the researchers found that adding carbohydrate antigen 19-9 — a well-known marker of pancreatic cancer — to the assay boosted the test’s accuracy to 97%.

The test performed the same whether the tumor was in the head or tail of the pancreas.

“We are very excited about this data,” said Dr. Goel.

The technology was recently licensed to Pharus Diagnostics for commercial development, which will likely include a prospective screening trial, he told this news organization.

Because pancreatic cancer is fairly uncommon, Dr. Goel did not anticipate the test being used for general screening but rather for screening high-risk patients such as those with newly diagnosed type 2 diabetes, a family history of pancreatic cancer, or predisposing genetic mutations.

“It should be a very inexpensive test; it doesn’t cost us much to do in the lab,” he added.

Study moderator Ryan Corcoran, MD, PhD, a gastrointestinal (GI) oncologist at Massachusetts General Hospital, Boston, saw the potential.

“As a GI oncologist, I know how lethal and hard to treat pancreatic cancer is,” he said. A test that could reliably detect pancreatic cancer early, with an acceptable false-positive rate, would be extremely useful.

“The cure rate is many, many times higher,” if we detect it before it has a chance to spread, he explained.

In the meantime, Dr. Goel said there’s more work to be done.

Almost 4,000 subjects have been enrolled in ongoing validation efforts, and efforts are underway to use the test to screen thousands of banked blood samples from the PLCO, a prospective cancer screening trial in healthy subjects.

The researchers also want to see if the test can distinguish benign pancreatic cysts from ones that turn cancerous.

The idea is to find the earliest possible signs of this disease to see if we can find it not “at the moment of clinical diagnosis, but possibly 6 months, 1 year, 2 years earlier” than with radiologic imaging, Dr. Goel said.

The work was funded by the National Cancer Institute and others. Dr. Goel is a consultant for Pharus Diagnostics and Cellomics. Dr. Corcoran is a consultant for, has grants from, and/or holds stock in numerous companies, including Pfizer, Novartis, Eli Lilly, and Revolution Medicines.

A version of this article appeared on Medscape.com.

SAN DIEGO — A liquid biopsy assay that combines a microRNA signature and a well-known biomarker for pancreatic cancer has demonstrated an accuracy of 97% for detecting stage I/II pancreatic ductal adenocarcinoma, the most common type of pancreatic cancer.

It is quite encouraging to know we have a blood test that could potentially find this disease early, said Ajay Goel, PhD, a molecular diagnostics specialist at City of Hope in Duarte, California, who presented the findings at the annual meeting of the American Association for Cancer Research (AACR).

Dr. Goel and colleagues developed a signature for pancreatic cancer based on microRNAs identified in the exomes shed from pancreatic cancers and cell-free DNA markers found in the blood of patients with the disease.

Their initial assay tested blood samples for this signature in a training cohort of 252 people in Japan, approximately 60% of whom had pancreatic cancer. The rest were healthy controls. The assay was then tested in validation cohorts of 400 subjects, half with pancreatic cancer and half controls, in China and South Korea.

In both the initial and validation tests, the microRNA assay had an accuracy of about 90% for stage I/II pancreatic cancer, already far better than commercially available assays.

In an additional validation cohort in the United States with 139 patients with pancreatic cancer and 193 controls at six centers across the country, the researchers found that adding carbohydrate antigen 19-9 — a well-known marker of pancreatic cancer — to the assay boosted the test’s accuracy to 97%.

The test performed the same whether the tumor was in the head or tail of the pancreas.

“We are very excited about this data,” said Dr. Goel.

The technology was recently licensed to Pharus Diagnostics for commercial development, which will likely include a prospective screening trial, he told this news organization.

Because pancreatic cancer is fairly uncommon, Dr. Goel did not anticipate the test being used for general screening but rather for screening high-risk patients such as those with newly diagnosed type 2 diabetes, a family history of pancreatic cancer, or predisposing genetic mutations.

“It should be a very inexpensive test; it doesn’t cost us much to do in the lab,” he added.

Study moderator Ryan Corcoran, MD, PhD, a gastrointestinal (GI) oncologist at Massachusetts General Hospital, Boston, saw the potential.

“As a GI oncologist, I know how lethal and hard to treat pancreatic cancer is,” he said. A test that could reliably detect pancreatic cancer early, with an acceptable false-positive rate, would be extremely useful.

“The cure rate is many, many times higher,” if we detect it before it has a chance to spread, he explained.

In the meantime, Dr. Goel said there’s more work to be done.

Almost 4,000 subjects have been enrolled in ongoing validation efforts, and efforts are underway to use the test to screen thousands of banked blood samples from the PLCO, a prospective cancer screening trial in healthy subjects.

The researchers also want to see if the test can distinguish benign pancreatic cysts from ones that turn cancerous.

The idea is to find the earliest possible signs of this disease to see if we can find it not “at the moment of clinical diagnosis, but possibly 6 months, 1 year, 2 years earlier” than with radiologic imaging, Dr. Goel said.

The work was funded by the National Cancer Institute and others. Dr. Goel is a consultant for Pharus Diagnostics and Cellomics. Dr. Corcoran is a consultant for, has grants from, and/or holds stock in numerous companies, including Pfizer, Novartis, Eli Lilly, and Revolution Medicines.

A version of this article appeared on Medscape.com.

SAN DIEGO — A liquid biopsy assay that combines a microRNA signature and a well-known biomarker for pancreatic cancer has demonstrated an accuracy of 97% for detecting stage I/II pancreatic ductal adenocarcinoma, the most common type of pancreatic cancer.

It is quite encouraging to know we have a blood test that could potentially find this disease early, said Ajay Goel, PhD, a molecular diagnostics specialist at City of Hope in Duarte, California, who presented the findings at the annual meeting of the American Association for Cancer Research (AACR).

Dr. Goel and colleagues developed a signature for pancreatic cancer based on microRNAs identified in the exomes shed from pancreatic cancers and cell-free DNA markers found in the blood of patients with the disease.

Their initial assay tested blood samples for this signature in a training cohort of 252 people in Japan, approximately 60% of whom had pancreatic cancer. The rest were healthy controls. The assay was then tested in validation cohorts of 400 subjects, half with pancreatic cancer and half controls, in China and South Korea.

In both the initial and validation tests, the microRNA assay had an accuracy of about 90% for stage I/II pancreatic cancer, already far better than commercially available assays.

In an additional validation cohort in the United States with 139 patients with pancreatic cancer and 193 controls at six centers across the country, the researchers found that adding carbohydrate antigen 19-9 — a well-known marker of pancreatic cancer — to the assay boosted the test’s accuracy to 97%.

The test performed the same whether the tumor was in the head or tail of the pancreas.

“We are very excited about this data,” said Dr. Goel.

The technology was recently licensed to Pharus Diagnostics for commercial development, which will likely include a prospective screening trial, he told this news organization.

Because pancreatic cancer is fairly uncommon, Dr. Goel did not anticipate the test being used for general screening but rather for screening high-risk patients such as those with newly diagnosed type 2 diabetes, a family history of pancreatic cancer, or predisposing genetic mutations.

“It should be a very inexpensive test; it doesn’t cost us much to do in the lab,” he added.

Study moderator Ryan Corcoran, MD, PhD, a gastrointestinal (GI) oncologist at Massachusetts General Hospital, Boston, saw the potential.

“As a GI oncologist, I know how lethal and hard to treat pancreatic cancer is,” he said. A test that could reliably detect pancreatic cancer early, with an acceptable false-positive rate, would be extremely useful.

“The cure rate is many, many times higher,” if we detect it before it has a chance to spread, he explained.

In the meantime, Dr. Goel said there’s more work to be done.

Almost 4,000 subjects have been enrolled in ongoing validation efforts, and efforts are underway to use the test to screen thousands of banked blood samples from the PLCO, a prospective cancer screening trial in healthy subjects.

The researchers also want to see if the test can distinguish benign pancreatic cysts from ones that turn cancerous.

The idea is to find the earliest possible signs of this disease to see if we can find it not “at the moment of clinical diagnosis, but possibly 6 months, 1 year, 2 years earlier” than with radiologic imaging, Dr. Goel said.

The work was funded by the National Cancer Institute and others. Dr. Goel is a consultant for Pharus Diagnostics and Cellomics. Dr. Corcoran is a consultant for, has grants from, and/or holds stock in numerous companies, including Pfizer, Novartis, Eli Lilly, and Revolution Medicines.

A version of this article appeared on Medscape.com.

The acronym AIDS is redundant, loaded with stigma, and potentially harmful, according to a group of specialists who suggest replacing the term with “advanced HIV.”

The acronym AIDS has “outlived its usefulness and we should transition toward a more descriptive language that aligns with contemporary challenges in HIV,” reports Isaac Núñez, MD, from the Department of Medical Education, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán in Mexico City, Mexico, and colleagues.

People generally associate the acronym AIDS with patients who have no available treatment options and a short life expectancy, said Dr. Núñez. That mischaracterization may affect treatment decisions by patients and clinicians and could result in exaggerated infection-control measures.

Using the HIV/AIDS combination erroneously implies equivalence and can mislead the public and clinicians, which the authors explained in their Viewpoint article published in The Lancet HIV.
 

Original Reason for the Term

AIDS, which stands for acquired immunodeficiency syndrome, was coined in 1982 by the US Centers for Disease Control and Prevention (CDC) to name a disease with an unknown cause that affected people with weakened cell-mediated immunity.

“When HIV was found to be the cause of the disease (labeled HIV in 1986), the term AIDS, strictly speaking, became unnecessary,” Dr. Núñez said.

AIDS was originally intended as a case definition for surveillance purposes, and treatment decisions were based on whether patients met the case definition for AIDS, he pointed out.

“The fact that some people still do so in this day and age shows that this is not only unhelpful, but misleading and even harmful,” he noted. Without the label AIDS, clinicians can focus on whether and for how long people have been on treatment, whether they recently switched treatment, and other factors that will help determine appropriate care.
 

Some Organizations Removed AIDS From Their Names

Some organizations have already removed AIDS from their names. For example, the International AIDS Society–USA, which issues guidelines on antiretroviral treatment, changed its name to the International Antiviral Society–USA. 

In 2017, the name of AIDS.gov was changed to HIV.gov. In its explanation, the group wrote, “Today, people with HIV who are diagnosed early, linked to care, start antiretroviral therapy, and take it as prescribed can achieve life-long viral suppression that prevents HIV infection from progressing to AIDS.”

A different view on the term AIDS comes from Greg Millett, MPH, vice president at the Foundation for AIDS Research (amfAR) and the director of amfAR’s Public Policy Office. 

Although he believes that AIDS is an anachronistic term, as a researcher for more than 30 years in the field; a policy director in Washington; a scientist; and a person living with HIV, “it feels like a distinction without a difference. At least from where I sit, there are far more pressing issues that we’re facing as an HIV community,” Millett shared. 

For instance, “we’re seeing that global, as well as domestic, HIV funding is in, by far, the most precarious position that I’ve ever seen in the field. Calling it AIDS or HIV makes no difference in trying to alleviate that jeopardy,” he said.

Millett also said that the stigma and persecution and, in some cases, criminalization of people living with HIV or AIDS is pervasive and won’t go away with a name change, which is a point the authors also acknowledged.

“We need to focus on the social determinants of health,” he said. “That is the thing that is going to move the needle among people living with HIV, not nomenclature.”

Millett likens the argument to the one between Black and African American. “As a Black American, I remember fierce debates in the early ‘90s over whether we should be called African Americans or Blacks. Some argued that African American carried greater dignity and would help with self-esteem and address inequities by emphasizing that we are American. Many others said that it doesn’t make a difference.”

“It is clear that being called African American has not fixed intractable issues like poverty, structural racism, or inequities in incarceration,” he pointed out.
 

End the Epidemic, Not the Name 

The authors misinterpret the impact of the term on stigma, said James W. Curran, MD, MPH, dean emeritus of the Rollins School of Public Health and professor of epidemiology and global health at Emory University, both in Atlanta, Georgia. The term AIDS “is more likely attributed to the fatal nature of the infection itself,” without treatment, he explained, and the mode of transmission, exacerbated by homophobia.

“The term has been in widespread use for 40 years and recognized worldwide,” Dr. Curran, who led the nation’s efforts in the battle against HIV and AIDS at the CDC for 15 years before joining Emory as dean, said.

He also worries about the continued trajectory of lives lost: “Over 35 million people worldwide have perished from HIV/AIDS, including over 500,000 per year now.”

Meanwhile, “global programs such as PEPFAR [the US President’s Emergency Plan for AIDS Relief] are under fire and threatened by Congress as no longer necessary. Removing AIDS from the terminology may add to confusion,” making people think “that the epidemic is over,” he said.

Although the authors argue that keeping the term may cause harm, eliminating it might worsen a different kind of harm. “There is a risk that abolishing the term will further de-emphasize the importance of the problem, with no significant impact on stigma,” Dr. Curran added.

A version of this article appeared on Medscape.com.

The acronym AIDS is redundant, loaded with stigma, and potentially harmful, according to a group of specialists who suggest replacing the term with “advanced HIV.”

The acronym AIDS has “outlived its usefulness and we should transition toward a more descriptive language that aligns with contemporary challenges in HIV,” reports Isaac Núñez, MD, from the Department of Medical Education, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán in Mexico City, Mexico, and colleagues.

People generally associate the acronym AIDS with patients who have no available treatment options and a short life expectancy, said Dr. Núñez. That mischaracterization may affect treatment decisions by patients and clinicians and could result in exaggerated infection-control measures.

Using the HIV/AIDS combination erroneously implies equivalence and can mislead the public and clinicians, which the authors explained in their Viewpoint article published in The Lancet HIV.
 

Original Reason for the Term

AIDS, which stands for acquired immunodeficiency syndrome, was coined in 1982 by the US Centers for Disease Control and Prevention (CDC) to name a disease with an unknown cause that affected people with weakened cell-mediated immunity.

“When HIV was found to be the cause of the disease (labeled HIV in 1986), the term AIDS, strictly speaking, became unnecessary,” Dr. Núñez said.

AIDS was originally intended as a case definition for surveillance purposes, and treatment decisions were based on whether patients met the case definition for AIDS, he pointed out.

“The fact that some people still do so in this day and age shows that this is not only unhelpful, but misleading and even harmful,” he noted. Without the label AIDS, clinicians can focus on whether and for how long people have been on treatment, whether they recently switched treatment, and other factors that will help determine appropriate care.
 

Some Organizations Removed AIDS From Their Names

Some organizations have already removed AIDS from their names. For example, the International AIDS Society–USA, which issues guidelines on antiretroviral treatment, changed its name to the International Antiviral Society–USA. 

In 2017, the name of AIDS.gov was changed to HIV.gov. In its explanation, the group wrote, “Today, people with HIV who are diagnosed early, linked to care, start antiretroviral therapy, and take it as prescribed can achieve life-long viral suppression that prevents HIV infection from progressing to AIDS.”

A different view on the term AIDS comes from Greg Millett, MPH, vice president at the Foundation for AIDS Research (amfAR) and the director of amfAR’s Public Policy Office. 

Although he believes that AIDS is an anachronistic term, as a researcher for more than 30 years in the field; a policy director in Washington; a scientist; and a person living with HIV, “it feels like a distinction without a difference. At least from where I sit, there are far more pressing issues that we’re facing as an HIV community,” Millett shared. 

For instance, “we’re seeing that global, as well as domestic, HIV funding is in, by far, the most precarious position that I’ve ever seen in the field. Calling it AIDS or HIV makes no difference in trying to alleviate that jeopardy,” he said.

Millett also said that the stigma and persecution and, in some cases, criminalization of people living with HIV or AIDS is pervasive and won’t go away with a name change, which is a point the authors also acknowledged.

“We need to focus on the social determinants of health,” he said. “That is the thing that is going to move the needle among people living with HIV, not nomenclature.”

Millett likens the argument to the one between Black and African American. “As a Black American, I remember fierce debates in the early ‘90s over whether we should be called African Americans or Blacks. Some argued that African American carried greater dignity and would help with self-esteem and address inequities by emphasizing that we are American. Many others said that it doesn’t make a difference.”

“It is clear that being called African American has not fixed intractable issues like poverty, structural racism, or inequities in incarceration,” he pointed out.
 

End the Epidemic, Not the Name 

The authors misinterpret the impact of the term on stigma, said James W. Curran, MD, MPH, dean emeritus of the Rollins School of Public Health and professor of epidemiology and global health at Emory University, both in Atlanta, Georgia. The term AIDS “is more likely attributed to the fatal nature of the infection itself,” without treatment, he explained, and the mode of transmission, exacerbated by homophobia.

“The term has been in widespread use for 40 years and recognized worldwide,” Dr. Curran, who led the nation’s efforts in the battle against HIV and AIDS at the CDC for 15 years before joining Emory as dean, said.

He also worries about the continued trajectory of lives lost: “Over 35 million people worldwide have perished from HIV/AIDS, including over 500,000 per year now.”

Meanwhile, “global programs such as PEPFAR [the US President’s Emergency Plan for AIDS Relief] are under fire and threatened by Congress as no longer necessary. Removing AIDS from the terminology may add to confusion,” making people think “that the epidemic is over,” he said.

Although the authors argue that keeping the term may cause harm, eliminating it might worsen a different kind of harm. “There is a risk that abolishing the term will further de-emphasize the importance of the problem, with no significant impact on stigma,” Dr. Curran added.

A version of this article appeared on Medscape.com.

The acronym AIDS is redundant, loaded with stigma, and potentially harmful, according to a group of specialists who suggest replacing the term with “advanced HIV.”

The acronym AIDS has “outlived its usefulness and we should transition toward a more descriptive language that aligns with contemporary challenges in HIV,” reports Isaac Núñez, MD, from the Department of Medical Education, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán in Mexico City, Mexico, and colleagues.

People generally associate the acronym AIDS with patients who have no available treatment options and a short life expectancy, said Dr. Núñez. That mischaracterization may affect treatment decisions by patients and clinicians and could result in exaggerated infection-control measures.

Using the HIV/AIDS combination erroneously implies equivalence and can mislead the public and clinicians, which the authors explained in their Viewpoint article published in The Lancet HIV.
 

Original Reason for the Term

AIDS, which stands for acquired immunodeficiency syndrome, was coined in 1982 by the US Centers for Disease Control and Prevention (CDC) to name a disease with an unknown cause that affected people with weakened cell-mediated immunity.

“When HIV was found to be the cause of the disease (labeled HIV in 1986), the term AIDS, strictly speaking, became unnecessary,” Dr. Núñez said.

AIDS was originally intended as a case definition for surveillance purposes, and treatment decisions were based on whether patients met the case definition for AIDS, he pointed out.

“The fact that some people still do so in this day and age shows that this is not only unhelpful, but misleading and even harmful,” he noted. Without the label AIDS, clinicians can focus on whether and for how long people have been on treatment, whether they recently switched treatment, and other factors that will help determine appropriate care.
 

Some Organizations Removed AIDS From Their Names

Some organizations have already removed AIDS from their names. For example, the International AIDS Society–USA, which issues guidelines on antiretroviral treatment, changed its name to the International Antiviral Society–USA. 

In 2017, the name of AIDS.gov was changed to HIV.gov. In its explanation, the group wrote, “Today, people with HIV who are diagnosed early, linked to care, start antiretroviral therapy, and take it as prescribed can achieve life-long viral suppression that prevents HIV infection from progressing to AIDS.”

A different view on the term AIDS comes from Greg Millett, MPH, vice president at the Foundation for AIDS Research (amfAR) and the director of amfAR’s Public Policy Office. 

Although he believes that AIDS is an anachronistic term, as a researcher for more than 30 years in the field; a policy director in Washington; a scientist; and a person living with HIV, “it feels like a distinction without a difference. At least from where I sit, there are far more pressing issues that we’re facing as an HIV community,” Millett shared. 

For instance, “we’re seeing that global, as well as domestic, HIV funding is in, by far, the most precarious position that I’ve ever seen in the field. Calling it AIDS or HIV makes no difference in trying to alleviate that jeopardy,” he said.

Millett also said that the stigma and persecution and, in some cases, criminalization of people living with HIV or AIDS is pervasive and won’t go away with a name change, which is a point the authors also acknowledged.

“We need to focus on the social determinants of health,” he said. “That is the thing that is going to move the needle among people living with HIV, not nomenclature.”

Millett likens the argument to the one between Black and African American. “As a Black American, I remember fierce debates in the early ‘90s over whether we should be called African Americans or Blacks. Some argued that African American carried greater dignity and would help with self-esteem and address inequities by emphasizing that we are American. Many others said that it doesn’t make a difference.”

“It is clear that being called African American has not fixed intractable issues like poverty, structural racism, or inequities in incarceration,” he pointed out.
 

End the Epidemic, Not the Name 

The authors misinterpret the impact of the term on stigma, said James W. Curran, MD, MPH, dean emeritus of the Rollins School of Public Health and professor of epidemiology and global health at Emory University, both in Atlanta, Georgia. The term AIDS “is more likely attributed to the fatal nature of the infection itself,” without treatment, he explained, and the mode of transmission, exacerbated by homophobia.

“The term has been in widespread use for 40 years and recognized worldwide,” Dr. Curran, who led the nation’s efforts in the battle against HIV and AIDS at the CDC for 15 years before joining Emory as dean, said.

He also worries about the continued trajectory of lives lost: “Over 35 million people worldwide have perished from HIV/AIDS, including over 500,000 per year now.”

Meanwhile, “global programs such as PEPFAR [the US President’s Emergency Plan for AIDS Relief] are under fire and threatened by Congress as no longer necessary. Removing AIDS from the terminology may add to confusion,” making people think “that the epidemic is over,” he said.

Although the authors argue that keeping the term may cause harm, eliminating it might worsen a different kind of harm. “There is a risk that abolishing the term will further de-emphasize the importance of the problem, with no significant impact on stigma,” Dr. Curran added.

A version of this article appeared on Medscape.com.

SAN DIEGO — A novel multicancer early detection (MCED) blood test has demonstrated promising real-world results in detecting new cancers, including several cases of early-stage disease.

This was the conclusion of recent data presented by Ora Karp Gordon, MD, MS, during a session at the American Association for Cancer Research annual meeting.

The MCED test, known as Galleri, was made clinically available in the United States in April 2021. Developed by GRAIL LLC, the test analyzes cell-free DNA in the blood using targeted methylation analysis and machine learning to detect the presence of a cancer signal and determine its organ of origin or cancer signal origin. The initial screening of over 53,000 individuals with the Galleri test detected a cancer signal in 1.1% of participants.

The new real-world analysis examines the outcomes of repeat MCED testing in 5,794 individuals.

The study looked at individuals who initially received a ‘no cancer signal detected’ result and then underwent a second Galleri test. Over 80% of participants received their follow-up test 10-18 months after the first, with a median interval between blood draws of 12.9 months.

“The repeat tests detect those cancer cases that have reached the detection threshold since their last MCED test, which should be less than one year of incidence,” Dr. Gordon, professor at Saint John’s Cancer Institute, Santa Monica, California, said in an interview. “We are just now starting to see results from patients who get their second and even third round of screening.”

“Galleri is recommended to be used annually in addition to USPSTF [US Preventive Services Task Force]–recommended cancer screening tests, like mammography and colonoscopy,” she said.

This recommendation is based on a modeling study suggesting that annual screening would improve stage shift, diagnostic yield, and potentially mortality when compared to biennial screening, although biennial screening was still favorable compared with no screening, she explained.
 

Early Real-World Evidence of Repeat Testing

Among the cohort of 5,794 individuals who received repeat testing, 26 received a positive cancer signal on their second test, yielding a cancer signal detection rate of 0.45% (95% CI: 0.31%-0.66%). The cancer signal detection rate was slightly higher in men. The rate was 0.50% (95% CI: 0.32%-0.81%; 17 of 3367) in men versus 0.37% (95% CI: 0.2%-0.7%; 9 of 2427) in women.

During her presentation, Dr. Gordon highlighted that the repeat testing signal detection rate was lower than the initial 0.95% rate (95% CI: 0.87-1.0; 510 of 53,744) seen in the previous larger cohort of patients who were retested at 1 year.

She acknowledged that the lower cancer signal detection rate of repeat testing may indicate some degree of ‘early adopter’ bias, where those who return for a second test are systematically different from the general screening population. This could suggest that broader population-level screening may yield different results, she continued.
 

Shift Toward Unscreened Cancers

The top cancer types identified in the second round of testing were lymphoid, head and neck, bladder/urothelial, colorectal, and anal cancers. Clinicians were able to confirm clinical outcomes in 12 of 26 cases, in which cancer signals were detected. Of those 12 cases, 8 individuals received a cancer diagnosis and 4 did not have cancer. The remaining 14 of 26 cases in which cancer signals were detected are still under investigation.

“We found a shift away from USPSTF screen-detected cancers, like breast, lung, and prostate, and relative increase in unscreened urinary, head and neck, and lymphoid cancers, with 75% of cancers being those without any screening guidelines,” Dr. Gordon said in an interview.

She added that patients who choose to retest may have different cancer rates for several reasons, including bias toward a population that is health conscious and adhered to all recommended cancer screening.

“So the shift toward unscreened cancers is not unexpected and highlights the value of Galleri,” she said, but also acknowledged that “continued monitoring is needed to see if this translates in a persistent finding over time and tests.”
 

Shift Toward Early-Stage Cancers

Staging information was available for five cases, and Dr. Gordon highlighted in her talk that four of these confirmed cancers were stage I, including cancers of the anus, head and neck, bladder, and lymphoma. The fifth confirmed cancer with staging information was stage IV ovarian cancer.

“It is still early, and the numbers are very small, but the detection of early-stage cancers with second annual testing is very encouraging as these are the cases where MCED testing could have the greatest impact in improving outcomes through earlier treatment,” Dr. Gordon told this publication.

During an interview after the talk, Kenneth L. Kehl, MD, MPH, echoed that data must be confirmed in larger cohorts.

“The shift toward earlier stage cancers that are less detectable by standard screening methods is an interesting result, but we need to be cautious since the numbers were relatively small, and we do not have data on cancers that were diagnosed among patients whose second MCED test was also negative,” said Dr. Kehl, a medical oncologist at Dana-Farber Cancer Institute, Boston.
 

MCED Results Could Help Direct Diagnostic Workup

The test’s ability to predict the organ of origin was highly accurate, correctly identifying the cancer type in all eight confirmed cases. Among the eight cases with a confirmed cancer diagnosis, the accuracy of the first prediction was 100%, and diagnoses included invasive cancers across multiple tissues and organs, including anus, colon, head and neck, urothelial tract, ovary, and the lymphatic system.

“The fact that the site of origin for 100% of confirmed cancers was accurately predicted with GRAIL’s CSO by Galleri test confirms the promise that this can guide workup when a cancer signal is detected,” Dr. Gordon noted in the interview.
 

Looking Ahead

Dr. Kehl, who was not involved in the MCED study, noted in an interview that “further data on test characteristics beyond positive predictive value, including the sensitivity, specificity, and negative predictive value, as well as demonstration of clinical benefit — ideally in a randomized trial — will likely be required for MCED testing to become a standard public health recommendation.”

He added that challenges associated with implementing annual screening with MCED tests include the risks of both false positives and false negatives as testing becomes more widely available.

“False positives cause anxiety and lead to additional testing that may carry its own risks, and we need to understand if potentially false negative tests will be associated with less uptake of established screening strategies,” Dr. Kehl said in an interview. However, he noted that serial testing could lead to more frequent diagnoses of early-stage cancers that may be less detectable by standard methods.

Dr. Gordon reported financial relationships with GRAIL LLC and Genetic Technologies Corporation. Dr. Kehl reported no relationships with entities whose primary business is producing, marketing, selling, reselling, or distributing healthcare products used by or on patients.

SAN DIEGO — A novel multicancer early detection (MCED) blood test has demonstrated promising real-world results in detecting new cancers, including several cases of early-stage disease.

This was the conclusion of recent data presented by Ora Karp Gordon, MD, MS, during a session at the American Association for Cancer Research annual meeting.

The MCED test, known as Galleri, was made clinically available in the United States in April 2021. Developed by GRAIL LLC, the test analyzes cell-free DNA in the blood using targeted methylation analysis and machine learning to detect the presence of a cancer signal and determine its organ of origin or cancer signal origin. The initial screening of over 53,000 individuals with the Galleri test detected a cancer signal in 1.1% of participants.

The new real-world analysis examines the outcomes of repeat MCED testing in 5,794 individuals.

The study looked at individuals who initially received a ‘no cancer signal detected’ result and then underwent a second Galleri test. Over 80% of participants received their follow-up test 10-18 months after the first, with a median interval between blood draws of 12.9 months.

“The repeat tests detect those cancer cases that have reached the detection threshold since their last MCED test, which should be less than one year of incidence,” Dr. Gordon, professor at Saint John’s Cancer Institute, Santa Monica, California, said in an interview. “We are just now starting to see results from patients who get their second and even third round of screening.”

“Galleri is recommended to be used annually in addition to USPSTF [US Preventive Services Task Force]–recommended cancer screening tests, like mammography and colonoscopy,” she said.

This recommendation is based on a modeling study suggesting that annual screening would improve stage shift, diagnostic yield, and potentially mortality when compared to biennial screening, although biennial screening was still favorable compared with no screening, she explained.
 

Early Real-World Evidence of Repeat Testing

Among the cohort of 5,794 individuals who received repeat testing, 26 received a positive cancer signal on their second test, yielding a cancer signal detection rate of 0.45% (95% CI: 0.31%-0.66%). The cancer signal detection rate was slightly higher in men. The rate was 0.50% (95% CI: 0.32%-0.81%; 17 of 3367) in men versus 0.37% (95% CI: 0.2%-0.7%; 9 of 2427) in women.

During her presentation, Dr. Gordon highlighted that the repeat testing signal detection rate was lower than the initial 0.95% rate (95% CI: 0.87-1.0; 510 of 53,744) seen in the previous larger cohort of patients who were retested at 1 year.

She acknowledged that the lower cancer signal detection rate of repeat testing may indicate some degree of ‘early adopter’ bias, where those who return for a second test are systematically different from the general screening population. This could suggest that broader population-level screening may yield different results, she continued.
 

Shift Toward Unscreened Cancers

The top cancer types identified in the second round of testing were lymphoid, head and neck, bladder/urothelial, colorectal, and anal cancers. Clinicians were able to confirm clinical outcomes in 12 of 26 cases, in which cancer signals were detected. Of those 12 cases, 8 individuals received a cancer diagnosis and 4 did not have cancer. The remaining 14 of 26 cases in which cancer signals were detected are still under investigation.

“We found a shift away from USPSTF screen-detected cancers, like breast, lung, and prostate, and relative increase in unscreened urinary, head and neck, and lymphoid cancers, with 75% of cancers being those without any screening guidelines,” Dr. Gordon said in an interview.

She added that patients who choose to retest may have different cancer rates for several reasons, including bias toward a population that is health conscious and adhered to all recommended cancer screening.

“So the shift toward unscreened cancers is not unexpected and highlights the value of Galleri,” she said, but also acknowledged that “continued monitoring is needed to see if this translates in a persistent finding over time and tests.”
 

Shift Toward Early-Stage Cancers

Staging information was available for five cases, and Dr. Gordon highlighted in her talk that four of these confirmed cancers were stage I, including cancers of the anus, head and neck, bladder, and lymphoma. The fifth confirmed cancer with staging information was stage IV ovarian cancer.

“It is still early, and the numbers are very small, but the detection of early-stage cancers with second annual testing is very encouraging as these are the cases where MCED testing could have the greatest impact in improving outcomes through earlier treatment,” Dr. Gordon told this publication.

During an interview after the talk, Kenneth L. Kehl, MD, MPH, echoed that data must be confirmed in larger cohorts.

“The shift toward earlier stage cancers that are less detectable by standard screening methods is an interesting result, but we need to be cautious since the numbers were relatively small, and we do not have data on cancers that were diagnosed among patients whose second MCED test was also negative,” said Dr. Kehl, a medical oncologist at Dana-Farber Cancer Institute, Boston.
 

MCED Results Could Help Direct Diagnostic Workup

The test’s ability to predict the organ of origin was highly accurate, correctly identifying the cancer type in all eight confirmed cases. Among the eight cases with a confirmed cancer diagnosis, the accuracy of the first prediction was 100%, and diagnoses included invasive cancers across multiple tissues and organs, including anus, colon, head and neck, urothelial tract, ovary, and the lymphatic system.

“The fact that the site of origin for 100% of confirmed cancers was accurately predicted with GRAIL’s CSO by Galleri test confirms the promise that this can guide workup when a cancer signal is detected,” Dr. Gordon noted in the interview.
 

Looking Ahead

Dr. Kehl, who was not involved in the MCED study, noted in an interview that “further data on test characteristics beyond positive predictive value, including the sensitivity, specificity, and negative predictive value, as well as demonstration of clinical benefit — ideally in a randomized trial — will likely be required for MCED testing to become a standard public health recommendation.”

He added that challenges associated with implementing annual screening with MCED tests include the risks of both false positives and false negatives as testing becomes more widely available.

“False positives cause anxiety and lead to additional testing that may carry its own risks, and we need to understand if potentially false negative tests will be associated with less uptake of established screening strategies,” Dr. Kehl said in an interview. However, he noted that serial testing could lead to more frequent diagnoses of early-stage cancers that may be less detectable by standard methods.

Dr. Gordon reported financial relationships with GRAIL LLC and Genetic Technologies Corporation. Dr. Kehl reported no relationships with entities whose primary business is producing, marketing, selling, reselling, or distributing healthcare products used by or on patients.

SAN DIEGO — A novel multicancer early detection (MCED) blood test has demonstrated promising real-world results in detecting new cancers, including several cases of early-stage disease.

This was the conclusion of recent data presented by Ora Karp Gordon, MD, MS, during a session at the American Association for Cancer Research annual meeting.

The MCED test, known as Galleri, was made clinically available in the United States in April 2021. Developed by GRAIL LLC, the test analyzes cell-free DNA in the blood using targeted methylation analysis and machine learning to detect the presence of a cancer signal and determine its organ of origin or cancer signal origin. The initial screening of over 53,000 individuals with the Galleri test detected a cancer signal in 1.1% of participants.

The new real-world analysis examines the outcomes of repeat MCED testing in 5,794 individuals.

The study looked at individuals who initially received a ‘no cancer signal detected’ result and then underwent a second Galleri test. Over 80% of participants received their follow-up test 10-18 months after the first, with a median interval between blood draws of 12.9 months.

“The repeat tests detect those cancer cases that have reached the detection threshold since their last MCED test, which should be less than one year of incidence,” Dr. Gordon, professor at Saint John’s Cancer Institute, Santa Monica, California, said in an interview. “We are just now starting to see results from patients who get their second and even third round of screening.”

“Galleri is recommended to be used annually in addition to USPSTF [US Preventive Services Task Force]–recommended cancer screening tests, like mammography and colonoscopy,” she said.

This recommendation is based on a modeling study suggesting that annual screening would improve stage shift, diagnostic yield, and potentially mortality when compared to biennial screening, although biennial screening was still favorable compared with no screening, she explained.
 

Early Real-World Evidence of Repeat Testing

Among the cohort of 5,794 individuals who received repeat testing, 26 received a positive cancer signal on their second test, yielding a cancer signal detection rate of 0.45% (95% CI: 0.31%-0.66%). The cancer signal detection rate was slightly higher in men. The rate was 0.50% (95% CI: 0.32%-0.81%; 17 of 3367) in men versus 0.37% (95% CI: 0.2%-0.7%; 9 of 2427) in women.

During her presentation, Dr. Gordon highlighted that the repeat testing signal detection rate was lower than the initial 0.95% rate (95% CI: 0.87-1.0; 510 of 53,744) seen in the previous larger cohort of patients who were retested at 1 year.

She acknowledged that the lower cancer signal detection rate of repeat testing may indicate some degree of ‘early adopter’ bias, where those who return for a second test are systematically different from the general screening population. This could suggest that broader population-level screening may yield different results, she continued.
 

Shift Toward Unscreened Cancers

The top cancer types identified in the second round of testing were lymphoid, head and neck, bladder/urothelial, colorectal, and anal cancers. Clinicians were able to confirm clinical outcomes in 12 of 26 cases, in which cancer signals were detected. Of those 12 cases, 8 individuals received a cancer diagnosis and 4 did not have cancer. The remaining 14 of 26 cases in which cancer signals were detected are still under investigation.

“We found a shift away from USPSTF screen-detected cancers, like breast, lung, and prostate, and relative increase in unscreened urinary, head and neck, and lymphoid cancers, with 75% of cancers being those without any screening guidelines,” Dr. Gordon said in an interview.

She added that patients who choose to retest may have different cancer rates for several reasons, including bias toward a population that is health conscious and adhered to all recommended cancer screening.

“So the shift toward unscreened cancers is not unexpected and highlights the value of Galleri,” she said, but also acknowledged that “continued monitoring is needed to see if this translates in a persistent finding over time and tests.”
 

Shift Toward Early-Stage Cancers

Staging information was available for five cases, and Dr. Gordon highlighted in her talk that four of these confirmed cancers were stage I, including cancers of the anus, head and neck, bladder, and lymphoma. The fifth confirmed cancer with staging information was stage IV ovarian cancer.

“It is still early, and the numbers are very small, but the detection of early-stage cancers with second annual testing is very encouraging as these are the cases where MCED testing could have the greatest impact in improving outcomes through earlier treatment,” Dr. Gordon told this publication.

During an interview after the talk, Kenneth L. Kehl, MD, MPH, echoed that data must be confirmed in larger cohorts.

“The shift toward earlier stage cancers that are less detectable by standard screening methods is an interesting result, but we need to be cautious since the numbers were relatively small, and we do not have data on cancers that were diagnosed among patients whose second MCED test was also negative,” said Dr. Kehl, a medical oncologist at Dana-Farber Cancer Institute, Boston.
 

MCED Results Could Help Direct Diagnostic Workup

The test’s ability to predict the organ of origin was highly accurate, correctly identifying the cancer type in all eight confirmed cases. Among the eight cases with a confirmed cancer diagnosis, the accuracy of the first prediction was 100%, and diagnoses included invasive cancers across multiple tissues and organs, including anus, colon, head and neck, urothelial tract, ovary, and the lymphatic system.

“The fact that the site of origin for 100% of confirmed cancers was accurately predicted with GRAIL’s CSO by Galleri test confirms the promise that this can guide workup when a cancer signal is detected,” Dr. Gordon noted in the interview.
 

Looking Ahead

Dr. Kehl, who was not involved in the MCED study, noted in an interview that “further data on test characteristics beyond positive predictive value, including the sensitivity, specificity, and negative predictive value, as well as demonstration of clinical benefit — ideally in a randomized trial — will likely be required for MCED testing to become a standard public health recommendation.”

He added that challenges associated with implementing annual screening with MCED tests include the risks of both false positives and false negatives as testing becomes more widely available.

“False positives cause anxiety and lead to additional testing that may carry its own risks, and we need to understand if potentially false negative tests will be associated with less uptake of established screening strategies,” Dr. Kehl said in an interview. However, he noted that serial testing could lead to more frequent diagnoses of early-stage cancers that may be less detectable by standard methods.

Dr. Gordon reported financial relationships with GRAIL LLC and Genetic Technologies Corporation. Dr. Kehl reported no relationships with entities whose primary business is producing, marketing, selling, reselling, or distributing healthcare products used by or on patients.

Statins raise the risks for increased glucose levels and the development of type 2 diabetes among people who don’t have it at baseline, but those risks are outweighed by the cardiovascular benefit, new data suggested.

The findings come from an analysis of individual participant data from a total of 23 randomized trials of statin therapy involving 154,664 individuals. In people without diabetes at baseline, statin therapy produces a dose-dependent increase in the risk for diabetes diagnosis, particularly among those whose glycemia marker levels are already at the diagnostic threshold.

Statins also tend to raise glucose levels in people who already have diabetes, but “the diabetes-related risks arising from the small changes in glycemia resulting from statin therapy are greatly outweighed by the benefits of statins on major vascular events when the direct clinical consequences of these outcomes are taken into consideration,” wrote the authors of the Cholesterol Treatment Trialists’ (CTT) Collaboration in their paper, published online in The Lancet Diabetes & Endocrinology.

Moreover, they say, “since the effect of statin therapy on measures of glycemia within an individual is small, there is likely to be little clinical benefit in measuring glucose concentrations and A1c values routinely after starting statin therapy with the aim of making comparisons to values taken before the initiation of a statin. However, people should continue to be screened for diabetes and associated risk factors and have their glycemic control monitored in accordance with current clinical guidelines.”

The CTT is co-led by Christina Reith, MBChB, PhD, and David Preiss, PhD, FRCPath, MRCP, both of the Nuffield Department of Population Health, University of Oxford, England.

In an accompanying editorial, Hertzel C. Gerstein, MD, and Marie Pigeyre, MD, PhD, both of McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada, noted that the decreased absolute annual incidence of life-threatening cardiovascular outcomes with statins in people at high risk for type 2 diabetes “clearly exceeds the 0.1%-1.3% per year increased absolute incidence of type 2 diabetes.”

Dr. Gerstein and Dr. Pigeyre also said “these findings emphasize the importance of holistic care. As people at risk for cardiovascular outcomes are also at risk for type 2 diabetes, any prescription of a statin should be accompanied by promoting proven strategies to prevent or delay diabetes, such as modest weight reduction and increased physical activity. Finally, these findings emphasize the importance of always being alert for harmful adverse effects, even with the most beneficial and successful preventive therapies.”
 

Statins Raise Diabetes Risk, Glucose Levels Slightly

The meta-analysis of trials in the CTT Collaboration included individual participant data from 19 double-blind randomized, controlled trials with a median follow-up of 4.3 years comparing statins with placebo in a total of 123,940 participants, including 18% who had known type 2 diabetes at randomization. Also analyzed were another four double-blind trials of lower- vs higher-intensity statins involving a total of 30,724 participants followed for a median of 4.9 years, with 15% having diabetes at baseline.

In the 19 trials of low- or moderate-intensity statins vs placebo, statins resulted in a significant 10% increase in new-onset diabetes compared with placebo (rate ratio, 1.10), while high-intensity statins raised the risk by an also significant 36% (1.36). This translated to a mean absolute excess of 0.12% per year of treatment.

Compared with less intensive statin therapy, more intensive statin therapy resulted in a significant 10% proportional increase in new-onset diabetes (1.10), giving an absolute annual excess of 0.22%.

In the statin vs placebo trials, differences in A1c values from placebo were 0.06 percentage points higher for low- or moderate-intensity statins and 0.08 points greater for high-intensity statins.

Nearly two thirds (62%) of the excess cases of new-onset diabetes occurred among participants in the highest quarter of the baseline glycemia distribution for both low-intensity or moderate-intensity and high-intensity statin therapy.

And among participants who already had diabetes at baseline, there was a significant 10% relative increase in worsening glycemia (defined by adverse glycemic event, A1c increase of ≥ 0.5 percentage points, or medication escalation) with low- or moderate-intensity statins compared with placebo and a 24% relative increase in the high-intensity trials.

The Nuffield Department of Population Health has an explicit policy of not accepting any personal honoraria payments directly or indirectly from the pharmaceutical and food industries. It seeks reimbursement to the University of Oxford for the costs of travel and accommodation to participate in scientific meetings. Dr. Reith reported receiving funding to the University of Oxford from the UK National Institute for Health and Care Research Health Technology Assessment Programme and holding unpaid roles on the Clinical Data Interchange Standards Consortium as a board member and WHO as a scientific advisor. Dr. Preiss reported receiving funding to his research institution (but no personal funding) from Novartis for the ORION 4 trial of inclisiran, Novo Nordisk for the ASCEND PLUS trial of semaglutide, and Boehringer Ingelheim and Eli Lilly for the EMPA-KIDNEY trial and being a committee member for a National Institute for Health and Care Excellence guideline.

Dr. Gerstein holds the McMaster-Sanofi Population Health Institute Chair in Diabetes Research and Care. He reported research grants from Eli Lilly, AstraZeneca, Novo Nordisk, Hanmi, and Merck; continuing medical education grants to McMaster University from Eli Lilly, Abbott, Sanofi, Novo Nordisk, and Boehringer Ingelheim; honoraria for speaking from AstraZeneca, Eli Lilly, Novo Nordisk, DKSH, Zuellig Pharma, Sanofi, and Jiangsu Hanson; and consulting fees from Abbott, Eli Lilly, Novo Nordisk, Pfizer, Carbon Brand, Sanofi, Kowa, and Hanmi. Pigeyre had no disclosures.
 

A version of this article appeared on Medscape.com.

Statins raise the risks for increased glucose levels and the development of type 2 diabetes among people who don’t have it at baseline, but those risks are outweighed by the cardiovascular benefit, new data suggested.

The findings come from an analysis of individual participant data from a total of 23 randomized trials of statin therapy involving 154,664 individuals. In people without diabetes at baseline, statin therapy produces a dose-dependent increase in the risk for diabetes diagnosis, particularly among those whose glycemia marker levels are already at the diagnostic threshold.

Statins also tend to raise glucose levels in people who already have diabetes, but “the diabetes-related risks arising from the small changes in glycemia resulting from statin therapy are greatly outweighed by the benefits of statins on major vascular events when the direct clinical consequences of these outcomes are taken into consideration,” wrote the authors of the Cholesterol Treatment Trialists’ (CTT) Collaboration in their paper, published online in The Lancet Diabetes & Endocrinology.

Moreover, they say, “since the effect of statin therapy on measures of glycemia within an individual is small, there is likely to be little clinical benefit in measuring glucose concentrations and A1c values routinely after starting statin therapy with the aim of making comparisons to values taken before the initiation of a statin. However, people should continue to be screened for diabetes and associated risk factors and have their glycemic control monitored in accordance with current clinical guidelines.”

The CTT is co-led by Christina Reith, MBChB, PhD, and David Preiss, PhD, FRCPath, MRCP, both of the Nuffield Department of Population Health, University of Oxford, England.

In an accompanying editorial, Hertzel C. Gerstein, MD, and Marie Pigeyre, MD, PhD, both of McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada, noted that the decreased absolute annual incidence of life-threatening cardiovascular outcomes with statins in people at high risk for type 2 diabetes “clearly exceeds the 0.1%-1.3% per year increased absolute incidence of type 2 diabetes.”

Dr. Gerstein and Dr. Pigeyre also said “these findings emphasize the importance of holistic care. As people at risk for cardiovascular outcomes are also at risk for type 2 diabetes, any prescription of a statin should be accompanied by promoting proven strategies to prevent or delay diabetes, such as modest weight reduction and increased physical activity. Finally, these findings emphasize the importance of always being alert for harmful adverse effects, even with the most beneficial and successful preventive therapies.”
 

Statins Raise Diabetes Risk, Glucose Levels Slightly

The meta-analysis of trials in the CTT Collaboration included individual participant data from 19 double-blind randomized, controlled trials with a median follow-up of 4.3 years comparing statins with placebo in a total of 123,940 participants, including 18% who had known type 2 diabetes at randomization. Also analyzed were another four double-blind trials of lower- vs higher-intensity statins involving a total of 30,724 participants followed for a median of 4.9 years, with 15% having diabetes at baseline.

In the 19 trials of low- or moderate-intensity statins vs placebo, statins resulted in a significant 10% increase in new-onset diabetes compared with placebo (rate ratio, 1.10), while high-intensity statins raised the risk by an also significant 36% (1.36). This translated to a mean absolute excess of 0.12% per year of treatment.

Compared with less intensive statin therapy, more intensive statin therapy resulted in a significant 10% proportional increase in new-onset diabetes (1.10), giving an absolute annual excess of 0.22%.

In the statin vs placebo trials, differences in A1c values from placebo were 0.06 percentage points higher for low- or moderate-intensity statins and 0.08 points greater for high-intensity statins.

Nearly two thirds (62%) of the excess cases of new-onset diabetes occurred among participants in the highest quarter of the baseline glycemia distribution for both low-intensity or moderate-intensity and high-intensity statin therapy.

And among participants who already had diabetes at baseline, there was a significant 10% relative increase in worsening glycemia (defined by adverse glycemic event, A1c increase of ≥ 0.5 percentage points, or medication escalation) with low- or moderate-intensity statins compared with placebo and a 24% relative increase in the high-intensity trials.

The Nuffield Department of Population Health has an explicit policy of not accepting any personal honoraria payments directly or indirectly from the pharmaceutical and food industries. It seeks reimbursement to the University of Oxford for the costs of travel and accommodation to participate in scientific meetings. Dr. Reith reported receiving funding to the University of Oxford from the UK National Institute for Health and Care Research Health Technology Assessment Programme and holding unpaid roles on the Clinical Data Interchange Standards Consortium as a board member and WHO as a scientific advisor. Dr. Preiss reported receiving funding to his research institution (but no personal funding) from Novartis for the ORION 4 trial of inclisiran, Novo Nordisk for the ASCEND PLUS trial of semaglutide, and Boehringer Ingelheim and Eli Lilly for the EMPA-KIDNEY trial and being a committee member for a National Institute for Health and Care Excellence guideline.

Dr. Gerstein holds the McMaster-Sanofi Population Health Institute Chair in Diabetes Research and Care. He reported research grants from Eli Lilly, AstraZeneca, Novo Nordisk, Hanmi, and Merck; continuing medical education grants to McMaster University from Eli Lilly, Abbott, Sanofi, Novo Nordisk, and Boehringer Ingelheim; honoraria for speaking from AstraZeneca, Eli Lilly, Novo Nordisk, DKSH, Zuellig Pharma, Sanofi, and Jiangsu Hanson; and consulting fees from Abbott, Eli Lilly, Novo Nordisk, Pfizer, Carbon Brand, Sanofi, Kowa, and Hanmi. Pigeyre had no disclosures.
 

A version of this article appeared on Medscape.com.

Statins raise the risks for increased glucose levels and the development of type 2 diabetes among people who don’t have it at baseline, but those risks are outweighed by the cardiovascular benefit, new data suggested.

The findings come from an analysis of individual participant data from a total of 23 randomized trials of statin therapy involving 154,664 individuals. In people without diabetes at baseline, statin therapy produces a dose-dependent increase in the risk for diabetes diagnosis, particularly among those whose glycemia marker levels are already at the diagnostic threshold.

Statins also tend to raise glucose levels in people who already have diabetes, but “the diabetes-related risks arising from the small changes in glycemia resulting from statin therapy are greatly outweighed by the benefits of statins on major vascular events when the direct clinical consequences of these outcomes are taken into consideration,” wrote the authors of the Cholesterol Treatment Trialists’ (CTT) Collaboration in their paper, published online in The Lancet Diabetes & Endocrinology.

Moreover, they say, “since the effect of statin therapy on measures of glycemia within an individual is small, there is likely to be little clinical benefit in measuring glucose concentrations and A1c values routinely after starting statin therapy with the aim of making comparisons to values taken before the initiation of a statin. However, people should continue to be screened for diabetes and associated risk factors and have their glycemic control monitored in accordance with current clinical guidelines.”

The CTT is co-led by Christina Reith, MBChB, PhD, and David Preiss, PhD, FRCPath, MRCP, both of the Nuffield Department of Population Health, University of Oxford, England.

In an accompanying editorial, Hertzel C. Gerstein, MD, and Marie Pigeyre, MD, PhD, both of McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada, noted that the decreased absolute annual incidence of life-threatening cardiovascular outcomes with statins in people at high risk for type 2 diabetes “clearly exceeds the 0.1%-1.3% per year increased absolute incidence of type 2 diabetes.”

Dr. Gerstein and Dr. Pigeyre also said “these findings emphasize the importance of holistic care. As people at risk for cardiovascular outcomes are also at risk for type 2 diabetes, any prescription of a statin should be accompanied by promoting proven strategies to prevent or delay diabetes, such as modest weight reduction and increased physical activity. Finally, these findings emphasize the importance of always being alert for harmful adverse effects, even with the most beneficial and successful preventive therapies.”
 

Statins Raise Diabetes Risk, Glucose Levels Slightly

The meta-analysis of trials in the CTT Collaboration included individual participant data from 19 double-blind randomized, controlled trials with a median follow-up of 4.3 years comparing statins with placebo in a total of 123,940 participants, including 18% who had known type 2 diabetes at randomization. Also analyzed were another four double-blind trials of lower- vs higher-intensity statins involving a total of 30,724 participants followed for a median of 4.9 years, with 15% having diabetes at baseline.

In the 19 trials of low- or moderate-intensity statins vs placebo, statins resulted in a significant 10% increase in new-onset diabetes compared with placebo (rate ratio, 1.10), while high-intensity statins raised the risk by an also significant 36% (1.36). This translated to a mean absolute excess of 0.12% per year of treatment.

Compared with less intensive statin therapy, more intensive statin therapy resulted in a significant 10% proportional increase in new-onset diabetes (1.10), giving an absolute annual excess of 0.22%.

In the statin vs placebo trials, differences in A1c values from placebo were 0.06 percentage points higher for low- or moderate-intensity statins and 0.08 points greater for high-intensity statins.

Nearly two thirds (62%) of the excess cases of new-onset diabetes occurred among participants in the highest quarter of the baseline glycemia distribution for both low-intensity or moderate-intensity and high-intensity statin therapy.

And among participants who already had diabetes at baseline, there was a significant 10% relative increase in worsening glycemia (defined by adverse glycemic event, A1c increase of ≥ 0.5 percentage points, or medication escalation) with low- or moderate-intensity statins compared with placebo and a 24% relative increase in the high-intensity trials.

The Nuffield Department of Population Health has an explicit policy of not accepting any personal honoraria payments directly or indirectly from the pharmaceutical and food industries. It seeks reimbursement to the University of Oxford for the costs of travel and accommodation to participate in scientific meetings. Dr. Reith reported receiving funding to the University of Oxford from the UK National Institute for Health and Care Research Health Technology Assessment Programme and holding unpaid roles on the Clinical Data Interchange Standards Consortium as a board member and WHO as a scientific advisor. Dr. Preiss reported receiving funding to his research institution (but no personal funding) from Novartis for the ORION 4 trial of inclisiran, Novo Nordisk for the ASCEND PLUS trial of semaglutide, and Boehringer Ingelheim and Eli Lilly for the EMPA-KIDNEY trial and being a committee member for a National Institute for Health and Care Excellence guideline.

Dr. Gerstein holds the McMaster-Sanofi Population Health Institute Chair in Diabetes Research and Care. He reported research grants from Eli Lilly, AstraZeneca, Novo Nordisk, Hanmi, and Merck; continuing medical education grants to McMaster University from Eli Lilly, Abbott, Sanofi, Novo Nordisk, and Boehringer Ingelheim; honoraria for speaking from AstraZeneca, Eli Lilly, Novo Nordisk, DKSH, Zuellig Pharma, Sanofi, and Jiangsu Hanson; and consulting fees from Abbott, Eli Lilly, Novo Nordisk, Pfizer, Carbon Brand, Sanofi, Kowa, and Hanmi. Pigeyre had no disclosures.
 

A version of this article appeared on Medscape.com.

ATLANTA — A novel antisense therapy called olezarsen reduced triglycerides (TGs) by approximately 50% with either of the two study doses relative to placebo and did so with a low relative risk for adverse events, new data from a phase 2b trial showed.

“The reduction in triglycerides was greater than that currently possible with any available therapy,” reported Brian A. Bergmark, MD, an interventional cardiologist at Brigham and Women’s Hospital, Boston.

The drug also produced meaningful improvements in multiple other lipid subfractions associated with increased cardiovascular (CV) risk, including ApoC-III, very low–density lipoprotein (VLDL) cholesterol, ApoB, and non-LDL cholesterol. High-density lipoprotein (HDL) cholesterol levels were significantly raised.

The results were presented on April 7 as a late breaker at the American College of Cardiology (ACC) Scientific Session 2024 and published online simultaneously in The New England Journal of Medicine.
 

No Major Subgroup Failed to Respond

The effect was seen across all the key subgroups evaluated, including women and patients with diabetes, obesity, and severe as well as moderate elevations in TGs at baseline, Dr. Bergmark reported.

Olezarsen is a N-acetylgalactosamine–conjugated antisense oligonucleotide targeting APOC3 RNA. The results of this randomized trial, called BRIDGE-TIMI 73a, are consistent with other evidence that inhibiting expression of ApoC-III lowers the levels of TGs and other lipid subfractions to a degree that would predict clinical benefit.

In this study, 154 patients at 24 sites in North America were randomized in a 1:1 ratio to 50 or 80 mg olezarsen. Those in each of these cohorts were then randomized in a 3:1 ratio to active therapy or placebo. All therapies were administered by subcutaneous injection once per month.

Patients were eligible for the trial if they had moderate hypertriglyceridemia, defined as a level of 150-499 mg/dL, and elevated CV risk or if they had severe hypertriglyceridemia (≥ 500 mg/dL) with or without other evidence of elevated CV risk. The primary endpoint was a change in TGs at 6 months. Complete follow-up was available in about 97% of patients regardless of treatment assignment.

With a slight numerical advantage for the higher dose, the TG reductions were 49.1% for the 50-mg dose and 53.1% for the 80-mg dose relative to no significant change in the placebo group (P < .001 for both olezarsen doses). The reductions in ApoC-III, an upstream driver of TG production and a CV risk factor, were 64.2% and 73.2% relative to placebo (both P < .001), respectively, Dr. Bergmark reported.

In those with moderate hypertriglyceridemia, normal TG levels, defined as < 150 mg/dL, were reached at 6 months in 85.7% and 93.3% in the 40-mg and 80-mg dose groups, respectively. Relative to these reductions, normalization was seen in only 11.8% of placebo patients (P < .001).
 

TG Lowering Might Not Be Best Endpoint

The primary endpoint in this trial was a change in TGs, but this target was questioned by an invited ACC discussant, Daniel Soffer, MD, who is both an adjunct professor assistant professor of medicine at Penn Medicine, Philadelphia, and current president of the National Lipid Association.

Dr. Soffer noted that highly elevated TGs are a major risk factor for acute pancreatitis, so this predicts a clinical benefit for this purpose, but he thought the other lipid subfractions are far more important for the goal of reducing atherosclerotic cardiovascular disease (ASCVD).

Indeed, he said categorically that it is not TGs that drive ASCVD risk and therefore not what is the real importance of these data. Rather, “it is the non-HDL cholesterol and ApoB lowering” that will drive the likely benefits from this therapy in CV disease.

In addition to the TG reductions, olezarsen did, in fact, produce significant reductions in many of the lipid subfractions associated with increased CV risk. While slightly more favorable in most cases with the higher dose of olezarsen, even the lower dose reduced Apo C-III from baseline by 64.2% (P < .001), VLDL by 46.2% (P < .001), remnant cholesterol by 46.6% (P < .001), ApoB by 18.2% (P < .001), and non-HDL cholesterol by 25.4% (P < .001). HDL cholesterol was increased by 39.6% (P < .001).

These favorable effects on TG and other lipid subfractions were achieved with a safety profile that was reassuring, Dr. Bergmark said. Serious adverse events leading to discontinuation occurred in 0%, 1.7%, and 1.8% of the placebo, lower-dose, and higher-dose arms, respectively. These rates did not differ significantly.
 

Increased Liver Enzymes Is Common

Liver enzymes were significantly elevated (P < .001) for both doses of olezarsen vs placebo, but liver enzymes > 3× the upper limit of normal did not reach significance on either dose of olezarsen relative to placebo. Low platelet counts and reductions in kidney function were observed in a minority of patients but were generally manageable, according to Dr. Bergmark. There was no impact on hemoglobin A1c levels.

Further evaluation of change in hepatic function is planned in the ongoing extension studies.

Characterizing these results as “exciting,” Neha J. Pagidipati, MD, a member of the Duke Clinical Research Institute and an assistant professor at the Duke School of Medicine, Durham, North Carolina, said that identifying a drug effective for hypertriglyceridemia is likely to be a major advance. While elevated TGs are “one of the toughest” lipid abnormalities to manage, “there is not much out there to offer for treatment.”

She, like Dr. Soffer, was encouraged by the favorable effects on multiple lipid abnormalities associated with increased CV risk, but she said the ultimate clinical utility of this or other agents that lower TGs for ASCVD requires a study showing a change in CV events.

Dr. Bergmark reported financial relationships with 15 pharmaceutical companies, including Ionis, which provided funding for the BRIDGE-TIMI 73a trial. Soffer had financial relationships with Akcea, Amgen, Amryt, AstraZeneca, Ionis, Novartis, Regeneron, and Verve. Dr. Pagidipati had financial relationships with more than 10 pharmaceutical companies but was not involved in the design of management of the BRIDGE-TIMI 73a trial.

A version of this article first appeared on Medscape.com.

ATLANTA — A novel antisense therapy called olezarsen reduced triglycerides (TGs) by approximately 50% with either of the two study doses relative to placebo and did so with a low relative risk for adverse events, new data from a phase 2b trial showed.

“The reduction in triglycerides was greater than that currently possible with any available therapy,” reported Brian A. Bergmark, MD, an interventional cardiologist at Brigham and Women’s Hospital, Boston.

The drug also produced meaningful improvements in multiple other lipid subfractions associated with increased cardiovascular (CV) risk, including ApoC-III, very low–density lipoprotein (VLDL) cholesterol, ApoB, and non-LDL cholesterol. High-density lipoprotein (HDL) cholesterol levels were significantly raised.

The results were presented on April 7 as a late breaker at the American College of Cardiology (ACC) Scientific Session 2024 and published online simultaneously in The New England Journal of Medicine.
 

No Major Subgroup Failed to Respond

The effect was seen across all the key subgroups evaluated, including women and patients with diabetes, obesity, and severe as well as moderate elevations in TGs at baseline, Dr. Bergmark reported.

Olezarsen is a N-acetylgalactosamine–conjugated antisense oligonucleotide targeting APOC3 RNA. The results of this randomized trial, called BRIDGE-TIMI 73a, are consistent with other evidence that inhibiting expression of ApoC-III lowers the levels of TGs and other lipid subfractions to a degree that would predict clinical benefit.

In this study, 154 patients at 24 sites in North America were randomized in a 1:1 ratio to 50 or 80 mg olezarsen. Those in each of these cohorts were then randomized in a 3:1 ratio to active therapy or placebo. All therapies were administered by subcutaneous injection once per month.

Patients were eligible for the trial if they had moderate hypertriglyceridemia, defined as a level of 150-499 mg/dL, and elevated CV risk or if they had severe hypertriglyceridemia (≥ 500 mg/dL) with or without other evidence of elevated CV risk. The primary endpoint was a change in TGs at 6 months. Complete follow-up was available in about 97% of patients regardless of treatment assignment.

With a slight numerical advantage for the higher dose, the TG reductions were 49.1% for the 50-mg dose and 53.1% for the 80-mg dose relative to no significant change in the placebo group (P < .001 for both olezarsen doses). The reductions in ApoC-III, an upstream driver of TG production and a CV risk factor, were 64.2% and 73.2% relative to placebo (both P < .001), respectively, Dr. Bergmark reported.

In those with moderate hypertriglyceridemia, normal TG levels, defined as < 150 mg/dL, were reached at 6 months in 85.7% and 93.3% in the 40-mg and 80-mg dose groups, respectively. Relative to these reductions, normalization was seen in only 11.8% of placebo patients (P < .001).
 

TG Lowering Might Not Be Best Endpoint

The primary endpoint in this trial was a change in TGs, but this target was questioned by an invited ACC discussant, Daniel Soffer, MD, who is both an adjunct professor assistant professor of medicine at Penn Medicine, Philadelphia, and current president of the National Lipid Association.

Dr. Soffer noted that highly elevated TGs are a major risk factor for acute pancreatitis, so this predicts a clinical benefit for this purpose, but he thought the other lipid subfractions are far more important for the goal of reducing atherosclerotic cardiovascular disease (ASCVD).

Indeed, he said categorically that it is not TGs that drive ASCVD risk and therefore not what is the real importance of these data. Rather, “it is the non-HDL cholesterol and ApoB lowering” that will drive the likely benefits from this therapy in CV disease.

In addition to the TG reductions, olezarsen did, in fact, produce significant reductions in many of the lipid subfractions associated with increased CV risk. While slightly more favorable in most cases with the higher dose of olezarsen, even the lower dose reduced Apo C-III from baseline by 64.2% (P < .001), VLDL by 46.2% (P < .001), remnant cholesterol by 46.6% (P < .001), ApoB by 18.2% (P < .001), and non-HDL cholesterol by 25.4% (P < .001). HDL cholesterol was increased by 39.6% (P < .001).

These favorable effects on TG and other lipid subfractions were achieved with a safety profile that was reassuring, Dr. Bergmark said. Serious adverse events leading to discontinuation occurred in 0%, 1.7%, and 1.8% of the placebo, lower-dose, and higher-dose arms, respectively. These rates did not differ significantly.
 

Increased Liver Enzymes Is Common

Liver enzymes were significantly elevated (P < .001) for both doses of olezarsen vs placebo, but liver enzymes > 3× the upper limit of normal did not reach significance on either dose of olezarsen relative to placebo. Low platelet counts and reductions in kidney function were observed in a minority of patients but were generally manageable, according to Dr. Bergmark. There was no impact on hemoglobin A1c levels.

Further evaluation of change in hepatic function is planned in the ongoing extension studies.

Characterizing these results as “exciting,” Neha J. Pagidipati, MD, a member of the Duke Clinical Research Institute and an assistant professor at the Duke School of Medicine, Durham, North Carolina, said that identifying a drug effective for hypertriglyceridemia is likely to be a major advance. While elevated TGs are “one of the toughest” lipid abnormalities to manage, “there is not much out there to offer for treatment.”

She, like Dr. Soffer, was encouraged by the favorable effects on multiple lipid abnormalities associated with increased CV risk, but she said the ultimate clinical utility of this or other agents that lower TGs for ASCVD requires a study showing a change in CV events.

Dr. Bergmark reported financial relationships with 15 pharmaceutical companies, including Ionis, which provided funding for the BRIDGE-TIMI 73a trial. Soffer had financial relationships with Akcea, Amgen, Amryt, AstraZeneca, Ionis, Novartis, Regeneron, and Verve. Dr. Pagidipati had financial relationships with more than 10 pharmaceutical companies but was not involved in the design of management of the BRIDGE-TIMI 73a trial.

A version of this article first appeared on Medscape.com.

ATLANTA — A novel antisense therapy called olezarsen reduced triglycerides (TGs) by approximately 50% with either of the two study doses relative to placebo and did so with a low relative risk for adverse events, new data from a phase 2b trial showed.

“The reduction in triglycerides was greater than that currently possible with any available therapy,” reported Brian A. Bergmark, MD, an interventional cardiologist at Brigham and Women’s Hospital, Boston.

The drug also produced meaningful improvements in multiple other lipid subfractions associated with increased cardiovascular (CV) risk, including ApoC-III, very low–density lipoprotein (VLDL) cholesterol, ApoB, and non-LDL cholesterol. High-density lipoprotein (HDL) cholesterol levels were significantly raised.

The results were presented on April 7 as a late breaker at the American College of Cardiology (ACC) Scientific Session 2024 and published online simultaneously in The New England Journal of Medicine.
 

No Major Subgroup Failed to Respond

The effect was seen across all the key subgroups evaluated, including women and patients with diabetes, obesity, and severe as well as moderate elevations in TGs at baseline, Dr. Bergmark reported.

Olezarsen is a N-acetylgalactosamine–conjugated antisense oligonucleotide targeting APOC3 RNA. The results of this randomized trial, called BRIDGE-TIMI 73a, are consistent with other evidence that inhibiting expression of ApoC-III lowers the levels of TGs and other lipid subfractions to a degree that would predict clinical benefit.

In this study, 154 patients at 24 sites in North America were randomized in a 1:1 ratio to 50 or 80 mg olezarsen. Those in each of these cohorts were then randomized in a 3:1 ratio to active therapy or placebo. All therapies were administered by subcutaneous injection once per month.

Patients were eligible for the trial if they had moderate hypertriglyceridemia, defined as a level of 150-499 mg/dL, and elevated CV risk or if they had severe hypertriglyceridemia (≥ 500 mg/dL) with or without other evidence of elevated CV risk. The primary endpoint was a change in TGs at 6 months. Complete follow-up was available in about 97% of patients regardless of treatment assignment.

With a slight numerical advantage for the higher dose, the TG reductions were 49.1% for the 50-mg dose and 53.1% for the 80-mg dose relative to no significant change in the placebo group (P < .001 for both olezarsen doses). The reductions in ApoC-III, an upstream driver of TG production and a CV risk factor, were 64.2% and 73.2% relative to placebo (both P < .001), respectively, Dr. Bergmark reported.

In those with moderate hypertriglyceridemia, normal TG levels, defined as < 150 mg/dL, were reached at 6 months in 85.7% and 93.3% in the 40-mg and 80-mg dose groups, respectively. Relative to these reductions, normalization was seen in only 11.8% of placebo patients (P < .001).
 

TG Lowering Might Not Be Best Endpoint

The primary endpoint in this trial was a change in TGs, but this target was questioned by an invited ACC discussant, Daniel Soffer, MD, who is both an adjunct professor assistant professor of medicine at Penn Medicine, Philadelphia, and current president of the National Lipid Association.

Dr. Soffer noted that highly elevated TGs are a major risk factor for acute pancreatitis, so this predicts a clinical benefit for this purpose, but he thought the other lipid subfractions are far more important for the goal of reducing atherosclerotic cardiovascular disease (ASCVD).

Indeed, he said categorically that it is not TGs that drive ASCVD risk and therefore not what is the real importance of these data. Rather, “it is the non-HDL cholesterol and ApoB lowering” that will drive the likely benefits from this therapy in CV disease.

In addition to the TG reductions, olezarsen did, in fact, produce significant reductions in many of the lipid subfractions associated with increased CV risk. While slightly more favorable in most cases with the higher dose of olezarsen, even the lower dose reduced Apo C-III from baseline by 64.2% (P < .001), VLDL by 46.2% (P < .001), remnant cholesterol by 46.6% (P < .001), ApoB by 18.2% (P < .001), and non-HDL cholesterol by 25.4% (P < .001). HDL cholesterol was increased by 39.6% (P < .001).

These favorable effects on TG and other lipid subfractions were achieved with a safety profile that was reassuring, Dr. Bergmark said. Serious adverse events leading to discontinuation occurred in 0%, 1.7%, and 1.8% of the placebo, lower-dose, and higher-dose arms, respectively. These rates did not differ significantly.
 

Increased Liver Enzymes Is Common

Liver enzymes were significantly elevated (P < .001) for both doses of olezarsen vs placebo, but liver enzymes > 3× the upper limit of normal did not reach significance on either dose of olezarsen relative to placebo. Low platelet counts and reductions in kidney function were observed in a minority of patients but were generally manageable, according to Dr. Bergmark. There was no impact on hemoglobin A1c levels.

Further evaluation of change in hepatic function is planned in the ongoing extension studies.

Characterizing these results as “exciting,” Neha J. Pagidipati, MD, a member of the Duke Clinical Research Institute and an assistant professor at the Duke School of Medicine, Durham, North Carolina, said that identifying a drug effective for hypertriglyceridemia is likely to be a major advance. While elevated TGs are “one of the toughest” lipid abnormalities to manage, “there is not much out there to offer for treatment.”

She, like Dr. Soffer, was encouraged by the favorable effects on multiple lipid abnormalities associated with increased CV risk, but she said the ultimate clinical utility of this or other agents that lower TGs for ASCVD requires a study showing a change in CV events.

Dr. Bergmark reported financial relationships with 15 pharmaceutical companies, including Ionis, which provided funding for the BRIDGE-TIMI 73a trial. Soffer had financial relationships with Akcea, Amgen, Amryt, AstraZeneca, Ionis, Novartis, Regeneron, and Verve. Dr. Pagidipati had financial relationships with more than 10 pharmaceutical companies but was not involved in the design of management of the BRIDGE-TIMI 73a trial.

A version of this article first appeared on Medscape.com.

TOPLINE:

Monthly cycles of a fasting-mimicking diet (FMD) may slow metabolic and immune system aging and reduce the risk for metabolic disease.

METHODOLOGY:

• In two clinical trials, monthly 5-day cycles of an FMD (a proprietary line of plant-based, low-calorie, and low-protein food products) showed lower body weight, body fat, and blood pressure at 3 months.
• Researchers assessed secondary outcomes for the impact of the diet on risk factors for metabolic syndrome and biomarkers associated with aging and age-related diseases.
• This study looked at data from nearly half of the original 184 participants (aged 18-70 years) from the two clinical trials who went through three to four monthly cycles, adhering to 5 days of an FMD in either a crossover design compared with a normal diet or an intervention group compared with people following a Mediterranean diet.
• Abdominal fat and hepatic fat were measured using an MRI in a subset of representative participants. The study also assessed metabolic blood markers and lipids and lymphoid-to-myeloid ratios (for immune aging).
• Biological age estimation was calculated from seven clinical chemistry measures, and life expectancy and mortality risk estimates and a simulation of continued FMD cycles were based on the National Health and Nutrition Examination Survey.

TAKEAWAY:

• In 15 volunteers measured by MRI, the body mass index (P = .0002), total body fat (P = .002), subcutaneous adipose tissue (P = .008), visceral adipose tissue (P = .002), and hepatic fat fraction (P = .049) reduced after the third FMD cycle, with a 50% reduction in liver fat for the five people with hepatic steatosis.
• In 11 participants with prediabetes, insulin resistance (measured by homeostatic model assessment) reduced from 1.473 to 1.209 (P = .046), while A1c levels dropped from 5.8 to 5.43 (P = .032) after the third FMD cycle.

• The lymphoid-to-myeloid ratio improved (P = .005) in all study participants receiving three FMD cycles, indicating an immune aging reversal.
• The estimated median biological age of the 86 participants who completed three FMD cycles in both trials decreased by nearly 2.5 years, independent of weight loss.

IN PRACTICE:

“Together our findings indicate that the FMD is a feasible periodic dietary intervention that reduces disease risk factors and biological age,” the authors wrote.

SOURCE:

The study, led by Sebastian Brandhorst, PhD, Leonard Davis School of Gerontology, University of Southern California (USC), Los Angeles, and Morgan E. Levine, PhD, Department of Pathology, Yale School of Medicine, New Haven, Connecticut, was published in Nature Communications.

LIMITATIONS:

The study estimated the effects of monthly FMD cycles based on results from two clinical trials and included a small subset of trial volunteers. By study measures, the cohort was healthier and biologically younger than average people of similar chronological age. Of the 86 participants, 24 who underwent FMD cycles exhibited increased biological age. The simulation did not consider compliance, dropout, mortality, or the bias that may arise owing to enthusiastic volunteers. Estimated risk reductions assume an effect of change in biological age, which hasn’t been proven. Projections from extending the effects of FMD to a lifelong intervention may require cautious interpretation.

DISCLOSURES:

The study was supported by the USC Edna Jones chair fund and funds from NIH/NIA and the Yale PEPPER Center. The experimental diet was provided by L-Nutra Inc. Some authors declared an equity interest in L-Nutra, with one author’s equity to be assigned to the nonprofit foundation Create Cures. Others disclosed no conflicts of interest.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Monthly cycles of a fasting-mimicking diet (FMD) may slow metabolic and immune system aging and reduce the risk for metabolic disease.

METHODOLOGY:

• In two clinical trials, monthly 5-day cycles of an FMD (a proprietary line of plant-based, low-calorie, and low-protein food products) showed lower body weight, body fat, and blood pressure at 3 months.
• Researchers assessed secondary outcomes for the impact of the diet on risk factors for metabolic syndrome and biomarkers associated with aging and age-related diseases.
• This study looked at data from nearly half of the original 184 participants (aged 18-70 years) from the two clinical trials who went through three to four monthly cycles, adhering to 5 days of an FMD in either a crossover design compared with a normal diet or an intervention group compared with people following a Mediterranean diet.
• Abdominal fat and hepatic fat were measured using an MRI in a subset of representative participants. The study also assessed metabolic blood markers and lipids and lymphoid-to-myeloid ratios (for immune aging).
• Biological age estimation was calculated from seven clinical chemistry measures, and life expectancy and mortality risk estimates and a simulation of continued FMD cycles were based on the National Health and Nutrition Examination Survey.

TAKEAWAY:

• In 15 volunteers measured by MRI, the body mass index (P = .0002), total body fat (P = .002), subcutaneous adipose tissue (P = .008), visceral adipose tissue (P = .002), and hepatic fat fraction (P = .049) reduced after the third FMD cycle, with a 50% reduction in liver fat for the five people with hepatic steatosis.
• In 11 participants with prediabetes, insulin resistance (measured by homeostatic model assessment) reduced from 1.473 to 1.209 (P = .046), while A1c levels dropped from 5.8 to 5.43 (P = .032) after the third FMD cycle.

• The lymphoid-to-myeloid ratio improved (P = .005) in all study participants receiving three FMD cycles, indicating an immune aging reversal.
• The estimated median biological age of the 86 participants who completed three FMD cycles in both trials decreased by nearly 2.5 years, independent of weight loss.

IN PRACTICE:

“Together our findings indicate that the FMD is a feasible periodic dietary intervention that reduces disease risk factors and biological age,” the authors wrote.

SOURCE:

The study, led by Sebastian Brandhorst, PhD, Leonard Davis School of Gerontology, University of Southern California (USC), Los Angeles, and Morgan E. Levine, PhD, Department of Pathology, Yale School of Medicine, New Haven, Connecticut, was published in Nature Communications.

LIMITATIONS:

The study estimated the effects of monthly FMD cycles based on results from two clinical trials and included a small subset of trial volunteers. By study measures, the cohort was healthier and biologically younger than average people of similar chronological age. Of the 86 participants, 24 who underwent FMD cycles exhibited increased biological age. The simulation did not consider compliance, dropout, mortality, or the bias that may arise owing to enthusiastic volunteers. Estimated risk reductions assume an effect of change in biological age, which hasn’t been proven. Projections from extending the effects of FMD to a lifelong intervention may require cautious interpretation.

DISCLOSURES:

The study was supported by the USC Edna Jones chair fund and funds from NIH/NIA and the Yale PEPPER Center. The experimental diet was provided by L-Nutra Inc. Some authors declared an equity interest in L-Nutra, with one author’s equity to be assigned to the nonprofit foundation Create Cures. Others disclosed no conflicts of interest.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Monthly cycles of a fasting-mimicking diet (FMD) may slow metabolic and immune system aging and reduce the risk for metabolic disease.

METHODOLOGY:

• In two clinical trials, monthly 5-day cycles of an FMD (a proprietary line of plant-based, low-calorie, and low-protein food products) showed lower body weight, body fat, and blood pressure at 3 months.
• Researchers assessed secondary outcomes for the impact of the diet on risk factors for metabolic syndrome and biomarkers associated with aging and age-related diseases.
• This study looked at data from nearly half of the original 184 participants (aged 18-70 years) from the two clinical trials who went through three to four monthly cycles, adhering to 5 days of an FMD in either a crossover design compared with a normal diet or an intervention group compared with people following a Mediterranean diet.
• Abdominal fat and hepatic fat were measured using an MRI in a subset of representative participants. The study also assessed metabolic blood markers and lipids and lymphoid-to-myeloid ratios (for immune aging).
• Biological age estimation was calculated from seven clinical chemistry measures, and life expectancy and mortality risk estimates and a simulation of continued FMD cycles were based on the National Health and Nutrition Examination Survey.

TAKEAWAY:

• In 15 volunteers measured by MRI, the body mass index (P = .0002), total body fat (P = .002), subcutaneous adipose tissue (P = .008), visceral adipose tissue (P = .002), and hepatic fat fraction (P = .049) reduced after the third FMD cycle, with a 50% reduction in liver fat for the five people with hepatic steatosis.
• In 11 participants with prediabetes, insulin resistance (measured by homeostatic model assessment) reduced from 1.473 to 1.209 (P = .046), while A1c levels dropped from 5.8 to 5.43 (P = .032) after the third FMD cycle.

• The lymphoid-to-myeloid ratio improved (P = .005) in all study participants receiving three FMD cycles, indicating an immune aging reversal.
• The estimated median biological age of the 86 participants who completed three FMD cycles in both trials decreased by nearly 2.5 years, independent of weight loss.

IN PRACTICE:

“Together our findings indicate that the FMD is a feasible periodic dietary intervention that reduces disease risk factors and biological age,” the authors wrote.

SOURCE:

The study, led by Sebastian Brandhorst, PhD, Leonard Davis School of Gerontology, University of Southern California (USC), Los Angeles, and Morgan E. Levine, PhD, Department of Pathology, Yale School of Medicine, New Haven, Connecticut, was published in Nature Communications.

LIMITATIONS:

The study estimated the effects of monthly FMD cycles based on results from two clinical trials and included a small subset of trial volunteers. By study measures, the cohort was healthier and biologically younger than average people of similar chronological age. Of the 86 participants, 24 who underwent FMD cycles exhibited increased biological age. The simulation did not consider compliance, dropout, mortality, or the bias that may arise owing to enthusiastic volunteers. Estimated risk reductions assume an effect of change in biological age, which hasn’t been proven. Projections from extending the effects of FMD to a lifelong intervention may require cautious interpretation.

DISCLOSURES:

The study was supported by the USC Edna Jones chair fund and funds from NIH/NIA and the Yale PEPPER Center. The experimental diet was provided by L-Nutra Inc. Some authors declared an equity interest in L-Nutra, with one author’s equity to be assigned to the nonprofit foundation Create Cures. Others disclosed no conflicts of interest.
 

A version of this article appeared on Medscape.com.