The federal government has charged a Florida addiction medicine specialist in what it says was a scheme to defraud Medicare and private insurers, charging them roughly $681 million over about a decade for lab tests, office visits, therapy sessions, and other services that were either unnecessary or never delivered.

The Department of Justice and the Attorney for the Southern District of Florida are prosecuting Michael Ligotti, DO, 46, saying that he preyed on individuals seeking substance abuse treatment. They have yet to issue a formal indictment.

“The substance abuse treatment fraud allegedly perpetrated by the defendant sacrificed the genuine care of vulnerable patients at a time when they urgently needed a trusted health care provider,” U.S. Attorney Ariana Fajardo Orshan, Southern District of Florida, said in a statement.

“Health care providers who allow greed to take precedence over their Hippocratic Oath and participate in these schemes are criminals and will be held accountable for their unscrupulous conduct,” she added.

Dr. Ligotti was charged July 31. The prosecutors were seeking to detain him until trial. However, a judge approved his bond today and he is free on bond, according to Ligotti’s attorney, Ben Curtis.

“As is always the case with any criminal matter, the burden of proof rests entirely with the government,” Mr. Curtis said in an interview.

“In this instance, we do not believe the US Department of Justice’s claims – and that is exactly what they are at this point, just one-sided claims – will reconcile with actual evidence at a future trial,” he said.

Mr. Curtis added that Dr. Ligotti “looks forward to establishing his innocence.”

Unnecessary urine tests

The government alleges that Dr. Ligotti played a central role in a scheme in which Medicare and private insurers paid about $121 million to cover some $680 million in charges from 2011 to 2020.

According to the prosecutors, Dr. Ligotti received a fee for becoming a “purported” medical director of about 50 addiction treatment facilities and sober homes – and that he issued 136 separate standing orders for medically unnecessary urinalysis (UA) tests.

The labs allegedly paid occasional kickbacks to the facilities and homes, and those facilities in turn were required to have their patients treated by Dr. Ligotti’s clinic, Whole Health, which is based in Delray Beach, Fla.

This allowed Dr. Ligotti to “bill hundreds of millions of dollars in additional fraudulent treatments, including unnecessary and expensive UAs, costly blood tests, nonexistent therapy sessions, office visits, and other unnecessary services, regardless of whether such treatment and testing were medically necessary and/or actually provided,” alleges the government.

Dr. Ligotti did not review results or use the results to inform patient treatment, according to the Department of Justice.

Urine tests have been exploited before by addiction treatment clinics as a revenue generator. Kaiser Health News reported in 2017 that a single nurse practitioner at one pain clinic in Tennessee generated $1 million in billings to Medicare for drug-related urine tests in a single year.

Also in 2017, The New York Times reported that a single patient had been billed $260,000 for urine tests by his treatment center.

The federal government alleges that Dr. Ligotti also “billed for psychiatric services and therapy sessions that never happened, and that he and his staff were not qualified to conduct.”

In addition, they assert that Dr. Ligotti improperly prescribed controlled substances, including large quantities of buprenorphine/Suboxone, often exceeding the number of patients he was legally authorized to treat or giving it to patients who did not require the medications.

Dr. Ligotti may not be practicing any longer. His clinic’s website features a message that the practice will be closed as of Aug. 7.
 

This article first appeared on Medscape.com.

The federal government has charged a Florida addiction medicine specialist in what it says was a scheme to defraud Medicare and private insurers, charging them roughly $681 million over about a decade for lab tests, office visits, therapy sessions, and other services that were either unnecessary or never delivered.

The Department of Justice and the Attorney for the Southern District of Florida are prosecuting Michael Ligotti, DO, 46, saying that he preyed on individuals seeking substance abuse treatment. They have yet to issue a formal indictment.

“The substance abuse treatment fraud allegedly perpetrated by the defendant sacrificed the genuine care of vulnerable patients at a time when they urgently needed a trusted health care provider,” U.S. Attorney Ariana Fajardo Orshan, Southern District of Florida, said in a statement.

“Health care providers who allow greed to take precedence over their Hippocratic Oath and participate in these schemes are criminals and will be held accountable for their unscrupulous conduct,” she added.

Dr. Ligotti was charged July 31. The prosecutors were seeking to detain him until trial. However, a judge approved his bond today and he is free on bond, according to Ligotti’s attorney, Ben Curtis.

“As is always the case with any criminal matter, the burden of proof rests entirely with the government,” Mr. Curtis said in an interview.

“In this instance, we do not believe the US Department of Justice’s claims – and that is exactly what they are at this point, just one-sided claims – will reconcile with actual evidence at a future trial,” he said.

Mr. Curtis added that Dr. Ligotti “looks forward to establishing his innocence.”

Unnecessary urine tests

The government alleges that Dr. Ligotti played a central role in a scheme in which Medicare and private insurers paid about $121 million to cover some $680 million in charges from 2011 to 2020.

According to the prosecutors, Dr. Ligotti received a fee for becoming a “purported” medical director of about 50 addiction treatment facilities and sober homes – and that he issued 136 separate standing orders for medically unnecessary urinalysis (UA) tests.

The labs allegedly paid occasional kickbacks to the facilities and homes, and those facilities in turn were required to have their patients treated by Dr. Ligotti’s clinic, Whole Health, which is based in Delray Beach, Fla.

This allowed Dr. Ligotti to “bill hundreds of millions of dollars in additional fraudulent treatments, including unnecessary and expensive UAs, costly blood tests, nonexistent therapy sessions, office visits, and other unnecessary services, regardless of whether such treatment and testing were medically necessary and/or actually provided,” alleges the government.

Dr. Ligotti did not review results or use the results to inform patient treatment, according to the Department of Justice.

Urine tests have been exploited before by addiction treatment clinics as a revenue generator. Kaiser Health News reported in 2017 that a single nurse practitioner at one pain clinic in Tennessee generated $1 million in billings to Medicare for drug-related urine tests in a single year.

Also in 2017, The New York Times reported that a single patient had been billed $260,000 for urine tests by his treatment center.

The federal government alleges that Dr. Ligotti also “billed for psychiatric services and therapy sessions that never happened, and that he and his staff were not qualified to conduct.”

In addition, they assert that Dr. Ligotti improperly prescribed controlled substances, including large quantities of buprenorphine/Suboxone, often exceeding the number of patients he was legally authorized to treat or giving it to patients who did not require the medications.

Dr. Ligotti may not be practicing any longer. His clinic’s website features a message that the practice will be closed as of Aug. 7.
 

This article first appeared on Medscape.com.

The federal government has charged a Florida addiction medicine specialist in what it says was a scheme to defraud Medicare and private insurers, charging them roughly $681 million over about a decade for lab tests, office visits, therapy sessions, and other services that were either unnecessary or never delivered.

The Department of Justice and the Attorney for the Southern District of Florida are prosecuting Michael Ligotti, DO, 46, saying that he preyed on individuals seeking substance abuse treatment. They have yet to issue a formal indictment.

“The substance abuse treatment fraud allegedly perpetrated by the defendant sacrificed the genuine care of vulnerable patients at a time when they urgently needed a trusted health care provider,” U.S. Attorney Ariana Fajardo Orshan, Southern District of Florida, said in a statement.

“Health care providers who allow greed to take precedence over their Hippocratic Oath and participate in these schemes are criminals and will be held accountable for their unscrupulous conduct,” she added.

Dr. Ligotti was charged July 31. The prosecutors were seeking to detain him until trial. However, a judge approved his bond today and he is free on bond, according to Ligotti’s attorney, Ben Curtis.

“As is always the case with any criminal matter, the burden of proof rests entirely with the government,” Mr. Curtis said in an interview.

“In this instance, we do not believe the US Department of Justice’s claims – and that is exactly what they are at this point, just one-sided claims – will reconcile with actual evidence at a future trial,” he said.

Mr. Curtis added that Dr. Ligotti “looks forward to establishing his innocence.”

Unnecessary urine tests

The government alleges that Dr. Ligotti played a central role in a scheme in which Medicare and private insurers paid about $121 million to cover some $680 million in charges from 2011 to 2020.

According to the prosecutors, Dr. Ligotti received a fee for becoming a “purported” medical director of about 50 addiction treatment facilities and sober homes – and that he issued 136 separate standing orders for medically unnecessary urinalysis (UA) tests.

The labs allegedly paid occasional kickbacks to the facilities and homes, and those facilities in turn were required to have their patients treated by Dr. Ligotti’s clinic, Whole Health, which is based in Delray Beach, Fla.

This allowed Dr. Ligotti to “bill hundreds of millions of dollars in additional fraudulent treatments, including unnecessary and expensive UAs, costly blood tests, nonexistent therapy sessions, office visits, and other unnecessary services, regardless of whether such treatment and testing were medically necessary and/or actually provided,” alleges the government.

Dr. Ligotti did not review results or use the results to inform patient treatment, according to the Department of Justice.

Urine tests have been exploited before by addiction treatment clinics as a revenue generator. Kaiser Health News reported in 2017 that a single nurse practitioner at one pain clinic in Tennessee generated $1 million in billings to Medicare for drug-related urine tests in a single year.

Also in 2017, The New York Times reported that a single patient had been billed $260,000 for urine tests by his treatment center.

The federal government alleges that Dr. Ligotti also “billed for psychiatric services and therapy sessions that never happened, and that he and his staff were not qualified to conduct.”

In addition, they assert that Dr. Ligotti improperly prescribed controlled substances, including large quantities of buprenorphine/Suboxone, often exceeding the number of patients he was legally authorized to treat or giving it to patients who did not require the medications.

Dr. Ligotti may not be practicing any longer. His clinic’s website features a message that the practice will be closed as of Aug. 7.
 

This article first appeared on Medscape.com.

The Diagnosis: Kaposi Varicelliform Eruption (Eczema Herpeticum) 

Polymerase chain reaction confirmed presence of herpes simplex virus (HSV) type 1, and the patient was started on intravenous acyclovir (10 mg/kg every 8 hours). Diagnosis was further supported by histopathologic examination with confirmatory immunohistochemistry (Figure 1). The patient's anemia and thrombocytopenia also were attributed to widespread HSV infection. 

Approximately 8 hours after the patient was started on acyclovir, he developed increasing tremors, confusion, and impaired speech. Lumbar puncture confirmed the presence of HSV-1 in the cerebrospinal fluid. Despite ongoing intravenous antiviral therapy, he required intubation 6 days after hospitalization due to impaired mental status and myoclonic jerking. He remained intubated, unresponsive, and in critical condition for 9 days before he gradually began to demonstrate cognitive recovery. He subsequently was weaned off the ventilator, his mental status returned to normal, and his skin rash slowly resolved (Figure 2). 

Hailey-Hailey disease (HHD), also known as familial benign chronic pemphigus, is a rare autosomal-dominant condition first described by Howard and Hugh Hailey in 1939.¹ It is a chronic blistering process characterized by epidermal fragility, often manifesting as macerated fissured erosions in areas exposed to heat and friction (eg, axillae, groin). Hailey-Hailey disease results from a defective calcium transporter (ATP2C1 gene), leading to impaired keratinocyte adhesion.² 

Eczema herpeticum refers to the dissemination of herpes infection to areas of compromised skin barrier. Although originally used to describe HSV infection in patients with atopic dermatitis, eczema herpeticum has been described in various conditions that affect the skin barrier function, including Darier disease, ichthyosis vulgaris, pemphigus foliaceus, pemphigus vulgaris, and mycosis fungoides, among others.³ When applied to skin conditions other than atopic dermatitis, it sometimes is referred to as Kaposi varicelliform eruption.² 

Hailey-Hailey disease commonly is complicated by a bacterial or fungal infection, including impetigo, tinea, or candidiasis. The first case of HHD complicated by HSV infection was reported in 1973.⁴ A PubMed search of articles indexed for MEDLINE using the terms benign familial pemphigus AND herpes, Hailey-Hailey AND herpes, Hailey-Hailey AND eczema herpeticum, Hailey-Hailey AND Kaposi varicelliform eruption, and Hailey-Hailey herpeticum revealed 15 cases of HHD complicated by eczema herpeticum.^4-6 Herpes simplex virus encephalitis is a rare and life-threatening complication of eczema herpeticum.^7,8 We report a case of HSV encephalitis resulting from eczema herpeticum in a patient with HHD.  

The clinical differential includes a flare of the patient's known HHD, secondary bacterial or fungal infection, or a superimposed viral infection (eg, HSV, zoster). Histologic evidence of herpetic infection would be absent in an uncomplicated flare of HHD. Impetigo is a superficial bacterial infection that can present in 2 clinical forms: a vesiculopustular type and less commonly a bullous type. It is caused by Staphylococcus aureus in most cases. In multiple myeloma with cutaneous dissemination, a monoclonal proliferation of plasma cells would be evident. Lastly, tinea corporis is caused by dermatophytes that can be seen on hematoxylin and eosin or periodic acid-Schiff staining.  

The diagnosis of eczema herpeticum in a patient with HHD should be considered in patients who present with grouped vesicles or hemorrhagic or punched-out erosions in areas of pre-existing HHD. The diagnosis can be confirmed by Tzanck smear, viral culture, polymerase chain reaction, or histopathology (with or without immunohistochemistry).^1,2,6 When eczema herpeticum is suspected, prompt antiviral administration is imperative to limit life-threatening systemic spread. 

The Diagnosis: Kaposi Varicelliform Eruption (Eczema Herpeticum) 

Polymerase chain reaction confirmed presence of herpes simplex virus (HSV) type 1, and the patient was started on intravenous acyclovir (10 mg/kg every 8 hours). Diagnosis was further supported by histopathologic examination with confirmatory immunohistochemistry (Figure 1). The patient's anemia and thrombocytopenia also were attributed to widespread HSV infection. 

Approximately 8 hours after the patient was started on acyclovir, he developed increasing tremors, confusion, and impaired speech. Lumbar puncture confirmed the presence of HSV-1 in the cerebrospinal fluid. Despite ongoing intravenous antiviral therapy, he required intubation 6 days after hospitalization due to impaired mental status and myoclonic jerking. He remained intubated, unresponsive, and in critical condition for 9 days before he gradually began to demonstrate cognitive recovery. He subsequently was weaned off the ventilator, his mental status returned to normal, and his skin rash slowly resolved (Figure 2). 

Hailey-Hailey disease (HHD), also known as familial benign chronic pemphigus, is a rare autosomal-dominant condition first described by Howard and Hugh Hailey in 1939.¹ It is a chronic blistering process characterized by epidermal fragility, often manifesting as macerated fissured erosions in areas exposed to heat and friction (eg, axillae, groin). Hailey-Hailey disease results from a defective calcium transporter (ATP2C1 gene), leading to impaired keratinocyte adhesion.² 

Eczema herpeticum refers to the dissemination of herpes infection to areas of compromised skin barrier. Although originally used to describe HSV infection in patients with atopic dermatitis, eczema herpeticum has been described in various conditions that affect the skin barrier function, including Darier disease, ichthyosis vulgaris, pemphigus foliaceus, pemphigus vulgaris, and mycosis fungoides, among others.³ When applied to skin conditions other than atopic dermatitis, it sometimes is referred to as Kaposi varicelliform eruption.² 

Hailey-Hailey disease commonly is complicated by a bacterial or fungal infection, including impetigo, tinea, or candidiasis. The first case of HHD complicated by HSV infection was reported in 1973.⁴ A PubMed search of articles indexed for MEDLINE using the terms benign familial pemphigus AND herpes, Hailey-Hailey AND herpes, Hailey-Hailey AND eczema herpeticum, Hailey-Hailey AND Kaposi varicelliform eruption, and Hailey-Hailey herpeticum revealed 15 cases of HHD complicated by eczema herpeticum.^4-6 Herpes simplex virus encephalitis is a rare and life-threatening complication of eczema herpeticum.^7,8 We report a case of HSV encephalitis resulting from eczema herpeticum in a patient with HHD.  

The clinical differential includes a flare of the patient's known HHD, secondary bacterial or fungal infection, or a superimposed viral infection (eg, HSV, zoster). Histologic evidence of herpetic infection would be absent in an uncomplicated flare of HHD. Impetigo is a superficial bacterial infection that can present in 2 clinical forms: a vesiculopustular type and less commonly a bullous type. It is caused by Staphylococcus aureus in most cases. In multiple myeloma with cutaneous dissemination, a monoclonal proliferation of plasma cells would be evident. Lastly, tinea corporis is caused by dermatophytes that can be seen on hematoxylin and eosin or periodic acid-Schiff staining.  

The diagnosis of eczema herpeticum in a patient with HHD should be considered in patients who present with grouped vesicles or hemorrhagic or punched-out erosions in areas of pre-existing HHD. The diagnosis can be confirmed by Tzanck smear, viral culture, polymerase chain reaction, or histopathology (with or without immunohistochemistry).^1,2,6 When eczema herpeticum is suspected, prompt antiviral administration is imperative to limit life-threatening systemic spread. 

The Diagnosis: Kaposi Varicelliform Eruption (Eczema Herpeticum) 

Polymerase chain reaction confirmed presence of herpes simplex virus (HSV) type 1, and the patient was started on intravenous acyclovir (10 mg/kg every 8 hours). Diagnosis was further supported by histopathologic examination with confirmatory immunohistochemistry (Figure 1). The patient's anemia and thrombocytopenia also were attributed to widespread HSV infection. 

Approximately 8 hours after the patient was started on acyclovir, he developed increasing tremors, confusion, and impaired speech. Lumbar puncture confirmed the presence of HSV-1 in the cerebrospinal fluid. Despite ongoing intravenous antiviral therapy, he required intubation 6 days after hospitalization due to impaired mental status and myoclonic jerking. He remained intubated, unresponsive, and in critical condition for 9 days before he gradually began to demonstrate cognitive recovery. He subsequently was weaned off the ventilator, his mental status returned to normal, and his skin rash slowly resolved (Figure 2). 

Hailey-Hailey disease (HHD), also known as familial benign chronic pemphigus, is a rare autosomal-dominant condition first described by Howard and Hugh Hailey in 1939.¹ It is a chronic blistering process characterized by epidermal fragility, often manifesting as macerated fissured erosions in areas exposed to heat and friction (eg, axillae, groin). Hailey-Hailey disease results from a defective calcium transporter (ATP2C1 gene), leading to impaired keratinocyte adhesion.² 

Eczema herpeticum refers to the dissemination of herpes infection to areas of compromised skin barrier. Although originally used to describe HSV infection in patients with atopic dermatitis, eczema herpeticum has been described in various conditions that affect the skin barrier function, including Darier disease, ichthyosis vulgaris, pemphigus foliaceus, pemphigus vulgaris, and mycosis fungoides, among others.³ When applied to skin conditions other than atopic dermatitis, it sometimes is referred to as Kaposi varicelliform eruption.² 

Hailey-Hailey disease commonly is complicated by a bacterial or fungal infection, including impetigo, tinea, or candidiasis. The first case of HHD complicated by HSV infection was reported in 1973.⁴ A PubMed search of articles indexed for MEDLINE using the terms benign familial pemphigus AND herpes, Hailey-Hailey AND herpes, Hailey-Hailey AND eczema herpeticum, Hailey-Hailey AND Kaposi varicelliform eruption, and Hailey-Hailey herpeticum revealed 15 cases of HHD complicated by eczema herpeticum.^4-6 Herpes simplex virus encephalitis is a rare and life-threatening complication of eczema herpeticum.^7,8 We report a case of HSV encephalitis resulting from eczema herpeticum in a patient with HHD.  

The clinical differential includes a flare of the patient's known HHD, secondary bacterial or fungal infection, or a superimposed viral infection (eg, HSV, zoster). Histologic evidence of herpetic infection would be absent in an uncomplicated flare of HHD. Impetigo is a superficial bacterial infection that can present in 2 clinical forms: a vesiculopustular type and less commonly a bullous type. It is caused by Staphylococcus aureus in most cases. In multiple myeloma with cutaneous dissemination, a monoclonal proliferation of plasma cells would be evident. Lastly, tinea corporis is caused by dermatophytes that can be seen on hematoxylin and eosin or periodic acid-Schiff staining.  

The diagnosis of eczema herpeticum in a patient with HHD should be considered in patients who present with grouped vesicles or hemorrhagic or punched-out erosions in areas of pre-existing HHD. The diagnosis can be confirmed by Tzanck smear, viral culture, polymerase chain reaction, or histopathology (with or without immunohistochemistry).^1,2,6 When eczema herpeticum is suspected, prompt antiviral administration is imperative to limit life-threatening systemic spread. 

Fellowship interviews are an essential step – arguably the most important step – in the process of matching candidates to training programs. Until recently, most programs relied exclusively on on-site face-to face interviews. Since the appearance of the COVID-19 pandemic, the medical field has utilized web-based platforms. Despite inherent limitations, virtual meetings appear to be effective in providing patient care and in conducting administrative meetings.^1,2

Because of uncertainty related to the pandemic, including changing guidelines regarding social distancing and travel restrictions, fellowship programs are expected to comply with CDC,³ state, and federal recommendations to avoid nonessential travel. Therefore, conducting web-based interviews exclusively will likely become a necessity.

While there may be some disadvantages to web-based interviews, many candidates find the overall experience satisfactory, thereby allowing them to understand the programs, express themselves, and comfortably rank the programs, as two studies have shown.^4,5 Programs and candidates are encouraged to adapt to this new reality in order to achieve a successful match. After all, there are many potential advantages of web-based interviews. In addition to eliminating the risk of COVID-19 acquisition, web-based interviews have been described as helping to improve scheduling flexibility, reduce the financial burden, and allow conducting more interviews for candidates and programs (Table 1).^6-8

There are different styles to the web-based interview.⁹ Some programs choose to offer a single group interview (or the so-called panel interview) in which all the interviewing faculties invite each candidate at a time. Alternatively, programs might choose to conduct separate interviews by each faculty in which the candidates would alternate. For the latter option, the program could use a single invitation link or multiple invitation links for each session.
 

General tips for a successful interview:⁹

1. Be pleasant and professional: Your communication with the program should reflect excellent manners and a professional attitude with everyone (i.e., faculties, coordinators, and fellows).

2. Know yourself and what you want: Review your CV and personal statement and reflect on your achievements, strengths and weaknesses. Identify examples from your experience that would speak well of you as a person and as a physician.

3. Communication is key:

• Respond to the interview invitations promptly.
• Send a brief thank you email to the interviewers and the coordinator. Avoid being generic; mention specific points of discussion and show your interest in the program.
• Proofread your emails carefully. Well-written emails that are devoid of grammatical or spelling errors send a positive message about the candidate.

4. Do your homework:

• Read the information posted on the website carefully and take notes. This should provide you with useful information to use when you rank the programs and could lead to questions that you might want to ask your interviewers. Besides, asking questions that are answered on the website reflects poorly on the candidate.
• Pay attention to various clues that could reflect how organized and how academically oriented a program is. For example, a program that provides details about their didactic lectures sends a message that quality teaching is a priority. On the other hand, a program that has a website that hasn’t been updated for years could dissuade rather than recruit applicants.
• Read about the faculty, their areas of interests, and publications. Learn how their names are pronounced and use them during the interview.
• Read about the city where the program is. It shows interest in the area where you might be living and will help you to stand out among candidates.

5. Be prepared for the classics; be honest, genuine, and authentic. Think about these common prompts:

• Tell me about yourself.
• Why did you choose gastroenterology?
• Where do you see yourself in 5 years?
• Why would you like to come to the city where the program is?
• Are there any certain areas in gastroenterology that you’re interested in more (e.g., hepatology, motility, IBD, advanced endoscopy)?

6. It is likely your interviewer will ask if you have questions. Ask questions that further allow you to assess the program and your fit into the program.

• What aspects of the program are you most proud of?
• Where would you like to see this program in 5 years?
• What keeps you at this program?

Tips for a successful web-based interview^9,10 (Table 2):

1. Pay attention to the time zone of the city of the program. Be ready at least 10 minutes before the interview.

2. Ensure a fast and stable Internet service for an uninterrupted interview experience. Consider using an ethernet cable. Have a back-up plan such as using a phone as a hotspot.

3. Use a quiet and private room, preferably at home. Be aware of the background. A simple decoration is acceptable.

4. Consider recording yourself using the same device you’ll use for the interview to make sure audio and video are functioning properly.

5. When scheduling more than one interview in 1 day, allow at least 2 hours between interviews to avoid scheduling conflicts caused by unanticipated delays related to technical issues.

6. Have immediate access to the invitation link(s) that you received. Add the interviews to your device’s calendar. Note that sometimes a new invitation link is generated last minute because of technical issues.

7. While the advice for physical interviews is to turn off your phone (and smart watch), you’ll have to keep your phone on but on silent for the virtual interviews. Sometimes, you’ll receive a phone call from the program to update you about any last-minute changes.

7. It is recommended that a laptop or a tablet with a camera with good resolution and a microphone be used rather than using a phone. A wide screen allows better communication. Disable notification on that device to avoid interruptions.

8. Sit comfortably with the device being at or just below eye level. Avoid distractions and maintain eye contact.

9. Familiarize yourself with the platform used and its functions. Double check the audio and video before each interview.

10. Put your device on a desk or table to improve stability; don’t hold it in your hand.

11. Find a place where the view is best and your face appears in the middle of the screen; not too far or too close. Use a well-lit room but don’t have a source of light behind you. Many platforms allow you to select a background or blur the background. A background that is monochromatic and not distracting is recommended.

12. Use a pen and a paper to take notes during the interview. You would use these notes to generate “thank you” or “interest in program” emails. Additionally, they will be a helpful reference when ranking programs.

13. Do not type. Typing is much louder to the interviewer and can be distracting.

14. Dress professionally, just as you dress for an on-site interview. You never know when you might have to stand up during the interview for unplanned reasons.

15. Do a practice interview. Have a colleague set up a virtual web session using any available platform. This will allow you to get feedback on your dress, background, acoustics, and general ability to answer questions.

References

1. Dig Dis Sci. 2019;64:1150-7.

2. BMJ Open. 2017;7:e016242.

3. Centers for Disease Control and Prevention. Coronavirus and Travel in the United States, 2020.

4. J Bone Joint Surg Am. 2017;99:e114.

5. Am J Gastroenterol. 2014;109:155-9.

6. West J Emerg Med. 2018;19:80-6.

7. Int J Med Educ. 2016;7:102-8.

8. Aparajit Naram M. How COVID-19 changed our fellowship interview process for the better. KevinMD.com. April 17, 2020.

9. Association of American Medical Colleges. Virtual interviews: Tips for medical school applicants, 2020. Updated May 14, 2020.

10. Top 5 video interviewing tips for residency and fellowship programs. Thalamus: Connecting the Docs. April 2, 2020, 2020.
 

Dr. Kiwan is chief fellow in gastroenterology, division of gastroenterology, at Wayne State University, Detroit Medical Center, John D. Dingell VA Medical Center, all in Detroit. Dr. Judd is an assistant professor and associate program director in the division of gastroenterology, Wayne State University, Detroit Medical Center, John D. Dingell VA Medical Center. Dr. Al Masalmeh is in the department of internal medicine, Wayne State University, Detroit Medical Center. Dr. Levine is professor and the vice chair for education, Wayne State University, Detroit Medical Center.

Fellowship interviews are an essential step – arguably the most important step – in the process of matching candidates to training programs. Until recently, most programs relied exclusively on on-site face-to face interviews. Since the appearance of the COVID-19 pandemic, the medical field has utilized web-based platforms. Despite inherent limitations, virtual meetings appear to be effective in providing patient care and in conducting administrative meetings.^1,2

Because of uncertainty related to the pandemic, including changing guidelines regarding social distancing and travel restrictions, fellowship programs are expected to comply with CDC,³ state, and federal recommendations to avoid nonessential travel. Therefore, conducting web-based interviews exclusively will likely become a necessity.

While there may be some disadvantages to web-based interviews, many candidates find the overall experience satisfactory, thereby allowing them to understand the programs, express themselves, and comfortably rank the programs, as two studies have shown.^4,5 Programs and candidates are encouraged to adapt to this new reality in order to achieve a successful match. After all, there are many potential advantages of web-based interviews. In addition to eliminating the risk of COVID-19 acquisition, web-based interviews have been described as helping to improve scheduling flexibility, reduce the financial burden, and allow conducting more interviews for candidates and programs (Table 1).^6-8

There are different styles to the web-based interview.⁹ Some programs choose to offer a single group interview (or the so-called panel interview) in which all the interviewing faculties invite each candidate at a time. Alternatively, programs might choose to conduct separate interviews by each faculty in which the candidates would alternate. For the latter option, the program could use a single invitation link or multiple invitation links for each session.
 

General tips for a successful interview:⁹

1. Be pleasant and professional: Your communication with the program should reflect excellent manners and a professional attitude with everyone (i.e., faculties, coordinators, and fellows).

2. Know yourself and what you want: Review your CV and personal statement and reflect on your achievements, strengths and weaknesses. Identify examples from your experience that would speak well of you as a person and as a physician.

3. Communication is key:

• Respond to the interview invitations promptly.
• Send a brief thank you email to the interviewers and the coordinator. Avoid being generic; mention specific points of discussion and show your interest in the program.
• Proofread your emails carefully. Well-written emails that are devoid of grammatical or spelling errors send a positive message about the candidate.

4. Do your homework:

• Read the information posted on the website carefully and take notes. This should provide you with useful information to use when you rank the programs and could lead to questions that you might want to ask your interviewers. Besides, asking questions that are answered on the website reflects poorly on the candidate.
• Pay attention to various clues that could reflect how organized and how academically oriented a program is. For example, a program that provides details about their didactic lectures sends a message that quality teaching is a priority. On the other hand, a program that has a website that hasn’t been updated for years could dissuade rather than recruit applicants.
• Read about the faculty, their areas of interests, and publications. Learn how their names are pronounced and use them during the interview.
• Read about the city where the program is. It shows interest in the area where you might be living and will help you to stand out among candidates.

5. Be prepared for the classics; be honest, genuine, and authentic. Think about these common prompts:

• Tell me about yourself.
• Why did you choose gastroenterology?
• Where do you see yourself in 5 years?
• Why would you like to come to the city where the program is?
• Are there any certain areas in gastroenterology that you’re interested in more (e.g., hepatology, motility, IBD, advanced endoscopy)?

6. It is likely your interviewer will ask if you have questions. Ask questions that further allow you to assess the program and your fit into the program.

• What aspects of the program are you most proud of?
• Where would you like to see this program in 5 years?
• What keeps you at this program?

Tips for a successful web-based interview^9,10 (Table 2):

1. Pay attention to the time zone of the city of the program. Be ready at least 10 minutes before the interview.

2. Ensure a fast and stable Internet service for an uninterrupted interview experience. Consider using an ethernet cable. Have a back-up plan such as using a phone as a hotspot.

3. Use a quiet and private room, preferably at home. Be aware of the background. A simple decoration is acceptable.

4. Consider recording yourself using the same device you’ll use for the interview to make sure audio and video are functioning properly.

5. When scheduling more than one interview in 1 day, allow at least 2 hours between interviews to avoid scheduling conflicts caused by unanticipated delays related to technical issues.

6. Have immediate access to the invitation link(s) that you received. Add the interviews to your device’s calendar. Note that sometimes a new invitation link is generated last minute because of technical issues.

7. While the advice for physical interviews is to turn off your phone (and smart watch), you’ll have to keep your phone on but on silent for the virtual interviews. Sometimes, you’ll receive a phone call from the program to update you about any last-minute changes.

7. It is recommended that a laptop or a tablet with a camera with good resolution and a microphone be used rather than using a phone. A wide screen allows better communication. Disable notification on that device to avoid interruptions.

8. Sit comfortably with the device being at or just below eye level. Avoid distractions and maintain eye contact.

9. Familiarize yourself with the platform used and its functions. Double check the audio and video before each interview.

10. Put your device on a desk or table to improve stability; don’t hold it in your hand.

11. Find a place where the view is best and your face appears in the middle of the screen; not too far or too close. Use a well-lit room but don’t have a source of light behind you. Many platforms allow you to select a background or blur the background. A background that is monochromatic and not distracting is recommended.

12. Use a pen and a paper to take notes during the interview. You would use these notes to generate “thank you” or “interest in program” emails. Additionally, they will be a helpful reference when ranking programs.

13. Do not type. Typing is much louder to the interviewer and can be distracting.

14. Dress professionally, just as you dress for an on-site interview. You never know when you might have to stand up during the interview for unplanned reasons.

15. Do a practice interview. Have a colleague set up a virtual web session using any available platform. This will allow you to get feedback on your dress, background, acoustics, and general ability to answer questions.

References

1. Dig Dis Sci. 2019;64:1150-7.

2. BMJ Open. 2017;7:e016242.

3. Centers for Disease Control and Prevention. Coronavirus and Travel in the United States, 2020.

4. J Bone Joint Surg Am. 2017;99:e114.

5. Am J Gastroenterol. 2014;109:155-9.

6. West J Emerg Med. 2018;19:80-6.

7. Int J Med Educ. 2016;7:102-8.

8. Aparajit Naram M. How COVID-19 changed our fellowship interview process for the better. KevinMD.com. April 17, 2020.

9. Association of American Medical Colleges. Virtual interviews: Tips for medical school applicants, 2020. Updated May 14, 2020.

10. Top 5 video interviewing tips for residency and fellowship programs. Thalamus: Connecting the Docs. April 2, 2020, 2020.
 

Dr. Kiwan is chief fellow in gastroenterology, division of gastroenterology, at Wayne State University, Detroit Medical Center, John D. Dingell VA Medical Center, all in Detroit. Dr. Judd is an assistant professor and associate program director in the division of gastroenterology, Wayne State University, Detroit Medical Center, John D. Dingell VA Medical Center. Dr. Al Masalmeh is in the department of internal medicine, Wayne State University, Detroit Medical Center. Dr. Levine is professor and the vice chair for education, Wayne State University, Detroit Medical Center.

Fellowship interviews are an essential step – arguably the most important step – in the process of matching candidates to training programs. Until recently, most programs relied exclusively on on-site face-to face interviews. Since the appearance of the COVID-19 pandemic, the medical field has utilized web-based platforms. Despite inherent limitations, virtual meetings appear to be effective in providing patient care and in conducting administrative meetings.^1,2

Because of uncertainty related to the pandemic, including changing guidelines regarding social distancing and travel restrictions, fellowship programs are expected to comply with CDC,³ state, and federal recommendations to avoid nonessential travel. Therefore, conducting web-based interviews exclusively will likely become a necessity.

While there may be some disadvantages to web-based interviews, many candidates find the overall experience satisfactory, thereby allowing them to understand the programs, express themselves, and comfortably rank the programs, as two studies have shown.^4,5 Programs and candidates are encouraged to adapt to this new reality in order to achieve a successful match. After all, there are many potential advantages of web-based interviews. In addition to eliminating the risk of COVID-19 acquisition, web-based interviews have been described as helping to improve scheduling flexibility, reduce the financial burden, and allow conducting more interviews for candidates and programs (Table 1).^6-8

There are different styles to the web-based interview.⁹ Some programs choose to offer a single group interview (or the so-called panel interview) in which all the interviewing faculties invite each candidate at a time. Alternatively, programs might choose to conduct separate interviews by each faculty in which the candidates would alternate. For the latter option, the program could use a single invitation link or multiple invitation links for each session.
 

General tips for a successful interview:⁹

1. Be pleasant and professional: Your communication with the program should reflect excellent manners and a professional attitude with everyone (i.e., faculties, coordinators, and fellows).

2. Know yourself and what you want: Review your CV and personal statement and reflect on your achievements, strengths and weaknesses. Identify examples from your experience that would speak well of you as a person and as a physician.

3. Communication is key:

• Respond to the interview invitations promptly.
• Send a brief thank you email to the interviewers and the coordinator. Avoid being generic; mention specific points of discussion and show your interest in the program.
• Proofread your emails carefully. Well-written emails that are devoid of grammatical or spelling errors send a positive message about the candidate.

4. Do your homework:

• Read the information posted on the website carefully and take notes. This should provide you with useful information to use when you rank the programs and could lead to questions that you might want to ask your interviewers. Besides, asking questions that are answered on the website reflects poorly on the candidate.
• Pay attention to various clues that could reflect how organized and how academically oriented a program is. For example, a program that provides details about their didactic lectures sends a message that quality teaching is a priority. On the other hand, a program that has a website that hasn’t been updated for years could dissuade rather than recruit applicants.
• Read about the faculty, their areas of interests, and publications. Learn how their names are pronounced and use them during the interview.
• Read about the city where the program is. It shows interest in the area where you might be living and will help you to stand out among candidates.

5. Be prepared for the classics; be honest, genuine, and authentic. Think about these common prompts:

• Tell me about yourself.
• Why did you choose gastroenterology?
• Where do you see yourself in 5 years?
• Why would you like to come to the city where the program is?
• Are there any certain areas in gastroenterology that you’re interested in more (e.g., hepatology, motility, IBD, advanced endoscopy)?

6. It is likely your interviewer will ask if you have questions. Ask questions that further allow you to assess the program and your fit into the program.

• What aspects of the program are you most proud of?
• Where would you like to see this program in 5 years?
• What keeps you at this program?

Tips for a successful web-based interview^9,10 (Table 2):

1. Pay attention to the time zone of the city of the program. Be ready at least 10 minutes before the interview.

2. Ensure a fast and stable Internet service for an uninterrupted interview experience. Consider using an ethernet cable. Have a back-up plan such as using a phone as a hotspot.

3. Use a quiet and private room, preferably at home. Be aware of the background. A simple decoration is acceptable.

4. Consider recording yourself using the same device you’ll use for the interview to make sure audio and video are functioning properly.

5. When scheduling more than one interview in 1 day, allow at least 2 hours between interviews to avoid scheduling conflicts caused by unanticipated delays related to technical issues.

6. Have immediate access to the invitation link(s) that you received. Add the interviews to your device’s calendar. Note that sometimes a new invitation link is generated last minute because of technical issues.

7. While the advice for physical interviews is to turn off your phone (and smart watch), you’ll have to keep your phone on but on silent for the virtual interviews. Sometimes, you’ll receive a phone call from the program to update you about any last-minute changes.

7. It is recommended that a laptop or a tablet with a camera with good resolution and a microphone be used rather than using a phone. A wide screen allows better communication. Disable notification on that device to avoid interruptions.

8. Sit comfortably with the device being at or just below eye level. Avoid distractions and maintain eye contact.

9. Familiarize yourself with the platform used and its functions. Double check the audio and video before each interview.

10. Put your device on a desk or table to improve stability; don’t hold it in your hand.

11. Find a place where the view is best and your face appears in the middle of the screen; not too far or too close. Use a well-lit room but don’t have a source of light behind you. Many platforms allow you to select a background or blur the background. A background that is monochromatic and not distracting is recommended.

12. Use a pen and a paper to take notes during the interview. You would use these notes to generate “thank you” or “interest in program” emails. Additionally, they will be a helpful reference when ranking programs.

13. Do not type. Typing is much louder to the interviewer and can be distracting.

14. Dress professionally, just as you dress for an on-site interview. You never know when you might have to stand up during the interview for unplanned reasons.

15. Do a practice interview. Have a colleague set up a virtual web session using any available platform. This will allow you to get feedback on your dress, background, acoustics, and general ability to answer questions.

References

1. Dig Dis Sci. 2019;64:1150-7.

2. BMJ Open. 2017;7:e016242.

3. Centers for Disease Control and Prevention. Coronavirus and Travel in the United States, 2020.

4. J Bone Joint Surg Am. 2017;99:e114.

5. Am J Gastroenterol. 2014;109:155-9.

6. West J Emerg Med. 2018;19:80-6.

7. Int J Med Educ. 2016;7:102-8.

8. Aparajit Naram M. How COVID-19 changed our fellowship interview process for the better. KevinMD.com. April 17, 2020.

9. Association of American Medical Colleges. Virtual interviews: Tips for medical school applicants, 2020. Updated May 14, 2020.

10. Top 5 video interviewing tips for residency and fellowship programs. Thalamus: Connecting the Docs. April 2, 2020, 2020.
 

Dr. Kiwan is chief fellow in gastroenterology, division of gastroenterology, at Wayne State University, Detroit Medical Center, John D. Dingell VA Medical Center, all in Detroit. Dr. Judd is an assistant professor and associate program director in the division of gastroenterology, Wayne State University, Detroit Medical Center, John D. Dingell VA Medical Center. Dr. Al Masalmeh is in the department of internal medicine, Wayne State University, Detroit Medical Center. Dr. Levine is professor and the vice chair for education, Wayne State University, Detroit Medical Center.

The state of health care in Massachusetts makes it the state for health care in 2020, according to the personal finance website WalletHub.

The Bay State finds itself at the top of the company’s annual ranking of state health care systems this year after finishing second in 2019 to Minnesota, which is now ranked second. Rhode Island is third this year, followed by Washington, D.C., and North Dakota, WalletHub reported Aug. 3.

The inclusion of Washington, D.C., allowed Georgia to finish 51st out of 50 states, just below the quartet of Louisiana (50th), Alabama (49th), North Carolina (48th), and Mississippi (47th). Alaska, which occupied the bottom spot in 2019, moved up to 42nd this year, the analysis showed.

The rankings are based on 44 (up from 43 last year) metrics that are grouped into three broad categories: cost (6 metrics), access (24 metrics), and outcomes (14 metrics). The one new measure added for 2020? That would be health infrastructure for coronavirus, which is itself based on a different WalletHub ranking.

Massachusetts’ top finish this year was driven by strong showings in such metrics as average monthly insurance premium (first), physicians per capita (second), insured children (first) and adults (first), and infant mortality rate (fourth). The state was 1st overall in outcomes and 4th in access but only 20th in cost, the company said.

Positive signs among the lowest-ranked states include Louisiana’s 18th-place finish in access, ahead of such top 10 states as Iowa and Hawaii, and Mississippi’s 17th in cost, which is higher than four of the states in the top 10, including Massachusetts, WalletHub said in the report.

Data for the analysis came from 22 different sources, including the Institute for Health Metrics and Evaluation, Centers for Medicare & Medicaid Services, Association of American Medical Colleges, and the American Telemedicine Association.

[email protected]

The state of health care in Massachusetts makes it the state for health care in 2020, according to the personal finance website WalletHub.

The Bay State finds itself at the top of the company’s annual ranking of state health care systems this year after finishing second in 2019 to Minnesota, which is now ranked second. Rhode Island is third this year, followed by Washington, D.C., and North Dakota, WalletHub reported Aug. 3.

The inclusion of Washington, D.C., allowed Georgia to finish 51st out of 50 states, just below the quartet of Louisiana (50th), Alabama (49th), North Carolina (48th), and Mississippi (47th). Alaska, which occupied the bottom spot in 2019, moved up to 42nd this year, the analysis showed.

The rankings are based on 44 (up from 43 last year) metrics that are grouped into three broad categories: cost (6 metrics), access (24 metrics), and outcomes (14 metrics). The one new measure added for 2020? That would be health infrastructure for coronavirus, which is itself based on a different WalletHub ranking.

Massachusetts’ top finish this year was driven by strong showings in such metrics as average monthly insurance premium (first), physicians per capita (second), insured children (first) and adults (first), and infant mortality rate (fourth). The state was 1st overall in outcomes and 4th in access but only 20th in cost, the company said.

Positive signs among the lowest-ranked states include Louisiana’s 18th-place finish in access, ahead of such top 10 states as Iowa and Hawaii, and Mississippi’s 17th in cost, which is higher than four of the states in the top 10, including Massachusetts, WalletHub said in the report.

Data for the analysis came from 22 different sources, including the Institute for Health Metrics and Evaluation, Centers for Medicare & Medicaid Services, Association of American Medical Colleges, and the American Telemedicine Association.

[email protected]

The state of health care in Massachusetts makes it the state for health care in 2020, according to the personal finance website WalletHub.

The Bay State finds itself at the top of the company’s annual ranking of state health care systems this year after finishing second in 2019 to Minnesota, which is now ranked second. Rhode Island is third this year, followed by Washington, D.C., and North Dakota, WalletHub reported Aug. 3.

The inclusion of Washington, D.C., allowed Georgia to finish 51st out of 50 states, just below the quartet of Louisiana (50th), Alabama (49th), North Carolina (48th), and Mississippi (47th). Alaska, which occupied the bottom spot in 2019, moved up to 42nd this year, the analysis showed.

The rankings are based on 44 (up from 43 last year) metrics that are grouped into three broad categories: cost (6 metrics), access (24 metrics), and outcomes (14 metrics). The one new measure added for 2020? That would be health infrastructure for coronavirus, which is itself based on a different WalletHub ranking.

Massachusetts’ top finish this year was driven by strong showings in such metrics as average monthly insurance premium (first), physicians per capita (second), insured children (first) and adults (first), and infant mortality rate (fourth). The state was 1st overall in outcomes and 4th in access but only 20th in cost, the company said.

Positive signs among the lowest-ranked states include Louisiana’s 18th-place finish in access, ahead of such top 10 states as Iowa and Hawaii, and Mississippi’s 17th in cost, which is higher than four of the states in the top 10, including Massachusetts, WalletHub said in the report.

Data for the analysis came from 22 different sources, including the Institute for Health Metrics and Evaluation, Centers for Medicare & Medicaid Services, Association of American Medical Colleges, and the American Telemedicine Association.

[email protected]

A 76-year-old woman presented recently to a Toronto-area hospital with acute onset muscle pain, limb weakness, difficulty walking, and rhabdomyolysis associated with a sharp spike in her plasma level of rosuvastatin – a drug she had been on uneventfully for more than 5 years, within days of starting for the first time treatment with the SGLT2 inhibitor canagliflozin (Invokana).

The patient’s Canadian clinicians stopped her treatment with both rosuvastatin and canagliflozin, administered intravenous crystalloid fluids, and within days her pain subsided and her limb weakness gradually improved, allowing her discharge 10 days later while she was ambulating with a walker.

“To our knowledge this is the first published report of a drug interaction between rosuvastatin and canagliflozin,” wrote the authors of the case report (Ann Intern Med. 2020 Aug 3. doi: 10.7326/L20-0549). They cited the importance of the observation given the widespread use today of rosuvastatin for lowering low density lipoprotein cholesterol and exerting pleiotropic effects; and canagliflozin for its modest effects for reducing hyperglycemia, as well as its important role in reducing adverse cardiovascular outcomes, slowing progression of chronic kidney disease, and having a mild but important diuretic effect. “We encourage clinicians to remain vigilant for features of myotoxicity when canagliflozin and rosuvastatin are coprescribed,” they wrote, avoiding discussion of whether this may represent class or drug-specific effects.

“It’s reasonable to be mindful of this risk, but this is not a reason to not use rosuvastatin and canagliflozin in a patient,” nor for the time being to avoid any other combination of a statin and SGLT2 (sodium-glucose cotransporter 2) inhibitor, said David Juurlink, MD, head of the division of clinical pharmacology and toxicology at Sunnybrook Health Sciences Centre in Toronto and lead author of the report. “Few drug interactions have absolute contraindications. The admonition is just to be careful. It’s premature to say they shouldn’t be used together,” he said in an interview.

“We don’t know how much of an outlier this patient is. But it would be important to tell patients” on this or a similar combination to alert their clinicians if they start to have muscle aches, which should be a “red flag” to stop the statin, the SGLT2 inhibitor, or both until the situation can be fully assessed, Dr. Juurlink advised.
 

Sky high rosuvastatin levels

The linchpin of the observed adverse effects appeared to be a startlingly high elevation of the patient’s plasma rosuvastatin level when she was hospitalized 15 days after starting canagliflozin and 12 days after the onset of her thigh pain and weakness. Testing showed a plasma rosuvastatin concentration of 176 ng/mL, “more than 15-fold higher than the mean value expected” in patients taking 40 mg rosuvastatin daily, the maximum labeled dosage for the drug and what the affected patient had been taking without prior incident for more than 5 years. The patient’s canagliflozin dosage was 100 mg/day, the standard starting dosage according to the drug’s label.

The report’s authors noted that genetic assessment of the patient, a woman originally from the Philippines who was “high functioning,” and diagnosed with type 2 diabetes, showed she was heterozygous for a polymorphism, c.421C>A, which is linked with increased rosuvastatin plasma levels in the plasma. They also cited a report that canagliflozin can interact with proteins involved in hepatic drug uptake.

“We speculate that, in our patient, the addition of canagliflozin enhanced intestinal rosuvastatin absorption, inhibited its hepatocellular uptake, and impaired its excretion into bile canaliculi and the proximal tubule, resulting in rosuvastatin accumulation and leading to hepatotoxicity and myotoxicity,” the clinicians wrote in their report.

“There is little doubt this was a drug interaction, but it does not apply uniformly to everyone.” The severity of the interaction would depend on the dosages, the comorbidities a patient has, and their genetic profile, Dr. Juurlink said.
 

Concern and skepticism

Other clinicians who regularly prescribe these drugs expressed concern about the observation as well as skepticism about the prevalence of patients who could potentially experience similar effects.

Catherine Hackett/MDedge News

“We don’t know how common are these genetic abnormalities. If this is extremely rare, then it doesn’t have many clinical implications, but if a large portion of the population has this [genetic] abnormality, it’s something we’d need to pay attention to,” Steven E. Nissen, MD, chair of cardiovascular medicine at the Cleveland Clinic Foundation, said in an interview. “It will be important to know the prevalence” of the genetic polymorphism carried by the reported patient, said Dr. Nissen, who has done research on lipid-lowering medications and drug safety.

“This could be important, or a very rare one-off. I can’t say which,” based on what’s currently known, he said. “There are many unanswered questions that make it hard to know how important this will be. It requires further investigation. There is a lot of uncertainty.”

Dr. Nissen particularly endorsed studies that approach this issue by looking at the prevalence rates of the implicated genetic polymorphism rather than pharmacovigilance studies that make epidemiologic assessments of adverse-effect prevalence. Studies that look for adverse-effect associations in large patient populations are “sloppy, and unless the interaction is incredibly intense they are not very sensitive,” he said.

But Dr. Juurlink, a pharmacoepidemiologist whose specialty includes studies of this sort, said that they could be useful if carefully designed. He suggested, for example, comparing in large patient databases the observed incidence of rhabdomyolysis among patients on an SGLT2 inhibitor and also on rosuvastatin with those on pravastatin, a statin with a different metabolic profile. Another approach to further examining the observation would be dosage studies with rosuvastatin and canagliflozin in healthy volunteers, he said.

Dr. Nissen noted that rosuvastatin is a key agent from the statin class because it’s the “most effective” for lowering low density lipoprotein cholesterol. “Rosuvastatin is a go-to drug,” he declared. On the other hand, canagliflozin is “a little less used” than other drugs in the SGLT2 inhibitor class, specifically dapagliflozin (Farxiga) and empagliflozin (Jardiance), he said.

One in a million?

“This was a freak accident. I don’t find it at all concerning. It was definitely one in a million,” Yehuda Handelsman, MD, an endocrinologist and diabetes specialist who is medical director of The Metabolic Institute of America in Tarzana, Calif., said in an interview. “None of us have seen it” in either the several cardiovascular outcome trials now run on multiple drugs in the SGLT2 inhibitor class that included many patients also taking a statin, or in routine practice, he said. Dr. Handelsman noted that in his practice he had never seen a similar case despite treating “hundreds if not thousands of patients” with type 2 diabetes, virtually all of whom were on a statin and were also treated with an SGLT2 inhibitor, including many with canagliflozin.

Dr. Handelsman cited the notably low estimated glomerular filtration rate in the reported patient, who was described as having a serum creatinine level of 150 mcmol/L (1.7 mg/dL) prior to canagliflozin treatment that then rose to 194 mcmol/L (2.19 mg/dL) at the time of hospitalization, which corresponds to estimated glomerular filtration rates of 29-31 and 21-23 mL/min per 1.73 m², respectively, depending on the calculator used, rates that were possibly below the labeled minimum rate of 30 mL/min per 1.73 m² for patients starting canagliflozin treatment. The case report cited the patient as having stage 3B chronic kidney disease, which corresponds to a eGFR of 30-44* mL/min per 1.73 m².

“I think the patient had acute kidney injury” on starting canagliflozin “that may have affected the [rosuvastatin] metabolism,” Dr. Handelsman suggested. “She had severe kidney dysfunction to start with that fell further with SGLT2 inhibitor treatment,” a well described and usually transient effect of starting drugs in this class because of changes the SGLT2 inhibitors cause in renal blood flow. He noted that the patient had not been receiving an angiotensin-converting enzyme inhibitor or angiotensin-receptor blocker, which may have contributed to her acute problems with fluid balance. Most similar patients with type 2 diabetes, cardiovascular disease risk, and chronic kidney disease would be on stable treatment with a drug that inhibits the renin-angiotensin system before starting an SGLT2 inhibitor, and not already having a RAS inhibitor on board before starting canagliflozin may have somehow contributed to the observed adverse effects, Dr. Handelsman said.

Dr. Juurlink was skeptical that the kidneys played a major role. “An abrupt change in renal function can influence statin clearance, but this was a 15-fold increase. You can’t explain such a dramatic increase by a transient reduction in renal function,” he said.

Dr. Juurlink and coauthors had no disclosures. Dr. Nissen had no relevant disclosures. Dr. Handelsman has been a consultant to companies that market drugs in the SGLT2 inhibitor class.

[email protected]

SOURCE: Brailovski E et al. Ann Intern Med. 2020 Aug 3. doi: 10.7326/L20-0549.

*Correction: This value was missing from the original article.

A 76-year-old woman presented recently to a Toronto-area hospital with acute onset muscle pain, limb weakness, difficulty walking, and rhabdomyolysis associated with a sharp spike in her plasma level of rosuvastatin – a drug she had been on uneventfully for more than 5 years, within days of starting for the first time treatment with the SGLT2 inhibitor canagliflozin (Invokana).

The patient’s Canadian clinicians stopped her treatment with both rosuvastatin and canagliflozin, administered intravenous crystalloid fluids, and within days her pain subsided and her limb weakness gradually improved, allowing her discharge 10 days later while she was ambulating with a walker.

“To our knowledge this is the first published report of a drug interaction between rosuvastatin and canagliflozin,” wrote the authors of the case report (Ann Intern Med. 2020 Aug 3. doi: 10.7326/L20-0549). They cited the importance of the observation given the widespread use today of rosuvastatin for lowering low density lipoprotein cholesterol and exerting pleiotropic effects; and canagliflozin for its modest effects for reducing hyperglycemia, as well as its important role in reducing adverse cardiovascular outcomes, slowing progression of chronic kidney disease, and having a mild but important diuretic effect. “We encourage clinicians to remain vigilant for features of myotoxicity when canagliflozin and rosuvastatin are coprescribed,” they wrote, avoiding discussion of whether this may represent class or drug-specific effects.

“It’s reasonable to be mindful of this risk, but this is not a reason to not use rosuvastatin and canagliflozin in a patient,” nor for the time being to avoid any other combination of a statin and SGLT2 (sodium-glucose cotransporter 2) inhibitor, said David Juurlink, MD, head of the division of clinical pharmacology and toxicology at Sunnybrook Health Sciences Centre in Toronto and lead author of the report. “Few drug interactions have absolute contraindications. The admonition is just to be careful. It’s premature to say they shouldn’t be used together,” he said in an interview.

“We don’t know how much of an outlier this patient is. But it would be important to tell patients” on this or a similar combination to alert their clinicians if they start to have muscle aches, which should be a “red flag” to stop the statin, the SGLT2 inhibitor, or both until the situation can be fully assessed, Dr. Juurlink advised.
 

Sky high rosuvastatin levels

The linchpin of the observed adverse effects appeared to be a startlingly high elevation of the patient’s plasma rosuvastatin level when she was hospitalized 15 days after starting canagliflozin and 12 days after the onset of her thigh pain and weakness. Testing showed a plasma rosuvastatin concentration of 176 ng/mL, “more than 15-fold higher than the mean value expected” in patients taking 40 mg rosuvastatin daily, the maximum labeled dosage for the drug and what the affected patient had been taking without prior incident for more than 5 years. The patient’s canagliflozin dosage was 100 mg/day, the standard starting dosage according to the drug’s label.

The report’s authors noted that genetic assessment of the patient, a woman originally from the Philippines who was “high functioning,” and diagnosed with type 2 diabetes, showed she was heterozygous for a polymorphism, c.421C>A, which is linked with increased rosuvastatin plasma levels in the plasma. They also cited a report that canagliflozin can interact with proteins involved in hepatic drug uptake.

“We speculate that, in our patient, the addition of canagliflozin enhanced intestinal rosuvastatin absorption, inhibited its hepatocellular uptake, and impaired its excretion into bile canaliculi and the proximal tubule, resulting in rosuvastatin accumulation and leading to hepatotoxicity and myotoxicity,” the clinicians wrote in their report.

“There is little doubt this was a drug interaction, but it does not apply uniformly to everyone.” The severity of the interaction would depend on the dosages, the comorbidities a patient has, and their genetic profile, Dr. Juurlink said.
 

Concern and skepticism

Other clinicians who regularly prescribe these drugs expressed concern about the observation as well as skepticism about the prevalence of patients who could potentially experience similar effects.

Catherine Hackett/MDedge News

“We don’t know how common are these genetic abnormalities. If this is extremely rare, then it doesn’t have many clinical implications, but if a large portion of the population has this [genetic] abnormality, it’s something we’d need to pay attention to,” Steven E. Nissen, MD, chair of cardiovascular medicine at the Cleveland Clinic Foundation, said in an interview. “It will be important to know the prevalence” of the genetic polymorphism carried by the reported patient, said Dr. Nissen, who has done research on lipid-lowering medications and drug safety.

“This could be important, or a very rare one-off. I can’t say which,” based on what’s currently known, he said. “There are many unanswered questions that make it hard to know how important this will be. It requires further investigation. There is a lot of uncertainty.”

Dr. Nissen particularly endorsed studies that approach this issue by looking at the prevalence rates of the implicated genetic polymorphism rather than pharmacovigilance studies that make epidemiologic assessments of adverse-effect prevalence. Studies that look for adverse-effect associations in large patient populations are “sloppy, and unless the interaction is incredibly intense they are not very sensitive,” he said.

But Dr. Juurlink, a pharmacoepidemiologist whose specialty includes studies of this sort, said that they could be useful if carefully designed. He suggested, for example, comparing in large patient databases the observed incidence of rhabdomyolysis among patients on an SGLT2 inhibitor and also on rosuvastatin with those on pravastatin, a statin with a different metabolic profile. Another approach to further examining the observation would be dosage studies with rosuvastatin and canagliflozin in healthy volunteers, he said.

Dr. Nissen noted that rosuvastatin is a key agent from the statin class because it’s the “most effective” for lowering low density lipoprotein cholesterol. “Rosuvastatin is a go-to drug,” he declared. On the other hand, canagliflozin is “a little less used” than other drugs in the SGLT2 inhibitor class, specifically dapagliflozin (Farxiga) and empagliflozin (Jardiance), he said.

One in a million?

“This was a freak accident. I don’t find it at all concerning. It was definitely one in a million,” Yehuda Handelsman, MD, an endocrinologist and diabetes specialist who is medical director of The Metabolic Institute of America in Tarzana, Calif., said in an interview. “None of us have seen it” in either the several cardiovascular outcome trials now run on multiple drugs in the SGLT2 inhibitor class that included many patients also taking a statin, or in routine practice, he said. Dr. Handelsman noted that in his practice he had never seen a similar case despite treating “hundreds if not thousands of patients” with type 2 diabetes, virtually all of whom were on a statin and were also treated with an SGLT2 inhibitor, including many with canagliflozin.

Dr. Handelsman cited the notably low estimated glomerular filtration rate in the reported patient, who was described as having a serum creatinine level of 150 mcmol/L (1.7 mg/dL) prior to canagliflozin treatment that then rose to 194 mcmol/L (2.19 mg/dL) at the time of hospitalization, which corresponds to estimated glomerular filtration rates of 29-31 and 21-23 mL/min per 1.73 m², respectively, depending on the calculator used, rates that were possibly below the labeled minimum rate of 30 mL/min per 1.73 m² for patients starting canagliflozin treatment. The case report cited the patient as having stage 3B chronic kidney disease, which corresponds to a eGFR of 30-44* mL/min per 1.73 m².

“I think the patient had acute kidney injury” on starting canagliflozin “that may have affected the [rosuvastatin] metabolism,” Dr. Handelsman suggested. “She had severe kidney dysfunction to start with that fell further with SGLT2 inhibitor treatment,” a well described and usually transient effect of starting drugs in this class because of changes the SGLT2 inhibitors cause in renal blood flow. He noted that the patient had not been receiving an angiotensin-converting enzyme inhibitor or angiotensin-receptor blocker, which may have contributed to her acute problems with fluid balance. Most similar patients with type 2 diabetes, cardiovascular disease risk, and chronic kidney disease would be on stable treatment with a drug that inhibits the renin-angiotensin system before starting an SGLT2 inhibitor, and not already having a RAS inhibitor on board before starting canagliflozin may have somehow contributed to the observed adverse effects, Dr. Handelsman said.

Dr. Juurlink was skeptical that the kidneys played a major role. “An abrupt change in renal function can influence statin clearance, but this was a 15-fold increase. You can’t explain such a dramatic increase by a transient reduction in renal function,” he said.

Dr. Juurlink and coauthors had no disclosures. Dr. Nissen had no relevant disclosures. Dr. Handelsman has been a consultant to companies that market drugs in the SGLT2 inhibitor class.

[email protected]

SOURCE: Brailovski E et al. Ann Intern Med. 2020 Aug 3. doi: 10.7326/L20-0549.

*Correction: This value was missing from the original article.

A 76-year-old woman presented recently to a Toronto-area hospital with acute onset muscle pain, limb weakness, difficulty walking, and rhabdomyolysis associated with a sharp spike in her plasma level of rosuvastatin – a drug she had been on uneventfully for more than 5 years, within days of starting for the first time treatment with the SGLT2 inhibitor canagliflozin (Invokana).

The patient’s Canadian clinicians stopped her treatment with both rosuvastatin and canagliflozin, administered intravenous crystalloid fluids, and within days her pain subsided and her limb weakness gradually improved, allowing her discharge 10 days later while she was ambulating with a walker.

“To our knowledge this is the first published report of a drug interaction between rosuvastatin and canagliflozin,” wrote the authors of the case report (Ann Intern Med. 2020 Aug 3. doi: 10.7326/L20-0549). They cited the importance of the observation given the widespread use today of rosuvastatin for lowering low density lipoprotein cholesterol and exerting pleiotropic effects; and canagliflozin for its modest effects for reducing hyperglycemia, as well as its important role in reducing adverse cardiovascular outcomes, slowing progression of chronic kidney disease, and having a mild but important diuretic effect. “We encourage clinicians to remain vigilant for features of myotoxicity when canagliflozin and rosuvastatin are coprescribed,” they wrote, avoiding discussion of whether this may represent class or drug-specific effects.

“It’s reasonable to be mindful of this risk, but this is not a reason to not use rosuvastatin and canagliflozin in a patient,” nor for the time being to avoid any other combination of a statin and SGLT2 (sodium-glucose cotransporter 2) inhibitor, said David Juurlink, MD, head of the division of clinical pharmacology and toxicology at Sunnybrook Health Sciences Centre in Toronto and lead author of the report. “Few drug interactions have absolute contraindications. The admonition is just to be careful. It’s premature to say they shouldn’t be used together,” he said in an interview.

“We don’t know how much of an outlier this patient is. But it would be important to tell patients” on this or a similar combination to alert their clinicians if they start to have muscle aches, which should be a “red flag” to stop the statin, the SGLT2 inhibitor, or both until the situation can be fully assessed, Dr. Juurlink advised.
 

Sky high rosuvastatin levels

The linchpin of the observed adverse effects appeared to be a startlingly high elevation of the patient’s plasma rosuvastatin level when she was hospitalized 15 days after starting canagliflozin and 12 days after the onset of her thigh pain and weakness. Testing showed a plasma rosuvastatin concentration of 176 ng/mL, “more than 15-fold higher than the mean value expected” in patients taking 40 mg rosuvastatin daily, the maximum labeled dosage for the drug and what the affected patient had been taking without prior incident for more than 5 years. The patient’s canagliflozin dosage was 100 mg/day, the standard starting dosage according to the drug’s label.

The report’s authors noted that genetic assessment of the patient, a woman originally from the Philippines who was “high functioning,” and diagnosed with type 2 diabetes, showed she was heterozygous for a polymorphism, c.421C>A, which is linked with increased rosuvastatin plasma levels in the plasma. They also cited a report that canagliflozin can interact with proteins involved in hepatic drug uptake.

“We speculate that, in our patient, the addition of canagliflozin enhanced intestinal rosuvastatin absorption, inhibited its hepatocellular uptake, and impaired its excretion into bile canaliculi and the proximal tubule, resulting in rosuvastatin accumulation and leading to hepatotoxicity and myotoxicity,” the clinicians wrote in their report.

“There is little doubt this was a drug interaction, but it does not apply uniformly to everyone.” The severity of the interaction would depend on the dosages, the comorbidities a patient has, and their genetic profile, Dr. Juurlink said.
 

Concern and skepticism

Other clinicians who regularly prescribe these drugs expressed concern about the observation as well as skepticism about the prevalence of patients who could potentially experience similar effects.

Catherine Hackett/MDedge News

“We don’t know how common are these genetic abnormalities. If this is extremely rare, then it doesn’t have many clinical implications, but if a large portion of the population has this [genetic] abnormality, it’s something we’d need to pay attention to,” Steven E. Nissen, MD, chair of cardiovascular medicine at the Cleveland Clinic Foundation, said in an interview. “It will be important to know the prevalence” of the genetic polymorphism carried by the reported patient, said Dr. Nissen, who has done research on lipid-lowering medications and drug safety.

“This could be important, or a very rare one-off. I can’t say which,” based on what’s currently known, he said. “There are many unanswered questions that make it hard to know how important this will be. It requires further investigation. There is a lot of uncertainty.”

Dr. Nissen particularly endorsed studies that approach this issue by looking at the prevalence rates of the implicated genetic polymorphism rather than pharmacovigilance studies that make epidemiologic assessments of adverse-effect prevalence. Studies that look for adverse-effect associations in large patient populations are “sloppy, and unless the interaction is incredibly intense they are not very sensitive,” he said.

But Dr. Juurlink, a pharmacoepidemiologist whose specialty includes studies of this sort, said that they could be useful if carefully designed. He suggested, for example, comparing in large patient databases the observed incidence of rhabdomyolysis among patients on an SGLT2 inhibitor and also on rosuvastatin with those on pravastatin, a statin with a different metabolic profile. Another approach to further examining the observation would be dosage studies with rosuvastatin and canagliflozin in healthy volunteers, he said.

Dr. Nissen noted that rosuvastatin is a key agent from the statin class because it’s the “most effective” for lowering low density lipoprotein cholesterol. “Rosuvastatin is a go-to drug,” he declared. On the other hand, canagliflozin is “a little less used” than other drugs in the SGLT2 inhibitor class, specifically dapagliflozin (Farxiga) and empagliflozin (Jardiance), he said.

One in a million?

“This was a freak accident. I don’t find it at all concerning. It was definitely one in a million,” Yehuda Handelsman, MD, an endocrinologist and diabetes specialist who is medical director of The Metabolic Institute of America in Tarzana, Calif., said in an interview. “None of us have seen it” in either the several cardiovascular outcome trials now run on multiple drugs in the SGLT2 inhibitor class that included many patients also taking a statin, or in routine practice, he said. Dr. Handelsman noted that in his practice he had never seen a similar case despite treating “hundreds if not thousands of patients” with type 2 diabetes, virtually all of whom were on a statin and were also treated with an SGLT2 inhibitor, including many with canagliflozin.

Dr. Handelsman cited the notably low estimated glomerular filtration rate in the reported patient, who was described as having a serum creatinine level of 150 mcmol/L (1.7 mg/dL) prior to canagliflozin treatment that then rose to 194 mcmol/L (2.19 mg/dL) at the time of hospitalization, which corresponds to estimated glomerular filtration rates of 29-31 and 21-23 mL/min per 1.73 m², respectively, depending on the calculator used, rates that were possibly below the labeled minimum rate of 30 mL/min per 1.73 m² for patients starting canagliflozin treatment. The case report cited the patient as having stage 3B chronic kidney disease, which corresponds to a eGFR of 30-44* mL/min per 1.73 m².

“I think the patient had acute kidney injury” on starting canagliflozin “that may have affected the [rosuvastatin] metabolism,” Dr. Handelsman suggested. “She had severe kidney dysfunction to start with that fell further with SGLT2 inhibitor treatment,” a well described and usually transient effect of starting drugs in this class because of changes the SGLT2 inhibitors cause in renal blood flow. He noted that the patient had not been receiving an angiotensin-converting enzyme inhibitor or angiotensin-receptor blocker, which may have contributed to her acute problems with fluid balance. Most similar patients with type 2 diabetes, cardiovascular disease risk, and chronic kidney disease would be on stable treatment with a drug that inhibits the renin-angiotensin system before starting an SGLT2 inhibitor, and not already having a RAS inhibitor on board before starting canagliflozin may have somehow contributed to the observed adverse effects, Dr. Handelsman said.

Dr. Juurlink was skeptical that the kidneys played a major role. “An abrupt change in renal function can influence statin clearance, but this was a 15-fold increase. You can’t explain such a dramatic increase by a transient reduction in renal function,” he said.

Dr. Juurlink and coauthors had no disclosures. Dr. Nissen had no relevant disclosures. Dr. Handelsman has been a consultant to companies that market drugs in the SGLT2 inhibitor class.

[email protected]

SOURCE: Brailovski E et al. Ann Intern Med. 2020 Aug 3. doi: 10.7326/L20-0549.

*Correction: This value was missing from the original article.

Plasma exchange with albumin replacement may be effective for slowing down symptoms of Alzheimer’s disease, new research suggests. Results from the phase 2b/3 AMBAR study showed that the treatment, which aims to remove amyloid-beta (Abeta) from plasma, was associated with a 60% decrease in functional and cognitive decline in patients with moderate Alzheimer’s disease.

The reduction in cognitive decline uncovered by the study is more striking than that reported for other investigational treatments targeting Abeta, such as monoclonal antibodies, said coinvestigator Antonio Páez, MD, medical director of the AMBAR program, Alzheimer’s Research Group, Grifols, Barcelona.

The results “open a new path for the development of plasma protein replacement therapies not only in Alzheimer’s disease but also in other degenerative diseases that we are planning to investigate,” Dr. Páez said.

The findings were presented at the virtual annual meeting of the Alzheimer’s Association International Conference and were simultaneously published in Alzheimer’s and Dementia.
 

Removing amyloid

Plasma exchange treatments, which have been available for several decades, are used to treat a range of neurologic, immunologic, and metabolic disorders. The treatment involves plasmapheresis, whereby plasma is separated from blood cells (red blood cells, white blood cells, platelets, etc) and toxic substances are removed. The albumin in plasma, to which plasma Abeta is bound, is replaced with a fresh commercial albumin product made from plasma from healthy donors.

“Our initial hypothesis was that, by removing albumin together with Abeta and substituting it with newer albumin periodically, we may be removing Abeta from the cerebrospinal fluid and eventually from the brain,” Dr. Páez said.

The AMBAR study included 347 men and women aged 55-85 years with probable Alzheimer’s disease dementia who were enrolled at 41 sites in Spain and the United States. All were diagnosed with mild Alzheimer’s disease, as shown by a baseline Mini-Mental State Examination score of 22-26, or moderate Alzheimer’s disease, having a baseline MMSE score of 18-21.

Investigators randomly assigned the participants to four groups; one group received placebo, and each of the other three treatment arms received different doses of albumin and intravenous immunoglobulin (IVIg) replacement.

During the first 6-week study phase, patients received weekly sham or conventional plasma exchange treatments of 2.5-3 liters of plasma, which Dr. Páez referred to as the “intensive-treatment phase to remove as much Abeta as possible.”

This was followed by a 12-month maintenance phase, which involved monthly low-volume (700-800 mL) plasma exchange or sham treatments.

Although the volume of plasma removed was the same in all three active-treatment groups, the amount of albumin and IVIg that was subsequently replaced varied. In one group, the same amount of albumin and IVIg that was removed was replaced; in another, half the amount removed was replaced; and in the third, only albumin was replaced.

The researchers collected cerebrospinal fluid (CSF) samples at baseline and after each treatment period. They assessed Abeta40, Abeta42, total tau, and phosphorylated-tau biomarkers.

The two primary outcomes were change from baseline to 14 months in scores on the Alzheimer’s Disease Cooperative Study–Activities of Daily Living (ADCS-ADL) scale and the Alzheimer’s Disease Assessment Scale–Cognitive Subscale (ADAS-Cog).
 

Symptom reduction

Results showed a reduction in the progression of symptoms in the plasma exchange–treated patients for both primary endpoints.

The ADCS-ADL showed 52% less decline in the plasma exchange–treated group, compared with the placebo group (P = .03); the ADAS-Cog showed 66% less decline (P = 0.06). In the moderate group, both endpoints showed 61% less decline (P = .002 and .05, respectively).

There were no clear differences between the three active-treatment groups, “suggesting that any of them could be considered for further investigation,” said Dr. Páez.

Differences in baseline demographic characteristics did not appear to have an influence on the outcomes. ADAS-Cog was more than twice as effective as some candidate monoclonal antibodies targeting Abeta that are being investigated for Alzheimer’s disease, Dr. Páez noted.

Although the plasma exchange approach is relatively invasive, so too are monoclonal antibody therapies that are infused intravenously through a pump, he said. In addition, a low-volume plasma exchange maintenance treatment takes less than 2 hours, which is on a par with some monoclonal antibody treatments.
 

Key secondary outcomes

For both primary outcomes, changes were found in those with moderate but not mild Alzheimer’s disease, possibly because the ADAS-Cog was designed for patients with more severe symptoms and may not be sensitive enough for patients with better cognitive performance, said Dr. Páez.

However, the difference between mild and moderate Alzheimer’s disease did not hold up in post hoc analyses that included additional baseline characteristics, including amyloid and APOE e4 status.

“We observed that both mild and moderate subjects performed better than placebo even in the two coprimary endpoints,” Dr. Páez said. “It suggested that the differences between mild and moderate patients was not so apparent.”

The study’s key secondary outcomes included scores on the Clinical Dementia Rating Sum of Boxes (CDR-sb) and the Alzheimer’s Disease Cooperative Study–Clinical Global Impression of Change (ADCS-CGIC) scales. Treated patients scored better than the placebo group on both the CDR-sb (71% less decline, P = .002) and the ADCS-CGIC (100% less decline, P < .0001) scales.

For disease biomarkers in the moderate Alzheimer’s disease study population, levels of CSF Abeta42 and tau protein remained stable in the treated patients. In the placebo group, Abeta42 was decreased and tau protein increased. Dr. Páez explained that, if amyloid in the brain comes from the CSF, this process may take some time.

The findings suggest that more than one mechanism may be involved in the plasma exchange approach, such as changes in oxidation status and inflammatory mediators, the investigators noted.
 

Safety profile

About 28% of the participants dropped out of the study, which the researchers note is a rate similar to that reported in studies of solanezumab and other treatments in patients with Alzheimer’s disease. “The high percentage (72%) of patients who completed the study further supports that this procedure is feasible in mild to moderate Alzheimer’s disease,” the investigators wrote.

Overall, adverse events were similar to the known safety profile of plasma exchange procedures for other indications. The two most common adverse events were catheter local reactions and hypotension.

Almost 90% of the apheresis procedures were “uneventful,” the researchers reported. Two patients (0.6%) died during the study, which is similar to the low mortality rates reported elsewhere.

However, the investigators stressed that, because many patients with Alzheimer’s disease are in fragile health, plasma exchange treatments should be undertaken with caution, because of its invasive nature.

Dr. Páez noted that a possible limitation of this treatment approach is the availability of plasma for manufacturing plasma products. In the future, this plasma exchange approach might be combined with current and future Alzheimer’s disease therapies.

They are currently in discussions with the American Society for Apheresis, which develops guidelines for plasma exchange. After additional research, the investigators hope to eventually receive Food and Drug Administration approval of plasma exchange with albumin replacement as a treatment for Alzheimer’s disease.
 

Speculative, yet reasonable approach

Commenting on the research findings, Pierre N. Tariot, MD, director of Banner Alzheimer’s Institute and research professor of psychiatry at the University of Arizona, both in Phoenix, said the study is “meaningful and large enough” to “come close” to determining whether the therapy is safe and effective. “The fundamental rationale for this experimental approach, while speculative, is reasonable and certainly seems to be worth testing,” said Dr. Tariot, who was not involved with the research.

However, “there’s a decent chance” that not all trial participants had Alzheimer’s disease. Although some CSF amyloid measures suggest levels consistent with AD, “this is not conclusive,” he said.

In addition, “there’s a slightly low rate of apolipoprotein E4 allele carriage [in the current study], compared with most Alzheimer’s disease trials,” Dr. Tariot said.

He also pointed out that the trial failed to show statistical significance on both coprimary outcomes. “It’s unclear what health authorities, if presented with these data, would decide to do with the file.”

Although it was “encouraging” that secondary endpoints were supportive, the fact that they had greater statistical significance than some of the other objective measures “raises at least the potential for partial unblinding as a result of side effects,” said Dr. Tariot. It is also unclear why changes would be more evident in the moderate subpopulation.

The study was funded by Grifols. Dr. Páez is an employee of Grifols. Dr. Tariot reported no relevant financial relationships.

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

Plasma exchange with albumin replacement may be effective for slowing down symptoms of Alzheimer’s disease, new research suggests. Results from the phase 2b/3 AMBAR study showed that the treatment, which aims to remove amyloid-beta (Abeta) from plasma, was associated with a 60% decrease in functional and cognitive decline in patients with moderate Alzheimer’s disease.

The reduction in cognitive decline uncovered by the study is more striking than that reported for other investigational treatments targeting Abeta, such as monoclonal antibodies, said coinvestigator Antonio Páez, MD, medical director of the AMBAR program, Alzheimer’s Research Group, Grifols, Barcelona.

The results “open a new path for the development of plasma protein replacement therapies not only in Alzheimer’s disease but also in other degenerative diseases that we are planning to investigate,” Dr. Páez said.

The findings were presented at the virtual annual meeting of the Alzheimer’s Association International Conference and were simultaneously published in Alzheimer’s and Dementia.
 

Removing amyloid

Plasma exchange treatments, which have been available for several decades, are used to treat a range of neurologic, immunologic, and metabolic disorders. The treatment involves plasmapheresis, whereby plasma is separated from blood cells (red blood cells, white blood cells, platelets, etc) and toxic substances are removed. The albumin in plasma, to which plasma Abeta is bound, is replaced with a fresh commercial albumin product made from plasma from healthy donors.

“Our initial hypothesis was that, by removing albumin together with Abeta and substituting it with newer albumin periodically, we may be removing Abeta from the cerebrospinal fluid and eventually from the brain,” Dr. Páez said.

The AMBAR study included 347 men and women aged 55-85 years with probable Alzheimer’s disease dementia who were enrolled at 41 sites in Spain and the United States. All were diagnosed with mild Alzheimer’s disease, as shown by a baseline Mini-Mental State Examination score of 22-26, or moderate Alzheimer’s disease, having a baseline MMSE score of 18-21.

Investigators randomly assigned the participants to four groups; one group received placebo, and each of the other three treatment arms received different doses of albumin and intravenous immunoglobulin (IVIg) replacement.

During the first 6-week study phase, patients received weekly sham or conventional plasma exchange treatments of 2.5-3 liters of plasma, which Dr. Páez referred to as the “intensive-treatment phase to remove as much Abeta as possible.”

This was followed by a 12-month maintenance phase, which involved monthly low-volume (700-800 mL) plasma exchange or sham treatments.

Although the volume of plasma removed was the same in all three active-treatment groups, the amount of albumin and IVIg that was subsequently replaced varied. In one group, the same amount of albumin and IVIg that was removed was replaced; in another, half the amount removed was replaced; and in the third, only albumin was replaced.

The researchers collected cerebrospinal fluid (CSF) samples at baseline and after each treatment period. They assessed Abeta40, Abeta42, total tau, and phosphorylated-tau biomarkers.

The two primary outcomes were change from baseline to 14 months in scores on the Alzheimer’s Disease Cooperative Study–Activities of Daily Living (ADCS-ADL) scale and the Alzheimer’s Disease Assessment Scale–Cognitive Subscale (ADAS-Cog).
 

Symptom reduction

Results showed a reduction in the progression of symptoms in the plasma exchange–treated patients for both primary endpoints.

The ADCS-ADL showed 52% less decline in the plasma exchange–treated group, compared with the placebo group (P = .03); the ADAS-Cog showed 66% less decline (P = 0.06). In the moderate group, both endpoints showed 61% less decline (P = .002 and .05, respectively).

There were no clear differences between the three active-treatment groups, “suggesting that any of them could be considered for further investigation,” said Dr. Páez.

Differences in baseline demographic characteristics did not appear to have an influence on the outcomes. ADAS-Cog was more than twice as effective as some candidate monoclonal antibodies targeting Abeta that are being investigated for Alzheimer’s disease, Dr. Páez noted.

Although the plasma exchange approach is relatively invasive, so too are monoclonal antibody therapies that are infused intravenously through a pump, he said. In addition, a low-volume plasma exchange maintenance treatment takes less than 2 hours, which is on a par with some monoclonal antibody treatments.
 

Key secondary outcomes

For both primary outcomes, changes were found in those with moderate but not mild Alzheimer’s disease, possibly because the ADAS-Cog was designed for patients with more severe symptoms and may not be sensitive enough for patients with better cognitive performance, said Dr. Páez.

However, the difference between mild and moderate Alzheimer’s disease did not hold up in post hoc analyses that included additional baseline characteristics, including amyloid and APOE e4 status.

“We observed that both mild and moderate subjects performed better than placebo even in the two coprimary endpoints,” Dr. Páez said. “It suggested that the differences between mild and moderate patients was not so apparent.”

The study’s key secondary outcomes included scores on the Clinical Dementia Rating Sum of Boxes (CDR-sb) and the Alzheimer’s Disease Cooperative Study–Clinical Global Impression of Change (ADCS-CGIC) scales. Treated patients scored better than the placebo group on both the CDR-sb (71% less decline, P = .002) and the ADCS-CGIC (100% less decline, P < .0001) scales.

For disease biomarkers in the moderate Alzheimer’s disease study population, levels of CSF Abeta42 and tau protein remained stable in the treated patients. In the placebo group, Abeta42 was decreased and tau protein increased. Dr. Páez explained that, if amyloid in the brain comes from the CSF, this process may take some time.

The findings suggest that more than one mechanism may be involved in the plasma exchange approach, such as changes in oxidation status and inflammatory mediators, the investigators noted.
 

Safety profile

About 28% of the participants dropped out of the study, which the researchers note is a rate similar to that reported in studies of solanezumab and other treatments in patients with Alzheimer’s disease. “The high percentage (72%) of patients who completed the study further supports that this procedure is feasible in mild to moderate Alzheimer’s disease,” the investigators wrote.

Overall, adverse events were similar to the known safety profile of plasma exchange procedures for other indications. The two most common adverse events were catheter local reactions and hypotension.

Almost 90% of the apheresis procedures were “uneventful,” the researchers reported. Two patients (0.6%) died during the study, which is similar to the low mortality rates reported elsewhere.

However, the investigators stressed that, because many patients with Alzheimer’s disease are in fragile health, plasma exchange treatments should be undertaken with caution, because of its invasive nature.

Dr. Páez noted that a possible limitation of this treatment approach is the availability of plasma for manufacturing plasma products. In the future, this plasma exchange approach might be combined with current and future Alzheimer’s disease therapies.

They are currently in discussions with the American Society for Apheresis, which develops guidelines for plasma exchange. After additional research, the investigators hope to eventually receive Food and Drug Administration approval of plasma exchange with albumin replacement as a treatment for Alzheimer’s disease.
 

Speculative, yet reasonable approach

Commenting on the research findings, Pierre N. Tariot, MD, director of Banner Alzheimer’s Institute and research professor of psychiatry at the University of Arizona, both in Phoenix, said the study is “meaningful and large enough” to “come close” to determining whether the therapy is safe and effective. “The fundamental rationale for this experimental approach, while speculative, is reasonable and certainly seems to be worth testing,” said Dr. Tariot, who was not involved with the research.

However, “there’s a decent chance” that not all trial participants had Alzheimer’s disease. Although some CSF amyloid measures suggest levels consistent with AD, “this is not conclusive,” he said.

In addition, “there’s a slightly low rate of apolipoprotein E4 allele carriage [in the current study], compared with most Alzheimer’s disease trials,” Dr. Tariot said.

He also pointed out that the trial failed to show statistical significance on both coprimary outcomes. “It’s unclear what health authorities, if presented with these data, would decide to do with the file.”

Although it was “encouraging” that secondary endpoints were supportive, the fact that they had greater statistical significance than some of the other objective measures “raises at least the potential for partial unblinding as a result of side effects,” said Dr. Tariot. It is also unclear why changes would be more evident in the moderate subpopulation.

The study was funded by Grifols. Dr. Páez is an employee of Grifols. Dr. Tariot reported no relevant financial relationships.

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

Plasma exchange with albumin replacement may be effective for slowing down symptoms of Alzheimer’s disease, new research suggests. Results from the phase 2b/3 AMBAR study showed that the treatment, which aims to remove amyloid-beta (Abeta) from plasma, was associated with a 60% decrease in functional and cognitive decline in patients with moderate Alzheimer’s disease.

The reduction in cognitive decline uncovered by the study is more striking than that reported for other investigational treatments targeting Abeta, such as monoclonal antibodies, said coinvestigator Antonio Páez, MD, medical director of the AMBAR program, Alzheimer’s Research Group, Grifols, Barcelona.

The results “open a new path for the development of plasma protein replacement therapies not only in Alzheimer’s disease but also in other degenerative diseases that we are planning to investigate,” Dr. Páez said.

The findings were presented at the virtual annual meeting of the Alzheimer’s Association International Conference and were simultaneously published in Alzheimer’s and Dementia.
 

Removing amyloid

Plasma exchange treatments, which have been available for several decades, are used to treat a range of neurologic, immunologic, and metabolic disorders. The treatment involves plasmapheresis, whereby plasma is separated from blood cells (red blood cells, white blood cells, platelets, etc) and toxic substances are removed. The albumin in plasma, to which plasma Abeta is bound, is replaced with a fresh commercial albumin product made from plasma from healthy donors.

“Our initial hypothesis was that, by removing albumin together with Abeta and substituting it with newer albumin periodically, we may be removing Abeta from the cerebrospinal fluid and eventually from the brain,” Dr. Páez said.

The AMBAR study included 347 men and women aged 55-85 years with probable Alzheimer’s disease dementia who were enrolled at 41 sites in Spain and the United States. All were diagnosed with mild Alzheimer’s disease, as shown by a baseline Mini-Mental State Examination score of 22-26, or moderate Alzheimer’s disease, having a baseline MMSE score of 18-21.

Investigators randomly assigned the participants to four groups; one group received placebo, and each of the other three treatment arms received different doses of albumin and intravenous immunoglobulin (IVIg) replacement.

During the first 6-week study phase, patients received weekly sham or conventional plasma exchange treatments of 2.5-3 liters of plasma, which Dr. Páez referred to as the “intensive-treatment phase to remove as much Abeta as possible.”

This was followed by a 12-month maintenance phase, which involved monthly low-volume (700-800 mL) plasma exchange or sham treatments.

Although the volume of plasma removed was the same in all three active-treatment groups, the amount of albumin and IVIg that was subsequently replaced varied. In one group, the same amount of albumin and IVIg that was removed was replaced; in another, half the amount removed was replaced; and in the third, only albumin was replaced.

The researchers collected cerebrospinal fluid (CSF) samples at baseline and after each treatment period. They assessed Abeta40, Abeta42, total tau, and phosphorylated-tau biomarkers.

The two primary outcomes were change from baseline to 14 months in scores on the Alzheimer’s Disease Cooperative Study–Activities of Daily Living (ADCS-ADL) scale and the Alzheimer’s Disease Assessment Scale–Cognitive Subscale (ADAS-Cog).
 

Symptom reduction

Results showed a reduction in the progression of symptoms in the plasma exchange–treated patients for both primary endpoints.

The ADCS-ADL showed 52% less decline in the plasma exchange–treated group, compared with the placebo group (P = .03); the ADAS-Cog showed 66% less decline (P = 0.06). In the moderate group, both endpoints showed 61% less decline (P = .002 and .05, respectively).

There were no clear differences between the three active-treatment groups, “suggesting that any of them could be considered for further investigation,” said Dr. Páez.

Differences in baseline demographic characteristics did not appear to have an influence on the outcomes. ADAS-Cog was more than twice as effective as some candidate monoclonal antibodies targeting Abeta that are being investigated for Alzheimer’s disease, Dr. Páez noted.

Although the plasma exchange approach is relatively invasive, so too are monoclonal antibody therapies that are infused intravenously through a pump, he said. In addition, a low-volume plasma exchange maintenance treatment takes less than 2 hours, which is on a par with some monoclonal antibody treatments.
 

Key secondary outcomes

For both primary outcomes, changes were found in those with moderate but not mild Alzheimer’s disease, possibly because the ADAS-Cog was designed for patients with more severe symptoms and may not be sensitive enough for patients with better cognitive performance, said Dr. Páez.

However, the difference between mild and moderate Alzheimer’s disease did not hold up in post hoc analyses that included additional baseline characteristics, including amyloid and APOE e4 status.

“We observed that both mild and moderate subjects performed better than placebo even in the two coprimary endpoints,” Dr. Páez said. “It suggested that the differences between mild and moderate patients was not so apparent.”

The study’s key secondary outcomes included scores on the Clinical Dementia Rating Sum of Boxes (CDR-sb) and the Alzheimer’s Disease Cooperative Study–Clinical Global Impression of Change (ADCS-CGIC) scales. Treated patients scored better than the placebo group on both the CDR-sb (71% less decline, P = .002) and the ADCS-CGIC (100% less decline, P < .0001) scales.

For disease biomarkers in the moderate Alzheimer’s disease study population, levels of CSF Abeta42 and tau protein remained stable in the treated patients. In the placebo group, Abeta42 was decreased and tau protein increased. Dr. Páez explained that, if amyloid in the brain comes from the CSF, this process may take some time.

The findings suggest that more than one mechanism may be involved in the plasma exchange approach, such as changes in oxidation status and inflammatory mediators, the investigators noted.
 

Safety profile

About 28% of the participants dropped out of the study, which the researchers note is a rate similar to that reported in studies of solanezumab and other treatments in patients with Alzheimer’s disease. “The high percentage (72%) of patients who completed the study further supports that this procedure is feasible in mild to moderate Alzheimer’s disease,” the investigators wrote.

Overall, adverse events were similar to the known safety profile of plasma exchange procedures for other indications. The two most common adverse events were catheter local reactions and hypotension.

Almost 90% of the apheresis procedures were “uneventful,” the researchers reported. Two patients (0.6%) died during the study, which is similar to the low mortality rates reported elsewhere.

However, the investigators stressed that, because many patients with Alzheimer’s disease are in fragile health, plasma exchange treatments should be undertaken with caution, because of its invasive nature.

Dr. Páez noted that a possible limitation of this treatment approach is the availability of plasma for manufacturing plasma products. In the future, this plasma exchange approach might be combined with current and future Alzheimer’s disease therapies.

They are currently in discussions with the American Society for Apheresis, which develops guidelines for plasma exchange. After additional research, the investigators hope to eventually receive Food and Drug Administration approval of plasma exchange with albumin replacement as a treatment for Alzheimer’s disease.
 

Speculative, yet reasonable approach

Commenting on the research findings, Pierre N. Tariot, MD, director of Banner Alzheimer’s Institute and research professor of psychiatry at the University of Arizona, both in Phoenix, said the study is “meaningful and large enough” to “come close” to determining whether the therapy is safe and effective. “The fundamental rationale for this experimental approach, while speculative, is reasonable and certainly seems to be worth testing,” said Dr. Tariot, who was not involved with the research.

However, “there’s a decent chance” that not all trial participants had Alzheimer’s disease. Although some CSF amyloid measures suggest levels consistent with AD, “this is not conclusive,” he said.

In addition, “there’s a slightly low rate of apolipoprotein E4 allele carriage [in the current study], compared with most Alzheimer’s disease trials,” Dr. Tariot said.

He also pointed out that the trial failed to show statistical significance on both coprimary outcomes. “It’s unclear what health authorities, if presented with these data, would decide to do with the file.”

Although it was “encouraging” that secondary endpoints were supportive, the fact that they had greater statistical significance than some of the other objective measures “raises at least the potential for partial unblinding as a result of side effects,” said Dr. Tariot. It is also unclear why changes would be more evident in the moderate subpopulation.

The study was funded by Grifols. Dr. Páez is an employee of Grifols. Dr. Tariot reported no relevant financial relationships.

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

Clinical guidelines for cholesterol management may have two blind spots when it comes to heart attack prevention: Most younger adults with premature coronary artery disease who’ve had a myocardial infarction don’t meet guideline criteria for preventative statin therapy, and survivors under age 55 don’t meet the criteria for continuing nonstatin lipid-lowering treatments, a large single-center retrospective study has shown.

“The classic approach we’ve taken to identifying young adults for prevention is inadequate in younger adults,” corresponding author Ann Marie Navar, MD, PhD, of Duke University, Durham, N.C., said in an interview. “While awaiting more definitive research we should at minimum be using all the tools at our disposal, including broader use of coronary artery calcium [CAC] scoring, to identify young people who may benefit from statin therapy.”

The retrospective observational study analyzed records of 6,639 adults who had cardiac catheterization at Duke University Medical Center from 1995 to 2012 for a first myocardial infarction with obstructive coronary artery disease. The study considered those under age 55 years as “younger” patients, comprising 41% of the study group (2,733); 35% were “middle-aged” at 55-65 years (2,324) and 24% were “older,” at 66-75 years (1,582).

The report, published online Aug. 3 in the Journal of the American College of Cardiology, noted that most of the adults with premature CAD did not meet criteria for preventative statin therapy before their first MI based on ACC/American Heart Association clinical guidelines from 2013 and 2018. It also noted that younger MI survivors are also less frequently eligible for secondary prevention with intensive nonstatin lipid-lowering therapies than are older adults despite a much longer potential life span – and opportunity for another MI – for the former.

The researchers sought to evaluate the real-world implications of changes made in the 2018 guideline for adults who develop premature ischemic heart disease, and found that fewer younger patients qualify for preventative statin therapy under the 2018 guidelines.

“Younger individuals with very high-risk criteria are at higher risk of major adverse cardiovascular events, a finding supporting the appropriate implementation of intensive lipid-lowering therapies in these patients,” wrote lead author Michel Zeitouni, MD, MSc, and colleagues.
 

Key findings

The investigators reported that younger adults were significantly less likely to meet a class I recommendation for statins under the 2013 guideline (42.9%), compared with their middle-aged (70%) and older (82.5%) counterparts; and under the 2018 guideline, at 39.4%, 59.5%, and 77.4%, respectively (both P < .001).

Similarly, when both class I and class IIa recommendations were accounted for, younger patients were significantly less likely than were middle-aged and older patients to be eligible for statins before their index MI under both the 2013 (56.7%, 79.5%, and 85.2%, respectively and 2018 guidelines (46.4%, 73.5%, and 88.2%, respectively (both P < .01).

After their first MI, one in four younger patients (28.3%) met the very high-risk criteria compared with 40% of middle-aged and 81.4% of older patients (P trend < .001). In 8 years of follow-up, patients with very high-risk criteria based on the 2018 guideline had twice the rate of death, nonfatal MI, or stroke (hazard ratio [HR]: 2.15; 95% confidence interval, 1.98-2.33; P < .001).

The researchers acknowledged that the 2018 guideline took the important step of implementing risk enhancers – patient characteristics such as obesity and metabolic syndrome – along with the 10-year atherosclerotic cardiovascular disease (ASCVD) risk score to better identify high-risk young individuals who need statins. However, they also noted that the ability of the guidelines to identify young adults before their first MI “remains suboptimal.”

How to protect younger patients

“The 2018 guidelines will be most effective if we as providers do our best to identify risk enhancers and if we can use CAC scoring more broadly,” Dr. Navar said, noting that although CAC scoring has been shown to improve risk prediction, insurance coverage can be problematic.

“We also need to be careful to screen for the presence of the risk enhancers, such as inflammatory disease, family history, and women-specific risk factors, to make sure we aren’t missing an important high-risk group,” she added.

Other solutions to better identify at-risk younger adults include considering upgrades to the guidelines’ class IIb recommendation to class IIa to emphasize the importance of recognizing lower-risk younger adults, and recommending statins for patients at higher lifetime risk than age- and sex-matched peers, the researchers noted. “In our cohort, young individuals admitted for a first MI had a higher lifetime ASCVD risk score than did patients in the older age categories,” Dr. Zeitouni and colleagues wrote.

Dr. Navar said that these findings are a reminder that guidelines aren’t mandates. “Guidelines are meant to be a starting point for patients and physicians,” she said. “The absence of a recommendation doesn’t mean something isn’t recommended, but that there is not enough data to say one way or another.” 

The study “provides important evidence” that the 2018 guidelines exempted about half of the younger adults who had a first MI from preventative statin therapy, Ron Blankstein, MD, and Avinainder Singh, MD, MMSc, noted in an editorial (J Am Coll Cardiol. 2020;76:665-8).

Brigham and Women&#039;s Hospital

“Data from both the Duke and Young-MI registries should force us to reexamine how we allocate statin use among young individuals,” they noted. Dr. Blankstein is with Brigham and Women’s Hospital, Harvard Medical School, Boston. Dr. Singh is with Yale University, New Haven, Conn.

Dr. Zeitouni reported receiving lecture fees from Bristol-Myers Squibb/Pfizer. Dr. Navar reported financial relationships with Amarin, Janssen, Amgen, Sanofi and Regeneron Pharmaceuticals, AstraZeneca, Esperion, Novo Nordisk, Novartis, The Medicine Company, New Amsterdam, Cerner and Pfizer. Dr. Blankstein reported receiving research support from Amgen. Dr. Singh has no relevant financial relationships to report.

SOURCE: M. Zeitouni et al. J Am Coll Cardiol 2020 Aug 3;76:653-64.

Clinical guidelines for cholesterol management may have two blind spots when it comes to heart attack prevention: Most younger adults with premature coronary artery disease who’ve had a myocardial infarction don’t meet guideline criteria for preventative statin therapy, and survivors under age 55 don’t meet the criteria for continuing nonstatin lipid-lowering treatments, a large single-center retrospective study has shown.

“The classic approach we’ve taken to identifying young adults for prevention is inadequate in younger adults,” corresponding author Ann Marie Navar, MD, PhD, of Duke University, Durham, N.C., said in an interview. “While awaiting more definitive research we should at minimum be using all the tools at our disposal, including broader use of coronary artery calcium [CAC] scoring, to identify young people who may benefit from statin therapy.”

The retrospective observational study analyzed records of 6,639 adults who had cardiac catheterization at Duke University Medical Center from 1995 to 2012 for a first myocardial infarction with obstructive coronary artery disease. The study considered those under age 55 years as “younger” patients, comprising 41% of the study group (2,733); 35% were “middle-aged” at 55-65 years (2,324) and 24% were “older,” at 66-75 years (1,582).

The report, published online Aug. 3 in the Journal of the American College of Cardiology, noted that most of the adults with premature CAD did not meet criteria for preventative statin therapy before their first MI based on ACC/American Heart Association clinical guidelines from 2013 and 2018. It also noted that younger MI survivors are also less frequently eligible for secondary prevention with intensive nonstatin lipid-lowering therapies than are older adults despite a much longer potential life span – and opportunity for another MI – for the former.

The researchers sought to evaluate the real-world implications of changes made in the 2018 guideline for adults who develop premature ischemic heart disease, and found that fewer younger patients qualify for preventative statin therapy under the 2018 guidelines.

“Younger individuals with very high-risk criteria are at higher risk of major adverse cardiovascular events, a finding supporting the appropriate implementation of intensive lipid-lowering therapies in these patients,” wrote lead author Michel Zeitouni, MD, MSc, and colleagues.
 

Key findings

The investigators reported that younger adults were significantly less likely to meet a class I recommendation for statins under the 2013 guideline (42.9%), compared with their middle-aged (70%) and older (82.5%) counterparts; and under the 2018 guideline, at 39.4%, 59.5%, and 77.4%, respectively (both P < .001).

Similarly, when both class I and class IIa recommendations were accounted for, younger patients were significantly less likely than were middle-aged and older patients to be eligible for statins before their index MI under both the 2013 (56.7%, 79.5%, and 85.2%, respectively and 2018 guidelines (46.4%, 73.5%, and 88.2%, respectively (both P < .01).

After their first MI, one in four younger patients (28.3%) met the very high-risk criteria compared with 40% of middle-aged and 81.4% of older patients (P trend < .001). In 8 years of follow-up, patients with very high-risk criteria based on the 2018 guideline had twice the rate of death, nonfatal MI, or stroke (hazard ratio [HR]: 2.15; 95% confidence interval, 1.98-2.33; P < .001).

The researchers acknowledged that the 2018 guideline took the important step of implementing risk enhancers – patient characteristics such as obesity and metabolic syndrome – along with the 10-year atherosclerotic cardiovascular disease (ASCVD) risk score to better identify high-risk young individuals who need statins. However, they also noted that the ability of the guidelines to identify young adults before their first MI “remains suboptimal.”

How to protect younger patients

“The 2018 guidelines will be most effective if we as providers do our best to identify risk enhancers and if we can use CAC scoring more broadly,” Dr. Navar said, noting that although CAC scoring has been shown to improve risk prediction, insurance coverage can be problematic.

“We also need to be careful to screen for the presence of the risk enhancers, such as inflammatory disease, family history, and women-specific risk factors, to make sure we aren’t missing an important high-risk group,” she added.

Other solutions to better identify at-risk younger adults include considering upgrades to the guidelines’ class IIb recommendation to class IIa to emphasize the importance of recognizing lower-risk younger adults, and recommending statins for patients at higher lifetime risk than age- and sex-matched peers, the researchers noted. “In our cohort, young individuals admitted for a first MI had a higher lifetime ASCVD risk score than did patients in the older age categories,” Dr. Zeitouni and colleagues wrote.

Dr. Navar said that these findings are a reminder that guidelines aren’t mandates. “Guidelines are meant to be a starting point for patients and physicians,” she said. “The absence of a recommendation doesn’t mean something isn’t recommended, but that there is not enough data to say one way or another.” 

The study “provides important evidence” that the 2018 guidelines exempted about half of the younger adults who had a first MI from preventative statin therapy, Ron Blankstein, MD, and Avinainder Singh, MD, MMSc, noted in an editorial (J Am Coll Cardiol. 2020;76:665-8).

Brigham and Women&#039;s Hospital

“Data from both the Duke and Young-MI registries should force us to reexamine how we allocate statin use among young individuals,” they noted. Dr. Blankstein is with Brigham and Women’s Hospital, Harvard Medical School, Boston. Dr. Singh is with Yale University, New Haven, Conn.

Dr. Zeitouni reported receiving lecture fees from Bristol-Myers Squibb/Pfizer. Dr. Navar reported financial relationships with Amarin, Janssen, Amgen, Sanofi and Regeneron Pharmaceuticals, AstraZeneca, Esperion, Novo Nordisk, Novartis, The Medicine Company, New Amsterdam, Cerner and Pfizer. Dr. Blankstein reported receiving research support from Amgen. Dr. Singh has no relevant financial relationships to report.

SOURCE: M. Zeitouni et al. J Am Coll Cardiol 2020 Aug 3;76:653-64.

Clinical guidelines for cholesterol management may have two blind spots when it comes to heart attack prevention: Most younger adults with premature coronary artery disease who’ve had a myocardial infarction don’t meet guideline criteria for preventative statin therapy, and survivors under age 55 don’t meet the criteria for continuing nonstatin lipid-lowering treatments, a large single-center retrospective study has shown.

“The classic approach we’ve taken to identifying young adults for prevention is inadequate in younger adults,” corresponding author Ann Marie Navar, MD, PhD, of Duke University, Durham, N.C., said in an interview. “While awaiting more definitive research we should at minimum be using all the tools at our disposal, including broader use of coronary artery calcium [CAC] scoring, to identify young people who may benefit from statin therapy.”

The retrospective observational study analyzed records of 6,639 adults who had cardiac catheterization at Duke University Medical Center from 1995 to 2012 for a first myocardial infarction with obstructive coronary artery disease. The study considered those under age 55 years as “younger” patients, comprising 41% of the study group (2,733); 35% were “middle-aged” at 55-65 years (2,324) and 24% were “older,” at 66-75 years (1,582).

The report, published online Aug. 3 in the Journal of the American College of Cardiology, noted that most of the adults with premature CAD did not meet criteria for preventative statin therapy before their first MI based on ACC/American Heart Association clinical guidelines from 2013 and 2018. It also noted that younger MI survivors are also less frequently eligible for secondary prevention with intensive nonstatin lipid-lowering therapies than are older adults despite a much longer potential life span – and opportunity for another MI – for the former.

The researchers sought to evaluate the real-world implications of changes made in the 2018 guideline for adults who develop premature ischemic heart disease, and found that fewer younger patients qualify for preventative statin therapy under the 2018 guidelines.

“Younger individuals with very high-risk criteria are at higher risk of major adverse cardiovascular events, a finding supporting the appropriate implementation of intensive lipid-lowering therapies in these patients,” wrote lead author Michel Zeitouni, MD, MSc, and colleagues.
 

Key findings

The investigators reported that younger adults were significantly less likely to meet a class I recommendation for statins under the 2013 guideline (42.9%), compared with their middle-aged (70%) and older (82.5%) counterparts; and under the 2018 guideline, at 39.4%, 59.5%, and 77.4%, respectively (both P < .001).

Similarly, when both class I and class IIa recommendations were accounted for, younger patients were significantly less likely than were middle-aged and older patients to be eligible for statins before their index MI under both the 2013 (56.7%, 79.5%, and 85.2%, respectively and 2018 guidelines (46.4%, 73.5%, and 88.2%, respectively (both P < .01).

After their first MI, one in four younger patients (28.3%) met the very high-risk criteria compared with 40% of middle-aged and 81.4% of older patients (P trend < .001). In 8 years of follow-up, patients with very high-risk criteria based on the 2018 guideline had twice the rate of death, nonfatal MI, or stroke (hazard ratio [HR]: 2.15; 95% confidence interval, 1.98-2.33; P < .001).

The researchers acknowledged that the 2018 guideline took the important step of implementing risk enhancers – patient characteristics such as obesity and metabolic syndrome – along with the 10-year atherosclerotic cardiovascular disease (ASCVD) risk score to better identify high-risk young individuals who need statins. However, they also noted that the ability of the guidelines to identify young adults before their first MI “remains suboptimal.”

How to protect younger patients

“The 2018 guidelines will be most effective if we as providers do our best to identify risk enhancers and if we can use CAC scoring more broadly,” Dr. Navar said, noting that although CAC scoring has been shown to improve risk prediction, insurance coverage can be problematic.

“We also need to be careful to screen for the presence of the risk enhancers, such as inflammatory disease, family history, and women-specific risk factors, to make sure we aren’t missing an important high-risk group,” she added.

Other solutions to better identify at-risk younger adults include considering upgrades to the guidelines’ class IIb recommendation to class IIa to emphasize the importance of recognizing lower-risk younger adults, and recommending statins for patients at higher lifetime risk than age- and sex-matched peers, the researchers noted. “In our cohort, young individuals admitted for a first MI had a higher lifetime ASCVD risk score than did patients in the older age categories,” Dr. Zeitouni and colleagues wrote.

Dr. Navar said that these findings are a reminder that guidelines aren’t mandates. “Guidelines are meant to be a starting point for patients and physicians,” she said. “The absence of a recommendation doesn’t mean something isn’t recommended, but that there is not enough data to say one way or another.” 

The study “provides important evidence” that the 2018 guidelines exempted about half of the younger adults who had a first MI from preventative statin therapy, Ron Blankstein, MD, and Avinainder Singh, MD, MMSc, noted in an editorial (J Am Coll Cardiol. 2020;76:665-8).

Brigham and Women&#039;s Hospital

“Data from both the Duke and Young-MI registries should force us to reexamine how we allocate statin use among young individuals,” they noted. Dr. Blankstein is with Brigham and Women’s Hospital, Harvard Medical School, Boston. Dr. Singh is with Yale University, New Haven, Conn.

Dr. Zeitouni reported receiving lecture fees from Bristol-Myers Squibb/Pfizer. Dr. Navar reported financial relationships with Amarin, Janssen, Amgen, Sanofi and Regeneron Pharmaceuticals, AstraZeneca, Esperion, Novo Nordisk, Novartis, The Medicine Company, New Amsterdam, Cerner and Pfizer. Dr. Blankstein reported receiving research support from Amgen. Dr. Singh has no relevant financial relationships to report.

SOURCE: M. Zeitouni et al. J Am Coll Cardiol 2020 Aug 3;76:653-64.

A novel drug, tafasitamab-cxix (Monjuvi, MorphoSys US), has been approved by the Food and Drug Administration for the treatment of adult patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL).

The product is a humanized Fc-modified cytolytic CD19 targeting monoclonal antibody. It mediates B-cell lysis through apoptosis and immune effector mechanism, including antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP).

It is indicated for use in combination with lenalidomide for adult patients with relapsed/refractory DLBCL that is not otherwise specified, including DLBCL arising from low-grade lymphoma, and in patients who are not eligible for autologous stem cell transplant (ASCT).

Tafasitamab-cxix in combination with lenalidomide is the first treatment that approved by the FDA for second-line use for patients with relapsed or refractory DLBCL, notes the manufacturer.

The approval “brings a new treatment option to patients in dire need across the United States,” said Gilles Salles, MD, chair of the clinical hematology department at the University of Lyon (France), and lead investigator of the L-MIND study.

The FDA granted an accelerated approval on the basis of overall response rate from an open-label, single-arm, phase 2 trial in 81 patients (known as L-MIND). Further trials are underway to confirm clinical benefit.

The L-MIND trial was conducted in patients with relapsed or refractory DLBCL who had received at least one, but no more than three, prior lines of therapy, including an anti-CD20 targeting therapy (e.g., rituximab), who were not eligible for high-dose chemotherapy or who refused subsequent ASCT.

All patients received tafasitamab-cxix 12 mg/kg intravenously with lenalidomide (25 mg orally on days 1-21 of each 28-day cycle) for a maximum of 12 cycles, followed by tafasitamab-cxix as monotherapy.

The best ORR (defined as complete and partial responders) in 71 patients with a diagnosis of DLBCL confirmed by central pathology was 55%, with complete responses in 37% and partial responses in 18% of patients. The median response duration was 21.7 months (range, 0-24).

The most common adverse reactions (≥20%) were neutropenia, fatigue, anemia, diarrhea, thrombocytopenia, cough, fever, peripheral edema, respiratory tract infection, and decreased appetite.

Precautions and warnings include infusion-related reactions (6%), serious or severe myelosuppression (including neutropenia [50%], thrombocytopenia [18%], and anemia [7%]), infections (73%), and embryo-fetal toxicity.

DLBCL is the most common type of non-Hodgkin lymphoma in adults worldwide, characterized by rapidly growing masses of malignant B-cells in the lymph nodes, spleen, liver, bone marrow or other organs. It is an aggressive disease with about one in three patients not responding to initial therapy or relapsing thereafter, notes the manufacturer. In the United States each year approximately 10,000 patients who are not eligible for ASCT are diagnosed with relapsed or refractory DLBCL.

This article first appeared on Medscape.com.

A novel drug, tafasitamab-cxix (Monjuvi, MorphoSys US), has been approved by the Food and Drug Administration for the treatment of adult patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL).

The product is a humanized Fc-modified cytolytic CD19 targeting monoclonal antibody. It mediates B-cell lysis through apoptosis and immune effector mechanism, including antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP).

It is indicated for use in combination with lenalidomide for adult patients with relapsed/refractory DLBCL that is not otherwise specified, including DLBCL arising from low-grade lymphoma, and in patients who are not eligible for autologous stem cell transplant (ASCT).

Tafasitamab-cxix in combination with lenalidomide is the first treatment that approved by the FDA for second-line use for patients with relapsed or refractory DLBCL, notes the manufacturer.

The approval “brings a new treatment option to patients in dire need across the United States,” said Gilles Salles, MD, chair of the clinical hematology department at the University of Lyon (France), and lead investigator of the L-MIND study.

The FDA granted an accelerated approval on the basis of overall response rate from an open-label, single-arm, phase 2 trial in 81 patients (known as L-MIND). Further trials are underway to confirm clinical benefit.

The L-MIND trial was conducted in patients with relapsed or refractory DLBCL who had received at least one, but no more than three, prior lines of therapy, including an anti-CD20 targeting therapy (e.g., rituximab), who were not eligible for high-dose chemotherapy or who refused subsequent ASCT.

All patients received tafasitamab-cxix 12 mg/kg intravenously with lenalidomide (25 mg orally on days 1-21 of each 28-day cycle) for a maximum of 12 cycles, followed by tafasitamab-cxix as monotherapy.

The best ORR (defined as complete and partial responders) in 71 patients with a diagnosis of DLBCL confirmed by central pathology was 55%, with complete responses in 37% and partial responses in 18% of patients. The median response duration was 21.7 months (range, 0-24).

The most common adverse reactions (≥20%) were neutropenia, fatigue, anemia, diarrhea, thrombocytopenia, cough, fever, peripheral edema, respiratory tract infection, and decreased appetite.

Precautions and warnings include infusion-related reactions (6%), serious or severe myelosuppression (including neutropenia [50%], thrombocytopenia [18%], and anemia [7%]), infections (73%), and embryo-fetal toxicity.

DLBCL is the most common type of non-Hodgkin lymphoma in adults worldwide, characterized by rapidly growing masses of malignant B-cells in the lymph nodes, spleen, liver, bone marrow or other organs. It is an aggressive disease with about one in three patients not responding to initial therapy or relapsing thereafter, notes the manufacturer. In the United States each year approximately 10,000 patients who are not eligible for ASCT are diagnosed with relapsed or refractory DLBCL.

This article first appeared on Medscape.com.

A novel drug, tafasitamab-cxix (Monjuvi, MorphoSys US), has been approved by the Food and Drug Administration for the treatment of adult patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL).

The product is a humanized Fc-modified cytolytic CD19 targeting monoclonal antibody. It mediates B-cell lysis through apoptosis and immune effector mechanism, including antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP).

It is indicated for use in combination with lenalidomide for adult patients with relapsed/refractory DLBCL that is not otherwise specified, including DLBCL arising from low-grade lymphoma, and in patients who are not eligible for autologous stem cell transplant (ASCT).

Tafasitamab-cxix in combination with lenalidomide is the first treatment that approved by the FDA for second-line use for patients with relapsed or refractory DLBCL, notes the manufacturer.

The approval “brings a new treatment option to patients in dire need across the United States,” said Gilles Salles, MD, chair of the clinical hematology department at the University of Lyon (France), and lead investigator of the L-MIND study.

The FDA granted an accelerated approval on the basis of overall response rate from an open-label, single-arm, phase 2 trial in 81 patients (known as L-MIND). Further trials are underway to confirm clinical benefit.

The L-MIND trial was conducted in patients with relapsed or refractory DLBCL who had received at least one, but no more than three, prior lines of therapy, including an anti-CD20 targeting therapy (e.g., rituximab), who were not eligible for high-dose chemotherapy or who refused subsequent ASCT.

All patients received tafasitamab-cxix 12 mg/kg intravenously with lenalidomide (25 mg orally on days 1-21 of each 28-day cycle) for a maximum of 12 cycles, followed by tafasitamab-cxix as monotherapy.

The best ORR (defined as complete and partial responders) in 71 patients with a diagnosis of DLBCL confirmed by central pathology was 55%, with complete responses in 37% and partial responses in 18% of patients. The median response duration was 21.7 months (range, 0-24).

The most common adverse reactions (≥20%) were neutropenia, fatigue, anemia, diarrhea, thrombocytopenia, cough, fever, peripheral edema, respiratory tract infection, and decreased appetite.

Precautions and warnings include infusion-related reactions (6%), serious or severe myelosuppression (including neutropenia [50%], thrombocytopenia [18%], and anemia [7%]), infections (73%), and embryo-fetal toxicity.

DLBCL is the most common type of non-Hodgkin lymphoma in adults worldwide, characterized by rapidly growing masses of malignant B-cells in the lymph nodes, spleen, liver, bone marrow or other organs. It is an aggressive disease with about one in three patients not responding to initial therapy or relapsing thereafter, notes the manufacturer. In the United States each year approximately 10,000 patients who are not eligible for ASCT are diagnosed with relapsed or refractory DLBCL.

This article first appeared on Medscape.com.

Older adults are being “overscreened” for cancer, say researchers who discovered that many patients reported undergoing screening for cancer even though they were older than the upper age limit recommended.

The U.S. Preventive Services Task Force recommends an upper age limit on cancer screening that varies by cancer type – 75 years old for colorectal cancer, 74 for breast cancer, and 65 for cervical cancer.

The study found that 59.3% of men and 56.2% of women being screening for colorectal cancer were above that cut-off age, as were 45.8% of women being screened for cervical cancer and 74.1% of women being screened for breast cancer.    

Overscreening was particularly high for women living in metropolitan areas.

The finding is of concern, say the researchers, because “continuing to screen patients who are older and/or who have limited life expectancy may cause more harms than benefits.”

“The development of successful interventions to address this problem are thus essential,” they write.

The study was published online July 27 in JAMA Network Open.

Clinicians, patients, and health care systems can be changed – and should be changed – to minimize overscreening,” said lead author Jennifer L. Moss, PhD, assistant professor of family and community medicine and public health sciences at Penn State University, Hershey.

“It will probably take many changes to meaningfully decrease overscreening,” she told Medscape Medical News.

One change that would help is if health insurance companies stopped reimbursing providers for screening after the recommended upper age limit, she continued. “Another change is if providers had evidence-based tools to guide conversations about stopping screening, given an individual patient’s demographics, health status, and risks and benefits of the screening test.”

Approached for comment on the study, Nancy Schoenborn, MD, MHS, an associate professor of medicine in the Division of Geriatric Medicine and Gerontology at Johns Hopkins University, Baltimore, noted that the finding of high overscreening is not surprising and is consistent with prior works that found similar results.

“One value of this paper is that the timing of the study is more recent and confirms that the issue of overscreening is one that is still ongoing,” she told Medscape Medical News. Schoenborn was not associated with the study.

As for what physicians should do about the findings in this study, Schoenborn suggested the first step is to simply recognize that overscreening is likely a problem and “to reflect if there are instances in one’s own practice where overscreening may occur.”

In her own work, Schoenborn continued, “I was recently surprised that a substantial minority of clinicians actually do not believe overscreening to be a problem in older adults, and they have a number of concerns about how overscreening is defined and about unintended consequences that can occur from efforts to reduce overscreening.”

She added that there are a number of reasons why overscreening occurs. These include guideline inconsistencies, inertia, patient request, clinician knowledge gaps, and discomfort with discussing stopping. “A lot of work is ongoing to address each of these issues, but I think the first step would be the clinician recognizing and agreeing that this is a problem that needs to be addressed,” she said.

Unnecessary screening

The authors note that the prevalence estimates for overscreening have not been reported on a national level, and it is also unclear how overscreening may vary among subgroups.

“The reason I focused on colorectal, cervical, and breast cancers is because USPSTF has very clear, age-based recommendations for these cancers in terms of who should and should not get screened routinely,” explained Moss. “This was important because it allowed me and my coauthors to clearly say, based on age alone, this person probably was screened unnecessarily, and this person was not.”

She noted that the age-based recommendations for routine screening are based on very large clinical trials to examine the effectiveness of the screening tool. “The recommendations for lung and prostate cancer screening are not so clear cut, and we would not be able to tell, based only on the available survey data, if someone was overscreened,” she said.

For their study, the team used data from the 2018 Behavioral Risk Factor Surveillance System, administered by the Centers for Disease Control and Prevention.

Overscreening was assessed in a cohort of 20,937 men and 34,244 women for colorectal cancer, 82,811 women for cervical cancer, and 38,356 women for breast cancer. Most the participants lived in a metropolitan area (about 80%) and were white (about 80%).

Being overscreened was also more common in metropolitan vs. nonmetropolitan areas for colorectal cancer in women (adjusted odds ratio, 1.23), cervical cancer (aOR, 1.20), and breast cancer (aOR, 1.36).

Overscreening for cervical and breast cancers was also associated with having a usual source of care, good/very good/excellent self-reported health, education beyond a high school diploma, and being married or living as married.

The study was carried out in 2018, and the situation is likely to have changed over recent months during the COVID-19 pandemic.

“We have already seen dramatic reductions in routine cancer screening among age-eligible adults, so part of this problem of overscreening among older adults will likely diminish,” said Moss. “State and national cancer surveillance systems will continue to monitor trends in cancer screening, including overscreening, cancer incidence, and cancer mortality.”

Johns Hopkins’ Schoenborn said one finding of particular interest was that the colorectal cancer overscreening rate was higher in those older than 80 and in those with higher mortality risk.

“It makes me wonder if this is due to the increasing use of noninvasive colorectal cancer screening modalities, such as the fecal immunochemical test FIT or Cologuard,” Schoenborn commented. “It would be important for clinicians to consider downstream effects even when the initial test is low risk, such as if the stool test screens positive, would the patient still need a colonoscopy, and is that something the patient can undergo and wants to undergo?”

The study was funded by the National Cancer Institute and American Cancer Society. Moss, study coauthors, and Schoenborn have disclosed no relevant financial relationships.

This article first appeared on Medscape.com.

Older adults are being “overscreened” for cancer, say researchers who discovered that many patients reported undergoing screening for cancer even though they were older than the upper age limit recommended.

The U.S. Preventive Services Task Force recommends an upper age limit on cancer screening that varies by cancer type – 75 years old for colorectal cancer, 74 for breast cancer, and 65 for cervical cancer.

The study found that 59.3% of men and 56.2% of women being screening for colorectal cancer were above that cut-off age, as were 45.8% of women being screened for cervical cancer and 74.1% of women being screened for breast cancer.    

Overscreening was particularly high for women living in metropolitan areas.

The finding is of concern, say the researchers, because “continuing to screen patients who are older and/or who have limited life expectancy may cause more harms than benefits.”

“The development of successful interventions to address this problem are thus essential,” they write.

The study was published online July 27 in JAMA Network Open.

Clinicians, patients, and health care systems can be changed – and should be changed – to minimize overscreening,” said lead author Jennifer L. Moss, PhD, assistant professor of family and community medicine and public health sciences at Penn State University, Hershey.

“It will probably take many changes to meaningfully decrease overscreening,” she told Medscape Medical News.

One change that would help is if health insurance companies stopped reimbursing providers for screening after the recommended upper age limit, she continued. “Another change is if providers had evidence-based tools to guide conversations about stopping screening, given an individual patient’s demographics, health status, and risks and benefits of the screening test.”

Approached for comment on the study, Nancy Schoenborn, MD, MHS, an associate professor of medicine in the Division of Geriatric Medicine and Gerontology at Johns Hopkins University, Baltimore, noted that the finding of high overscreening is not surprising and is consistent with prior works that found similar results.

“One value of this paper is that the timing of the study is more recent and confirms that the issue of overscreening is one that is still ongoing,” she told Medscape Medical News. Schoenborn was not associated with the study.

As for what physicians should do about the findings in this study, Schoenborn suggested the first step is to simply recognize that overscreening is likely a problem and “to reflect if there are instances in one’s own practice where overscreening may occur.”

In her own work, Schoenborn continued, “I was recently surprised that a substantial minority of clinicians actually do not believe overscreening to be a problem in older adults, and they have a number of concerns about how overscreening is defined and about unintended consequences that can occur from efforts to reduce overscreening.”

She added that there are a number of reasons why overscreening occurs. These include guideline inconsistencies, inertia, patient request, clinician knowledge gaps, and discomfort with discussing stopping. “A lot of work is ongoing to address each of these issues, but I think the first step would be the clinician recognizing and agreeing that this is a problem that needs to be addressed,” she said.

Unnecessary screening

The authors note that the prevalence estimates for overscreening have not been reported on a national level, and it is also unclear how overscreening may vary among subgroups.

“The reason I focused on colorectal, cervical, and breast cancers is because USPSTF has very clear, age-based recommendations for these cancers in terms of who should and should not get screened routinely,” explained Moss. “This was important because it allowed me and my coauthors to clearly say, based on age alone, this person probably was screened unnecessarily, and this person was not.”

She noted that the age-based recommendations for routine screening are based on very large clinical trials to examine the effectiveness of the screening tool. “The recommendations for lung and prostate cancer screening are not so clear cut, and we would not be able to tell, based only on the available survey data, if someone was overscreened,” she said.

For their study, the team used data from the 2018 Behavioral Risk Factor Surveillance System, administered by the Centers for Disease Control and Prevention.

Overscreening was assessed in a cohort of 20,937 men and 34,244 women for colorectal cancer, 82,811 women for cervical cancer, and 38,356 women for breast cancer. Most the participants lived in a metropolitan area (about 80%) and were white (about 80%).

Being overscreened was also more common in metropolitan vs. nonmetropolitan areas for colorectal cancer in women (adjusted odds ratio, 1.23), cervical cancer (aOR, 1.20), and breast cancer (aOR, 1.36).

Overscreening for cervical and breast cancers was also associated with having a usual source of care, good/very good/excellent self-reported health, education beyond a high school diploma, and being married or living as married.

The study was carried out in 2018, and the situation is likely to have changed over recent months during the COVID-19 pandemic.

“We have already seen dramatic reductions in routine cancer screening among age-eligible adults, so part of this problem of overscreening among older adults will likely diminish,” said Moss. “State and national cancer surveillance systems will continue to monitor trends in cancer screening, including overscreening, cancer incidence, and cancer mortality.”

Johns Hopkins’ Schoenborn said one finding of particular interest was that the colorectal cancer overscreening rate was higher in those older than 80 and in those with higher mortality risk.

“It makes me wonder if this is due to the increasing use of noninvasive colorectal cancer screening modalities, such as the fecal immunochemical test FIT or Cologuard,” Schoenborn commented. “It would be important for clinicians to consider downstream effects even when the initial test is low risk, such as if the stool test screens positive, would the patient still need a colonoscopy, and is that something the patient can undergo and wants to undergo?”

The study was funded by the National Cancer Institute and American Cancer Society. Moss, study coauthors, and Schoenborn have disclosed no relevant financial relationships.

This article first appeared on Medscape.com.

Older adults are being “overscreened” for cancer, say researchers who discovered that many patients reported undergoing screening for cancer even though they were older than the upper age limit recommended.

The U.S. Preventive Services Task Force recommends an upper age limit on cancer screening that varies by cancer type – 75 years old for colorectal cancer, 74 for breast cancer, and 65 for cervical cancer.

The study found that 59.3% of men and 56.2% of women being screening for colorectal cancer were above that cut-off age, as were 45.8% of women being screened for cervical cancer and 74.1% of women being screened for breast cancer.    

Overscreening was particularly high for women living in metropolitan areas.

The finding is of concern, say the researchers, because “continuing to screen patients who are older and/or who have limited life expectancy may cause more harms than benefits.”

“The development of successful interventions to address this problem are thus essential,” they write.

The study was published online July 27 in JAMA Network Open.

Clinicians, patients, and health care systems can be changed – and should be changed – to minimize overscreening,” said lead author Jennifer L. Moss, PhD, assistant professor of family and community medicine and public health sciences at Penn State University, Hershey.

“It will probably take many changes to meaningfully decrease overscreening,” she told Medscape Medical News.

One change that would help is if health insurance companies stopped reimbursing providers for screening after the recommended upper age limit, she continued. “Another change is if providers had evidence-based tools to guide conversations about stopping screening, given an individual patient’s demographics, health status, and risks and benefits of the screening test.”

Approached for comment on the study, Nancy Schoenborn, MD, MHS, an associate professor of medicine in the Division of Geriatric Medicine and Gerontology at Johns Hopkins University, Baltimore, noted that the finding of high overscreening is not surprising and is consistent with prior works that found similar results.

“One value of this paper is that the timing of the study is more recent and confirms that the issue of overscreening is one that is still ongoing,” she told Medscape Medical News. Schoenborn was not associated with the study.

As for what physicians should do about the findings in this study, Schoenborn suggested the first step is to simply recognize that overscreening is likely a problem and “to reflect if there are instances in one’s own practice where overscreening may occur.”

In her own work, Schoenborn continued, “I was recently surprised that a substantial minority of clinicians actually do not believe overscreening to be a problem in older adults, and they have a number of concerns about how overscreening is defined and about unintended consequences that can occur from efforts to reduce overscreening.”

She added that there are a number of reasons why overscreening occurs. These include guideline inconsistencies, inertia, patient request, clinician knowledge gaps, and discomfort with discussing stopping. “A lot of work is ongoing to address each of these issues, but I think the first step would be the clinician recognizing and agreeing that this is a problem that needs to be addressed,” she said.

Unnecessary screening

The authors note that the prevalence estimates for overscreening have not been reported on a national level, and it is also unclear how overscreening may vary among subgroups.

“The reason I focused on colorectal, cervical, and breast cancers is because USPSTF has very clear, age-based recommendations for these cancers in terms of who should and should not get screened routinely,” explained Moss. “This was important because it allowed me and my coauthors to clearly say, based on age alone, this person probably was screened unnecessarily, and this person was not.”

She noted that the age-based recommendations for routine screening are based on very large clinical trials to examine the effectiveness of the screening tool. “The recommendations for lung and prostate cancer screening are not so clear cut, and we would not be able to tell, based only on the available survey data, if someone was overscreened,” she said.

For their study, the team used data from the 2018 Behavioral Risk Factor Surveillance System, administered by the Centers for Disease Control and Prevention.

Overscreening was assessed in a cohort of 20,937 men and 34,244 women for colorectal cancer, 82,811 women for cervical cancer, and 38,356 women for breast cancer. Most the participants lived in a metropolitan area (about 80%) and were white (about 80%).

Being overscreened was also more common in metropolitan vs. nonmetropolitan areas for colorectal cancer in women (adjusted odds ratio, 1.23), cervical cancer (aOR, 1.20), and breast cancer (aOR, 1.36).

Overscreening for cervical and breast cancers was also associated with having a usual source of care, good/very good/excellent self-reported health, education beyond a high school diploma, and being married or living as married.

The study was carried out in 2018, and the situation is likely to have changed over recent months during the COVID-19 pandemic.

“We have already seen dramatic reductions in routine cancer screening among age-eligible adults, so part of this problem of overscreening among older adults will likely diminish,” said Moss. “State and national cancer surveillance systems will continue to monitor trends in cancer screening, including overscreening, cancer incidence, and cancer mortality.”

Johns Hopkins’ Schoenborn said one finding of particular interest was that the colorectal cancer overscreening rate was higher in those older than 80 and in those with higher mortality risk.

“It makes me wonder if this is due to the increasing use of noninvasive colorectal cancer screening modalities, such as the fecal immunochemical test FIT or Cologuard,” Schoenborn commented. “It would be important for clinicians to consider downstream effects even when the initial test is low risk, such as if the stool test screens positive, would the patient still need a colonoscopy, and is that something the patient can undergo and wants to undergo?”

The study was funded by the National Cancer Institute and American Cancer Society. Moss, study coauthors, and Schoenborn have disclosed no relevant financial relationships.

This article first appeared on Medscape.com.

Editor’s note: The Hospitalist is excited to debut a quarterly Pediatric Hospital Medicine Fellows column with this article by pediatric hospitalist Dr. Adam Cohen.

In June 2019, I was offered the new role of chief fellow of pediatric hospital medicine at Baylor College of Medicine and Texas Children’s Hospital, both in Houston. After messaging colleagues and friends at PHM fellowships across the country, I discovered that I wasn’t only Baylor’s first chief fellow of PHM, but I was the only chief fellow of PHM in the nation.

At first, this seemed to be a daunting prospect that left me wondering what my experiences would be like. However, as any good academician knows, the only way to properly answer a question with such existential considerations is a literature review.

While the role of chief fellow exists in other pediatric subspecialty fellowships, the literature on this role is not yet developed. I focused my literature review on using the chief resident role as a surrogate. The chief resident position is filled with opportunities to work administratively and educationally and even has the potential to drive interinstitutional educational change.¹ However, many chief residents feel their administrative roles outweigh their educational ones.^2,3 This worried me, as the administrative side of program leadership was something that I had little experience in. Would I be weighed down with answering emails and fielding grievances from other fellows? While I did occasionally have that responsibility, my experiences as a chief fellow meant being intimately involved in one program’s response and growth during a national change to PHM as a field, while also coaching those from other programs on how to respond to these many changes.

The dawn of this new era of PHM saw the first board-certified hospitalists crowned and the first fellowships accredited by the Accreditation Council for Graduate Medical Education within the past academic year. I experienced this in a unique position as a chief fellow – an insider as part of the administration and an outsider as a prospective specialist. Prior to the recent accreditation and certification, PHM fellowship graduates were becoming successful academic physicians. A 2014 study of over 80% of all graduated PHM fellows showed nearly all had academic positions in which they taught students and residents. Many of these graduates also participated in research, with two-thirds being the first author on at least one peer-reviewed article.⁴

However, we also know that, prior to accreditation, fellowship training was varied, with clinical time ranging from 20% to 65%, in addition to wide variability in billing practices, scholarly practices, and the ability to pursue advanced nonclinical training, such as coursework or master’s degrees in quality improvement or education.⁵ With PHM fellowships becoming accredited and hospitalists becoming board certified, this is going to change, hopefully for the better.

National accrediting bodies like the ACGME create standards for programs to follow, but as a field we have to make sure we know what those standards mean for our future fellows and our educators. At my own program, these standards meant a significant reduction in clinical time, which was the main way fellows obtained content mastery in PHM. There were also concerns from practicing hospitalists about what it would mean if they did not or could not “grandfather in” to board certification. Would they be pushed out of their jobs or forced into less desirable ones? Would they be able to continue teaching and working with fellows?

As I reflect on experiencing this tumultuous time of change for our specialty, my main takeaway is that board certification of PHM faculty and accreditation of fellowships is an important step to creating the next generation of productive academic hospitalists. The greatest benefit for PHM fellows is that ACGME accreditation mandates that they be treated as learners, and not just junior attendings who are paid less. Many programs rely on fellow billing to fund fellowships, which can create a culture where the focus falls away from exploring a wide variety of educational opportunities and toward an exclusive or near-exclusive service-learning model.

This old model can come at the expense of opportunities such as conferences or secondary degrees. Under ACGME accreditation, fellowships will also be required to provide a regimented system of mentorship and support, more than just nonclinical time, to allow fellows to follow their interests and passions, whether that be in clinical hospital medicine, education, quality, advocacy or more. When these fellows graduate and become board certified, they will truly have recognition as specialists in the field, and be able to advance the field in any setting they choose to practice.

Like any change, this shift in our field also comes with our fair share of risks. Fellowship programs have to be careful about what they take away from an accreditation process that can be incredibly time-consuming and difficult. Leadership at these programs need to look critically at the changes they are required to make, and ensure they are integrated intelligently in a way that benefits the fellows.

At Baylor, while a decrease in clinical time was required, our leadership saw it as an opportunity to implement active learning and assessment techniques to improve clinical mastery with less clinical time. While many programs may need to make significant changes to align with ACGME standards, a key lesson in education is that these changes also need to reflect the goal of the program, to create expert academicians, clinicians, and leaders in PHM.

One of the largest challenges brought about by these changes is how we take into account pediatric hospitalists with clinical expertise who either are not academically oriented or are not eligible for board certification. Excluding them from participating in fellowship training or as productive members of our groups can create a hidden curriculum that board certification and academic practice are the only way forward in our field. We also risk excluding those with the ability to fill the largest need in our specialty, those who practice clinically in the community.⁶

We must ensure that our desire to have productive academic faculty does not result in the loss of those with clinical expertise, both for the care of our patients and the education of our learners. Whether that solution lies with alternative certification procedures or through thoughtful hiring and educational policies is yet to be seen.

Overall, as PHM’s chief fellow this past academic year, I found that we have a lot to be excited for as our field continues to grow. With this growth, we need be careful about how we move forward with the standardization of our training, education, and faculty practices to align with our core values of excellent care for children and advancement of our field to meet their needs and the needs of our medical system. I am grateful to the many PHM leaders and providers who have thoughtfully stimulated so much growth in the field and paved the way for current and future generations of fellows to benefit from that growth.

Dr. Cohen is an assistant professor of pediatrics in the section of hospital medicine at Baylor College of Medicine and Texas Children’s Hospital. He graduated from PHM fellowship in June 2020 at Baylor, dedicating himself to developing expertise in medical education. He would like to thank Dr. Michelle Lopez for her assistance in revising this article.

References

1. Myers RE et al. Pediatric chief resident exchange program: A novel method to share educational ideas across training programs. Acad Pediatr. 2019. doi: S1876-2859(19)30386-9.

2. Norris T et al. Do program directors and their chief residents view the role of chief resident similarly? Family Medicine. 1996;28(5):343-5.

3. Dabrow SM et al. Two perspectives on the educational and administrative roles of the pediatric chief resident. J Grad Med Educ. 2011;3(1):17-20.

4. Oshimura JM et al. Current roles and perceived needs of pediatric hospital medicine fellowship graduates. Hosp Pediatr. 2016;6(10):633-7.

5. Shah NH et al. The current state of pediatric hospital medicine fellowships: A survey of program directors. J Hosp Med. 2016;11(5):324-8.

6. Leyenaar JK et al. Epidemiology of pediatric hospitalizations at general hospitals and freestanding children’s hospitals in the United States. J Hosp Med. 2016;11(11):743-9.

Editor’s note: The Hospitalist is excited to debut a quarterly Pediatric Hospital Medicine Fellows column with this article by pediatric hospitalist Dr. Adam Cohen.

In June 2019, I was offered the new role of chief fellow of pediatric hospital medicine at Baylor College of Medicine and Texas Children’s Hospital, both in Houston. After messaging colleagues and friends at PHM fellowships across the country, I discovered that I wasn’t only Baylor’s first chief fellow of PHM, but I was the only chief fellow of PHM in the nation.

At first, this seemed to be a daunting prospect that left me wondering what my experiences would be like. However, as any good academician knows, the only way to properly answer a question with such existential considerations is a literature review.

While the role of chief fellow exists in other pediatric subspecialty fellowships, the literature on this role is not yet developed. I focused my literature review on using the chief resident role as a surrogate. The chief resident position is filled with opportunities to work administratively and educationally and even has the potential to drive interinstitutional educational change.¹ However, many chief residents feel their administrative roles outweigh their educational ones.^2,3 This worried me, as the administrative side of program leadership was something that I had little experience in. Would I be weighed down with answering emails and fielding grievances from other fellows? While I did occasionally have that responsibility, my experiences as a chief fellow meant being intimately involved in one program’s response and growth during a national change to PHM as a field, while also coaching those from other programs on how to respond to these many changes.

The dawn of this new era of PHM saw the first board-certified hospitalists crowned and the first fellowships accredited by the Accreditation Council for Graduate Medical Education within the past academic year. I experienced this in a unique position as a chief fellow – an insider as part of the administration and an outsider as a prospective specialist. Prior to the recent accreditation and certification, PHM fellowship graduates were becoming successful academic physicians. A 2014 study of over 80% of all graduated PHM fellows showed nearly all had academic positions in which they taught students and residents. Many of these graduates also participated in research, with two-thirds being the first author on at least one peer-reviewed article.⁴

However, we also know that, prior to accreditation, fellowship training was varied, with clinical time ranging from 20% to 65%, in addition to wide variability in billing practices, scholarly practices, and the ability to pursue advanced nonclinical training, such as coursework or master’s degrees in quality improvement or education.⁵ With PHM fellowships becoming accredited and hospitalists becoming board certified, this is going to change, hopefully for the better.

National accrediting bodies like the ACGME create standards for programs to follow, but as a field we have to make sure we know what those standards mean for our future fellows and our educators. At my own program, these standards meant a significant reduction in clinical time, which was the main way fellows obtained content mastery in PHM. There were also concerns from practicing hospitalists about what it would mean if they did not or could not “grandfather in” to board certification. Would they be pushed out of their jobs or forced into less desirable ones? Would they be able to continue teaching and working with fellows?

As I reflect on experiencing this tumultuous time of change for our specialty, my main takeaway is that board certification of PHM faculty and accreditation of fellowships is an important step to creating the next generation of productive academic hospitalists. The greatest benefit for PHM fellows is that ACGME accreditation mandates that they be treated as learners, and not just junior attendings who are paid less. Many programs rely on fellow billing to fund fellowships, which can create a culture where the focus falls away from exploring a wide variety of educational opportunities and toward an exclusive or near-exclusive service-learning model.

This old model can come at the expense of opportunities such as conferences or secondary degrees. Under ACGME accreditation, fellowships will also be required to provide a regimented system of mentorship and support, more than just nonclinical time, to allow fellows to follow their interests and passions, whether that be in clinical hospital medicine, education, quality, advocacy or more. When these fellows graduate and become board certified, they will truly have recognition as specialists in the field, and be able to advance the field in any setting they choose to practice.

Like any change, this shift in our field also comes with our fair share of risks. Fellowship programs have to be careful about what they take away from an accreditation process that can be incredibly time-consuming and difficult. Leadership at these programs need to look critically at the changes they are required to make, and ensure they are integrated intelligently in a way that benefits the fellows.

At Baylor, while a decrease in clinical time was required, our leadership saw it as an opportunity to implement active learning and assessment techniques to improve clinical mastery with less clinical time. While many programs may need to make significant changes to align with ACGME standards, a key lesson in education is that these changes also need to reflect the goal of the program, to create expert academicians, clinicians, and leaders in PHM.

One of the largest challenges brought about by these changes is how we take into account pediatric hospitalists with clinical expertise who either are not academically oriented or are not eligible for board certification. Excluding them from participating in fellowship training or as productive members of our groups can create a hidden curriculum that board certification and academic practice are the only way forward in our field. We also risk excluding those with the ability to fill the largest need in our specialty, those who practice clinically in the community.⁶

We must ensure that our desire to have productive academic faculty does not result in the loss of those with clinical expertise, both for the care of our patients and the education of our learners. Whether that solution lies with alternative certification procedures or through thoughtful hiring and educational policies is yet to be seen.

Overall, as PHM’s chief fellow this past academic year, I found that we have a lot to be excited for as our field continues to grow. With this growth, we need be careful about how we move forward with the standardization of our training, education, and faculty practices to align with our core values of excellent care for children and advancement of our field to meet their needs and the needs of our medical system. I am grateful to the many PHM leaders and providers who have thoughtfully stimulated so much growth in the field and paved the way for current and future generations of fellows to benefit from that growth.

Dr. Cohen is an assistant professor of pediatrics in the section of hospital medicine at Baylor College of Medicine and Texas Children’s Hospital. He graduated from PHM fellowship in June 2020 at Baylor, dedicating himself to developing expertise in medical education. He would like to thank Dr. Michelle Lopez for her assistance in revising this article.

References

1. Myers RE et al. Pediatric chief resident exchange program: A novel method to share educational ideas across training programs. Acad Pediatr. 2019. doi: S1876-2859(19)30386-9.

2. Norris T et al. Do program directors and their chief residents view the role of chief resident similarly? Family Medicine. 1996;28(5):343-5.

3. Dabrow SM et al. Two perspectives on the educational and administrative roles of the pediatric chief resident. J Grad Med Educ. 2011;3(1):17-20.

4. Oshimura JM et al. Current roles and perceived needs of pediatric hospital medicine fellowship graduates. Hosp Pediatr. 2016;6(10):633-7.

5. Shah NH et al. The current state of pediatric hospital medicine fellowships: A survey of program directors. J Hosp Med. 2016;11(5):324-8.

6. Leyenaar JK et al. Epidemiology of pediatric hospitalizations at general hospitals and freestanding children’s hospitals in the United States. J Hosp Med. 2016;11(11):743-9.

Editor’s note: The Hospitalist is excited to debut a quarterly Pediatric Hospital Medicine Fellows column with this article by pediatric hospitalist Dr. Adam Cohen.

In June 2019, I was offered the new role of chief fellow of pediatric hospital medicine at Baylor College of Medicine and Texas Children’s Hospital, both in Houston. After messaging colleagues and friends at PHM fellowships across the country, I discovered that I wasn’t only Baylor’s first chief fellow of PHM, but I was the only chief fellow of PHM in the nation.

At first, this seemed to be a daunting prospect that left me wondering what my experiences would be like. However, as any good academician knows, the only way to properly answer a question with such existential considerations is a literature review.

While the role of chief fellow exists in other pediatric subspecialty fellowships, the literature on this role is not yet developed. I focused my literature review on using the chief resident role as a surrogate. The chief resident position is filled with opportunities to work administratively and educationally and even has the potential to drive interinstitutional educational change.¹ However, many chief residents feel their administrative roles outweigh their educational ones.^2,3 This worried me, as the administrative side of program leadership was something that I had little experience in. Would I be weighed down with answering emails and fielding grievances from other fellows? While I did occasionally have that responsibility, my experiences as a chief fellow meant being intimately involved in one program’s response and growth during a national change to PHM as a field, while also coaching those from other programs on how to respond to these many changes.

The dawn of this new era of PHM saw the first board-certified hospitalists crowned and the first fellowships accredited by the Accreditation Council for Graduate Medical Education within the past academic year. I experienced this in a unique position as a chief fellow – an insider as part of the administration and an outsider as a prospective specialist. Prior to the recent accreditation and certification, PHM fellowship graduates were becoming successful academic physicians. A 2014 study of over 80% of all graduated PHM fellows showed nearly all had academic positions in which they taught students and residents. Many of these graduates also participated in research, with two-thirds being the first author on at least one peer-reviewed article.⁴

However, we also know that, prior to accreditation, fellowship training was varied, with clinical time ranging from 20% to 65%, in addition to wide variability in billing practices, scholarly practices, and the ability to pursue advanced nonclinical training, such as coursework or master’s degrees in quality improvement or education.⁵ With PHM fellowships becoming accredited and hospitalists becoming board certified, this is going to change, hopefully for the better.

National accrediting bodies like the ACGME create standards for programs to follow, but as a field we have to make sure we know what those standards mean for our future fellows and our educators. At my own program, these standards meant a significant reduction in clinical time, which was the main way fellows obtained content mastery in PHM. There were also concerns from practicing hospitalists about what it would mean if they did not or could not “grandfather in” to board certification. Would they be pushed out of their jobs or forced into less desirable ones? Would they be able to continue teaching and working with fellows?

As I reflect on experiencing this tumultuous time of change for our specialty, my main takeaway is that board certification of PHM faculty and accreditation of fellowships is an important step to creating the next generation of productive academic hospitalists. The greatest benefit for PHM fellows is that ACGME accreditation mandates that they be treated as learners, and not just junior attendings who are paid less. Many programs rely on fellow billing to fund fellowships, which can create a culture where the focus falls away from exploring a wide variety of educational opportunities and toward an exclusive or near-exclusive service-learning model.

This old model can come at the expense of opportunities such as conferences or secondary degrees. Under ACGME accreditation, fellowships will also be required to provide a regimented system of mentorship and support, more than just nonclinical time, to allow fellows to follow their interests and passions, whether that be in clinical hospital medicine, education, quality, advocacy or more. When these fellows graduate and become board certified, they will truly have recognition as specialists in the field, and be able to advance the field in any setting they choose to practice.

Like any change, this shift in our field also comes with our fair share of risks. Fellowship programs have to be careful about what they take away from an accreditation process that can be incredibly time-consuming and difficult. Leadership at these programs need to look critically at the changes they are required to make, and ensure they are integrated intelligently in a way that benefits the fellows.

At Baylor, while a decrease in clinical time was required, our leadership saw it as an opportunity to implement active learning and assessment techniques to improve clinical mastery with less clinical time. While many programs may need to make significant changes to align with ACGME standards, a key lesson in education is that these changes also need to reflect the goal of the program, to create expert academicians, clinicians, and leaders in PHM.

One of the largest challenges brought about by these changes is how we take into account pediatric hospitalists with clinical expertise who either are not academically oriented or are not eligible for board certification. Excluding them from participating in fellowship training or as productive members of our groups can create a hidden curriculum that board certification and academic practice are the only way forward in our field. We also risk excluding those with the ability to fill the largest need in our specialty, those who practice clinically in the community.⁶

We must ensure that our desire to have productive academic faculty does not result in the loss of those with clinical expertise, both for the care of our patients and the education of our learners. Whether that solution lies with alternative certification procedures or through thoughtful hiring and educational policies is yet to be seen.

Overall, as PHM’s chief fellow this past academic year, I found that we have a lot to be excited for as our field continues to grow. With this growth, we need be careful about how we move forward with the standardization of our training, education, and faculty practices to align with our core values of excellent care for children and advancement of our field to meet their needs and the needs of our medical system. I am grateful to the many PHM leaders and providers who have thoughtfully stimulated so much growth in the field and paved the way for current and future generations of fellows to benefit from that growth.

Dr. Cohen is an assistant professor of pediatrics in the section of hospital medicine at Baylor College of Medicine and Texas Children’s Hospital. He graduated from PHM fellowship in June 2020 at Baylor, dedicating himself to developing expertise in medical education. He would like to thank Dr. Michelle Lopez for her assistance in revising this article.

References

1. Myers RE et al. Pediatric chief resident exchange program: A novel method to share educational ideas across training programs. Acad Pediatr. 2019. doi: S1876-2859(19)30386-9.

2. Norris T et al. Do program directors and their chief residents view the role of chief resident similarly? Family Medicine. 1996;28(5):343-5.

3. Dabrow SM et al. Two perspectives on the educational and administrative roles of the pediatric chief resident. J Grad Med Educ. 2011;3(1):17-20.

4. Oshimura JM et al. Current roles and perceived needs of pediatric hospital medicine fellowship graduates. Hosp Pediatr. 2016;6(10):633-7.

5. Shah NH et al. The current state of pediatric hospital medicine fellowships: A survey of program directors. J Hosp Med. 2016;11(5):324-8.

6. Leyenaar JK et al. Epidemiology of pediatric hospitalizations at general hospitals and freestanding children’s hospitals in the United States. J Hosp Med. 2016;11(11):743-9.