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The easy way to talk about penises
This transcript has been edited for clarity.
I mean it. Penis problems are very common and are an early sign that patients could have a cardiac event. Think about it: Clogging the arteries of the heart is called a heart attack; clogging the arteries to the penis is a penis attack, or as doctors like to call it, erectile dysfunction.
The arteries to the penis are only 1 mm in diameter. They develop plaque and clog the circulation long before the 3-mm cardiac arteries. So, it’s very important for primary care doctors to talk to their patients about erection health. And I’ll be honest: It’s easier to talk to patients about how lifestyle is affecting their penis health than it is to discuss how lifestyle affects longevity or prevents cancer. I get a lot of men to quit smoking because I tell them what it’s doing to their penises.
It can be challenging for doctors and patients to talk about penises. It doesn’t come naturally for many of us. If a 20-year-old comes in to my office with his 85-year-old grandfather and they both say their penises aren’t working, how do you figure out what’s going on? Do they even have the same thing wrong with them?
Here’s a fun and helpful tool that I use in my office. It’s called the Erection Hardness Score. It was developed around the time that Viagra came out, in 1998. It’s been game-changing for me to get patients more comfortable talking about their erection issues.
I tell them it’s a 4-number scale. A “1” is no erection at all. A “2” is when it gets harder and larger, but it’s not going to penetrate. A “3” will penetrate, but it’s pretty wobbly. A “4” is that perfect cucumber–porn star erection that everyone is seeking. I have the patient tell me a story. They may say, “When I wake up in the morning, I’m at a 2. When I stimulate myself, I can get up to a 3. When I’m with my partner, sometimes I can get up to a 4.”
This is really helpful because they can talk in numbers. And after I give them treatments such as lifestyle changes, sex therapy, testosterone, a PDE5 inhibitor such as Viagra or Cialis, or an injection, they can come back and tell me how the story has changed. I have an objective measure that shows me how the treatment is affecting their erections. Not only do I feel more confident having those objective measures, but my patients feel more confident in the care that they’re getting, and they feel more comfortable talking to me about the changes. So, I encourage all of you to bring that EHS tool into your office. Show it to patients and get them more comfortable talking about erections.
Dr. Rubin is assistant clinical professor, department of urology, Georgetown University, Washington. She disclosed financial relationships with Absorption Pharmaceuticals, GlaxoSmithKline, and Endo Pharmaceuticals; has served as a speaker for Sprout; and has received research grant from Maternal Medical.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
I mean it. Penis problems are very common and are an early sign that patients could have a cardiac event. Think about it: Clogging the arteries of the heart is called a heart attack; clogging the arteries to the penis is a penis attack, or as doctors like to call it, erectile dysfunction.
The arteries to the penis are only 1 mm in diameter. They develop plaque and clog the circulation long before the 3-mm cardiac arteries. So, it’s very important for primary care doctors to talk to their patients about erection health. And I’ll be honest: It’s easier to talk to patients about how lifestyle is affecting their penis health than it is to discuss how lifestyle affects longevity or prevents cancer. I get a lot of men to quit smoking because I tell them what it’s doing to their penises.
It can be challenging for doctors and patients to talk about penises. It doesn’t come naturally for many of us. If a 20-year-old comes in to my office with his 85-year-old grandfather and they both say their penises aren’t working, how do you figure out what’s going on? Do they even have the same thing wrong with them?
Here’s a fun and helpful tool that I use in my office. It’s called the Erection Hardness Score. It was developed around the time that Viagra came out, in 1998. It’s been game-changing for me to get patients more comfortable talking about their erection issues.
I tell them it’s a 4-number scale. A “1” is no erection at all. A “2” is when it gets harder and larger, but it’s not going to penetrate. A “3” will penetrate, but it’s pretty wobbly. A “4” is that perfect cucumber–porn star erection that everyone is seeking. I have the patient tell me a story. They may say, “When I wake up in the morning, I’m at a 2. When I stimulate myself, I can get up to a 3. When I’m with my partner, sometimes I can get up to a 4.”
This is really helpful because they can talk in numbers. And after I give them treatments such as lifestyle changes, sex therapy, testosterone, a PDE5 inhibitor such as Viagra or Cialis, or an injection, they can come back and tell me how the story has changed. I have an objective measure that shows me how the treatment is affecting their erections. Not only do I feel more confident having those objective measures, but my patients feel more confident in the care that they’re getting, and they feel more comfortable talking to me about the changes. So, I encourage all of you to bring that EHS tool into your office. Show it to patients and get them more comfortable talking about erections.
Dr. Rubin is assistant clinical professor, department of urology, Georgetown University, Washington. She disclosed financial relationships with Absorption Pharmaceuticals, GlaxoSmithKline, and Endo Pharmaceuticals; has served as a speaker for Sprout; and has received research grant from Maternal Medical.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
I mean it. Penis problems are very common and are an early sign that patients could have a cardiac event. Think about it: Clogging the arteries of the heart is called a heart attack; clogging the arteries to the penis is a penis attack, or as doctors like to call it, erectile dysfunction.
The arteries to the penis are only 1 mm in diameter. They develop plaque and clog the circulation long before the 3-mm cardiac arteries. So, it’s very important for primary care doctors to talk to their patients about erection health. And I’ll be honest: It’s easier to talk to patients about how lifestyle is affecting their penis health than it is to discuss how lifestyle affects longevity or prevents cancer. I get a lot of men to quit smoking because I tell them what it’s doing to their penises.
It can be challenging for doctors and patients to talk about penises. It doesn’t come naturally for many of us. If a 20-year-old comes in to my office with his 85-year-old grandfather and they both say their penises aren’t working, how do you figure out what’s going on? Do they even have the same thing wrong with them?
Here’s a fun and helpful tool that I use in my office. It’s called the Erection Hardness Score. It was developed around the time that Viagra came out, in 1998. It’s been game-changing for me to get patients more comfortable talking about their erection issues.
I tell them it’s a 4-number scale. A “1” is no erection at all. A “2” is when it gets harder and larger, but it’s not going to penetrate. A “3” will penetrate, but it’s pretty wobbly. A “4” is that perfect cucumber–porn star erection that everyone is seeking. I have the patient tell me a story. They may say, “When I wake up in the morning, I’m at a 2. When I stimulate myself, I can get up to a 3. When I’m with my partner, sometimes I can get up to a 4.”
This is really helpful because they can talk in numbers. And after I give them treatments such as lifestyle changes, sex therapy, testosterone, a PDE5 inhibitor such as Viagra or Cialis, or an injection, they can come back and tell me how the story has changed. I have an objective measure that shows me how the treatment is affecting their erections. Not only do I feel more confident having those objective measures, but my patients feel more confident in the care that they’re getting, and they feel more comfortable talking to me about the changes. So, I encourage all of you to bring that EHS tool into your office. Show it to patients and get them more comfortable talking about erections.
Dr. Rubin is assistant clinical professor, department of urology, Georgetown University, Washington. She disclosed financial relationships with Absorption Pharmaceuticals, GlaxoSmithKline, and Endo Pharmaceuticals; has served as a speaker for Sprout; and has received research grant from Maternal Medical.
A version of this article appeared on Medscape.com.
Renewing the dream
The dream of family practice began more than 6 decades ago with a movement toward personal physicians who have “… the feeling of warm personal regard and concern of doctor for patient, the feeling that the doctor treats people, not illnesses ….” The personal family physician helps patients “… not because of the interesting medical problems they may present but because they are human beings in need of help.”1 One of the most influential founders of family medicine, Dr. Gayle Stephens, expounded on this idea in a series of essays that tapped into the intellectual, philosophical, historical, and moral underpinnings of our discipline.2
Following the dream and the birth of family medicine—like any organization—its lifecycle can be envisioned as proceeding through the rest of the 7 stages of organizational life (TABLE).3 Now allow me to give you some numbers. There are more than 118,000 family physicians in the United States, 784 family medicine residencies filled by 4530 medical school graduates, more than 150 departments of family medicine, multiple national family medicine organizations, and even a World Organization of Family Doctors.4,5 The American Board of Family Medicine is the second largest medical specialty board in the country. Family doctors make up nearly 40% of our total primary care workforce.6 We launched the venture, got organized, made it. We are an institution.
The threat at the institution stage is that we are on the precipice of “closing in.” Many factors are driving this stage: commoditization in health care, market influences and competition for patients, alternative primary care models, erosion of the patient-physician relationship (partly driven by technology), narrowing scope of care, clinician burnout, and the challenges of implementing value-based care, to name a few. You see what comes next in the TABLE.3 The good news is that there is an alternative to the “natural” progression to the ending stage: the path of renewal.3
In the lifecycle of an organization, the path of renewal starts the cycle anew, with dreaming the dream. I recently had the opportunity to visit Singapore to learn about their health system. Singapore is one of the wealthiest countries in the world. I was impressed with their many innovations, including technological ones, as well as new models of care. However, I was most impressed that the country is betting big on family medicine. Their Ministry of Health has launched an initiative they are calling Healthier SG.7 The goal is for “all Singaporeans to have a trusted and lifelong relationship with [their] family doctor.” Their dream is to bring personal doctoring to everyone in the country to make Singapore healthier.
While their path of renewal is occurring halfway around the world, here at home, our path of renewal has been ignited over the past several years by the work of the Robert Graham Center; the Keystone Conferences; the American Board of Family Medicine; and the National Academies of Science, Engineering, and Medicine, among others.8-11 These organizations are aligning around re-centering on patient-clinician relationships, measuring what is important, care by interprofessional teams, payment reform, professionalism, health equity, improved information technology, and adherence to the best available evidence. We are working toward the solution shop as opposed to the production line.12 We are indeed dreaming a new dream.
While I write about this renewal, I close with an ending. This is the final issue of The Journal of Family Practice. It marks the end of an era of nearly 50 years of publication. The Journal of Family Practice has left a lasting mark, providing generations of clinicians with evidence-based, practical guidance to help care for patients as well as serving as an important venue for scholarly work by the family medicine community. Although I have had the privilege of serving the discipline as an editor-in-chief for only a brief time, I am grateful I had the opportunity. Most of all, I appreciate being on the journey of family medicine with you, renewing the dream together.
The references for this Editorial are available in the online version of the article at www.mdedge.com/familymedicine.
1. Fox TF. The personal doctor and his relation to the hospital. Observations and reflections on some American experiments in general practice by groups. Lancet. 1960;2:743-760.
2. Stephens, GG. The Intellectual Basis of Family Practice. Winter Publishing and Society of Teachers of Family Medicine; 1982.
3. Bridges W, Bridges S. Managing Transitions: Making the Most of Change. 4th ed. Da Capo Press; 2016.
4. Association of American Medical Colleges. Physician specialty data report. Accessed October 25, 2023. www.aamc.org/data-reports/workforce/data/active-physicians-us-doctor-medicine-us-md-degree-specialty-2019
5. American Academy of Family Physicians. 2023 match results for family medicine. Accessed October 25, 2023. www.aafp.org/students-residents/residency-program-directors/national-resident-matching-program-results.html
6. Robert Graham Center. Primary Care in the US: A Chartbook of Facts and Statistics. Accessed October 25, 2023. www.graham-center.org/content/dam/rgc/documents/publications-reports/reports/PrimaryCareChartbook2021.pdf
7. Ministry of Health Singapore. What is Healthier SG? Accessed October 25, 2023. www.healthiersg.gov.sg/about/what-is-healthier-sg/
8. The Robert Graham Center. Accessed October 25, 2023. www.graham-center.org/home.html
9. Stange KC. Holding on and letting go: a perspective from the Keystone IV Conference. J Am Board Fam Med. 2016;29:S32-S39.
10. American Board of Family Medicine. Family medicine certification. Accessed October 25, 2023. www.theabfm.org/research-articles/family-medicine-certification?page=1
11. National Academies of Sciences, Engineering, and Medicine. Implementing high-quality primary care. Accessed October 25, 2023. www.nationalacademies.org/our-work/implementing-high-quality-primary-care
12. Sinsky CA, Panzer J. The solution shop and the production line—the case for a frameshift for physician practices. N Engl J Med. 2022;386:2452-2453.
The dream of family practice began more than 6 decades ago with a movement toward personal physicians who have “… the feeling of warm personal regard and concern of doctor for patient, the feeling that the doctor treats people, not illnesses ….” The personal family physician helps patients “… not because of the interesting medical problems they may present but because they are human beings in need of help.”1 One of the most influential founders of family medicine, Dr. Gayle Stephens, expounded on this idea in a series of essays that tapped into the intellectual, philosophical, historical, and moral underpinnings of our discipline.2
Following the dream and the birth of family medicine—like any organization—its lifecycle can be envisioned as proceeding through the rest of the 7 stages of organizational life (TABLE).3 Now allow me to give you some numbers. There are more than 118,000 family physicians in the United States, 784 family medicine residencies filled by 4530 medical school graduates, more than 150 departments of family medicine, multiple national family medicine organizations, and even a World Organization of Family Doctors.4,5 The American Board of Family Medicine is the second largest medical specialty board in the country. Family doctors make up nearly 40% of our total primary care workforce.6 We launched the venture, got organized, made it. We are an institution.
The threat at the institution stage is that we are on the precipice of “closing in.” Many factors are driving this stage: commoditization in health care, market influences and competition for patients, alternative primary care models, erosion of the patient-physician relationship (partly driven by technology), narrowing scope of care, clinician burnout, and the challenges of implementing value-based care, to name a few. You see what comes next in the TABLE.3 The good news is that there is an alternative to the “natural” progression to the ending stage: the path of renewal.3
In the lifecycle of an organization, the path of renewal starts the cycle anew, with dreaming the dream. I recently had the opportunity to visit Singapore to learn about their health system. Singapore is one of the wealthiest countries in the world. I was impressed with their many innovations, including technological ones, as well as new models of care. However, I was most impressed that the country is betting big on family medicine. Their Ministry of Health has launched an initiative they are calling Healthier SG.7 The goal is for “all Singaporeans to have a trusted and lifelong relationship with [their] family doctor.” Their dream is to bring personal doctoring to everyone in the country to make Singapore healthier.
While their path of renewal is occurring halfway around the world, here at home, our path of renewal has been ignited over the past several years by the work of the Robert Graham Center; the Keystone Conferences; the American Board of Family Medicine; and the National Academies of Science, Engineering, and Medicine, among others.8-11 These organizations are aligning around re-centering on patient-clinician relationships, measuring what is important, care by interprofessional teams, payment reform, professionalism, health equity, improved information technology, and adherence to the best available evidence. We are working toward the solution shop as opposed to the production line.12 We are indeed dreaming a new dream.
While I write about this renewal, I close with an ending. This is the final issue of The Journal of Family Practice. It marks the end of an era of nearly 50 years of publication. The Journal of Family Practice has left a lasting mark, providing generations of clinicians with evidence-based, practical guidance to help care for patients as well as serving as an important venue for scholarly work by the family medicine community. Although I have had the privilege of serving the discipline as an editor-in-chief for only a brief time, I am grateful I had the opportunity. Most of all, I appreciate being on the journey of family medicine with you, renewing the dream together.
The references for this Editorial are available in the online version of the article at www.mdedge.com/familymedicine.
The dream of family practice began more than 6 decades ago with a movement toward personal physicians who have “… the feeling of warm personal regard and concern of doctor for patient, the feeling that the doctor treats people, not illnesses ….” The personal family physician helps patients “… not because of the interesting medical problems they may present but because they are human beings in need of help.”1 One of the most influential founders of family medicine, Dr. Gayle Stephens, expounded on this idea in a series of essays that tapped into the intellectual, philosophical, historical, and moral underpinnings of our discipline.2
Following the dream and the birth of family medicine—like any organization—its lifecycle can be envisioned as proceeding through the rest of the 7 stages of organizational life (TABLE).3 Now allow me to give you some numbers. There are more than 118,000 family physicians in the United States, 784 family medicine residencies filled by 4530 medical school graduates, more than 150 departments of family medicine, multiple national family medicine organizations, and even a World Organization of Family Doctors.4,5 The American Board of Family Medicine is the second largest medical specialty board in the country. Family doctors make up nearly 40% of our total primary care workforce.6 We launched the venture, got organized, made it. We are an institution.
The threat at the institution stage is that we are on the precipice of “closing in.” Many factors are driving this stage: commoditization in health care, market influences and competition for patients, alternative primary care models, erosion of the patient-physician relationship (partly driven by technology), narrowing scope of care, clinician burnout, and the challenges of implementing value-based care, to name a few. You see what comes next in the TABLE.3 The good news is that there is an alternative to the “natural” progression to the ending stage: the path of renewal.3
In the lifecycle of an organization, the path of renewal starts the cycle anew, with dreaming the dream. I recently had the opportunity to visit Singapore to learn about their health system. Singapore is one of the wealthiest countries in the world. I was impressed with their many innovations, including technological ones, as well as new models of care. However, I was most impressed that the country is betting big on family medicine. Their Ministry of Health has launched an initiative they are calling Healthier SG.7 The goal is for “all Singaporeans to have a trusted and lifelong relationship with [their] family doctor.” Their dream is to bring personal doctoring to everyone in the country to make Singapore healthier.
While their path of renewal is occurring halfway around the world, here at home, our path of renewal has been ignited over the past several years by the work of the Robert Graham Center; the Keystone Conferences; the American Board of Family Medicine; and the National Academies of Science, Engineering, and Medicine, among others.8-11 These organizations are aligning around re-centering on patient-clinician relationships, measuring what is important, care by interprofessional teams, payment reform, professionalism, health equity, improved information technology, and adherence to the best available evidence. We are working toward the solution shop as opposed to the production line.12 We are indeed dreaming a new dream.
While I write about this renewal, I close with an ending. This is the final issue of The Journal of Family Practice. It marks the end of an era of nearly 50 years of publication. The Journal of Family Practice has left a lasting mark, providing generations of clinicians with evidence-based, practical guidance to help care for patients as well as serving as an important venue for scholarly work by the family medicine community. Although I have had the privilege of serving the discipline as an editor-in-chief for only a brief time, I am grateful I had the opportunity. Most of all, I appreciate being on the journey of family medicine with you, renewing the dream together.
The references for this Editorial are available in the online version of the article at www.mdedge.com/familymedicine.
1. Fox TF. The personal doctor and his relation to the hospital. Observations and reflections on some American experiments in general practice by groups. Lancet. 1960;2:743-760.
2. Stephens, GG. The Intellectual Basis of Family Practice. Winter Publishing and Society of Teachers of Family Medicine; 1982.
3. Bridges W, Bridges S. Managing Transitions: Making the Most of Change. 4th ed. Da Capo Press; 2016.
4. Association of American Medical Colleges. Physician specialty data report. Accessed October 25, 2023. www.aamc.org/data-reports/workforce/data/active-physicians-us-doctor-medicine-us-md-degree-specialty-2019
5. American Academy of Family Physicians. 2023 match results for family medicine. Accessed October 25, 2023. www.aafp.org/students-residents/residency-program-directors/national-resident-matching-program-results.html
6. Robert Graham Center. Primary Care in the US: A Chartbook of Facts and Statistics. Accessed October 25, 2023. www.graham-center.org/content/dam/rgc/documents/publications-reports/reports/PrimaryCareChartbook2021.pdf
7. Ministry of Health Singapore. What is Healthier SG? Accessed October 25, 2023. www.healthiersg.gov.sg/about/what-is-healthier-sg/
8. The Robert Graham Center. Accessed October 25, 2023. www.graham-center.org/home.html
9. Stange KC. Holding on and letting go: a perspective from the Keystone IV Conference. J Am Board Fam Med. 2016;29:S32-S39.
10. American Board of Family Medicine. Family medicine certification. Accessed October 25, 2023. www.theabfm.org/research-articles/family-medicine-certification?page=1
11. National Academies of Sciences, Engineering, and Medicine. Implementing high-quality primary care. Accessed October 25, 2023. www.nationalacademies.org/our-work/implementing-high-quality-primary-care
12. Sinsky CA, Panzer J. The solution shop and the production line—the case for a frameshift for physician practices. N Engl J Med. 2022;386:2452-2453.
1. Fox TF. The personal doctor and his relation to the hospital. Observations and reflections on some American experiments in general practice by groups. Lancet. 1960;2:743-760.
2. Stephens, GG. The Intellectual Basis of Family Practice. Winter Publishing and Society of Teachers of Family Medicine; 1982.
3. Bridges W, Bridges S. Managing Transitions: Making the Most of Change. 4th ed. Da Capo Press; 2016.
4. Association of American Medical Colleges. Physician specialty data report. Accessed October 25, 2023. www.aamc.org/data-reports/workforce/data/active-physicians-us-doctor-medicine-us-md-degree-specialty-2019
5. American Academy of Family Physicians. 2023 match results for family medicine. Accessed October 25, 2023. www.aafp.org/students-residents/residency-program-directors/national-resident-matching-program-results.html
6. Robert Graham Center. Primary Care in the US: A Chartbook of Facts and Statistics. Accessed October 25, 2023. www.graham-center.org/content/dam/rgc/documents/publications-reports/reports/PrimaryCareChartbook2021.pdf
7. Ministry of Health Singapore. What is Healthier SG? Accessed October 25, 2023. www.healthiersg.gov.sg/about/what-is-healthier-sg/
8. The Robert Graham Center. Accessed October 25, 2023. www.graham-center.org/home.html
9. Stange KC. Holding on and letting go: a perspective from the Keystone IV Conference. J Am Board Fam Med. 2016;29:S32-S39.
10. American Board of Family Medicine. Family medicine certification. Accessed October 25, 2023. www.theabfm.org/research-articles/family-medicine-certification?page=1
11. National Academies of Sciences, Engineering, and Medicine. Implementing high-quality primary care. Accessed October 25, 2023. www.nationalacademies.org/our-work/implementing-high-quality-primary-care
12. Sinsky CA, Panzer J. The solution shop and the production line—the case for a frameshift for physician practices. N Engl J Med. 2022;386:2452-2453.
The steep costs of disrupting gut-barrier harmony
An interview with Elena Ivanina, DO, MPH
From Ayurveda to the teachings of Hippocrates, medicine’s earliest traditions advanced a belief that the gut was the foundation of all health and disease. It wasn’t until recently, however, that Western medicine has adopted the notion of gut-barrier dysfunction as a pathologic phenomenon critical to not only digestive health but also chronic allergic, inflammatory, and autoimmune disease.
To learn more, Medscape contributor Akash Goel, MD, interviewed Elena Ivanina, DO, MPH, an integrative gastroenterologist, on the role of the gut barrier. Dr. Ivanina is the founder of the Center for Integrative Gut Health and the former director of Neurogastroenterology and Motility at Lenox Hill Hospital in New York. She runs the educational platform for all things gut health, gutlove.com.
What is the role of the gut barrier in overall health and disease?
The gut contains the human body’s largest interface between a person and their external environment. The actual interface is at the gut barrier, where there needs to be an ideal homeostasis and selectivity mechanism to allow the absorption of healthy nutrients, but on the other hand prevent the penetration of harmful microbes, food antigens, and other proinflammatory factors and toxins.
The gut barrier is made up of the mucus layer, gut microbiome, epithelial cells, and immune cells in the lamina propria. When this apparatus is disrupted by factors such as infection, low-fiber diet, antibiotics, and alcohol, then it cannot function normally to selectively keep out the harmful intraluminal substances.
Gut-barrier disruption leads to translocation of dangerous intraluminal components, such as bacteria and their components, into the gut wall and, most importantly, exposes the immune system to them. This causes improper immune activation and dysregulation, which has been shown to lead to various diseases, including gastrointestinal inflammatory disorders such as inflammatory bowel disease (IBD) and celiac disease, systemic autoimmune diseases such as multiple sclerosis and rheumatoid arthritis, and metabolic diseases such as obesity and diabetes.
Is disruption of this barrier what is usually referred to as “leaky gut”?
Leaky gut is a colloquial term for increased intestinal permeability or intestinal hyperpermeability. In a 2019 review article, Dr. Michael Camilleri exposes leaky gut as a term that can be misleading and confusing to the general population. It calls upon clinicians to have an increased awareness of the potential of barrier dysfunction in diseases, and to consider the barrier as a target for treatment.
Is leaky gut more of a mechanism of underlying chronic disease or is it a disease of its own?
Intestinal permeability is a pathophysiologic process in the gut with certain risk factors that in some conditions has been shown to precede chronic disease. There has not been any convincing evidence that it can be diagnosed and treated as its own entity, but research is ongoing.
In IBD, the Crohn’s and Colitis Canada Genetic, Environmental, Microbial Project research consortium has been studying individuals at increased risk for Crohn’s disease because of a first-degree family member with Crohn’s disease. They found an increased abundance of Ruminococcus torques in the microbiomes of at-risk individuals who went on to develop the disease. R. torques are mucin degraders that induce an increase in other mucin-using bacteria, which can contribute to gut-barrier compromise.
In other studies, patients have been found to have asymptomatic intestinal hyperpermeability years before their diagnosis of Crohn’s disease. This supports understanding more about the potential of intestinal hyperpermeability as its own diagnosis that, if addressed, could possibly prevent disease development.
The many possible sources of gut-barrier disruption
What causes leaky gut, and when should physicians and patients be suspicious if they have it?
There are many risk factors that have been associated with leaky gut in both human studies and animal studies, including acrolein (food toxin), aging, alcohol, antacid drugs, antibiotics, burn injury, chemotherapy, circadian rhythm disruption, corticosteroids, emulsifiers (food additives), strenuous exercise (≥ 2 hours) at 60% VO2 max, starvation, fructose, fructans, gliadin (wheat protein), high-fat diet, high-salt diet, high-sugar diet, hyperglycemia, low-fiber diet, nonsteroidal anti-inflammatory drugs, pesticide, proinflammatory cytokines, psychological stress, radiation, sleep deprivation, smoking, and sweeteners.
Patients may be completely asymptomatic with leaky gut. Physicians should be suspicious if there is a genetic predisposition to chronic disease or if any risk factors are unveiled after assessing diet and lifestyle exposures.
What is the role of the Western diet and processed food consumption in driving disruptions of the gut barrier?
The Western diet reduces gut-barrier mucus thickness, leading to increased gut permeability. People who consume a Western diet typically eat less than 15 grams of fiber per day, which is significantly less than many other cultures, including the hunter-gatherers of Tanzania (Hadza), who get 100 or more grams of fiber a day in their food.
With a fiber-depleted diet, gut microbiota that normally feed on fiber gradually disappear and other commensals shift their metabolism to degrade the gut-barrier mucus layer.
A low-fiber diet also decreases short-chain fatty acid production, which reduces production of mucus and affects tight junction regulation.
Emerging evidence on causality
New evidence is demonstrating that previous functional conditions of the gastrointestinal tract, like functional dyspepsia, are associated with abnormalities to the intestinal barrier. What is the association between conditions like functional dyspepsia and irritable bowel syndrome (IBS) with gut-barrier disruption?
Conditions such as functional dyspepsia and IBS are similar in that their pathophysiology is incompletely understood and likely attributable to contributions from many different underlying mechanisms. This makes it difficult for clinicians to explain the condition to patients and often to treat without specific therapeutic targets.
Emerging evidence with new diagnostic tools, such as confocal laser endomicroscopy, has demonstrated altered mucosal barrier function in both conditions.
In patients with IBS who have a suspected food intolerance, studies looking at exposure to the food antigens found that the food caused immediate breaks, increased intervillous spaces, and increased inflammatory cells in the gut mucosa. These changes were associated with patient responses to exclusion diets.
In functional dyspepsia, another study, using confocal laser endomicroscopy, has shown that affected patients have significantly greater epithelial gap density in the duodenum, compared with healthy controls. There was also impaired duodenal-epithelial barrier integrity and evidence of increased cellular pyroptosis in the duodenal mucosa.
These findings suggest that while IBS and functional dyspepsia are still likely multifactorial, there may be a common preclinical state that can be further investigated as far as preventing its development and using it as a therapeutic target.
What diagnostic testing are you using to determine whether patients have disruptions to the gut barrier? Are they validated or more experimental?
There are various testing strategies that have been used in research to diagnose intestinal hyperpermeability. In a 2021 analysis, Dr. Michael Camilleri found that the optimal probes for measuring small intestinal and colonic permeability are the mass excreted of 13C-mannitol at 0-2 hours and lactulose during 2-8 hours or sucralose during 8-24 hours. Studies looking at postinfectious IBS have incorporated elevated urinary lactulose/mannitol ratios. Dr. Alessio Fasano and others have looked at using zonulin as a biomarker of impaired gut-barrier function. These tests are still considered experimental.
Is there an association between alterations in the gut microbiome and gut-barrier disruption?
There is an integral relationship between the gut microbiome and gut-barrier function, and dysbiosis can disrupt gut-barrier functionality.
The microbiota produce a variety of metabolites in close proximity to the gut epithelium, impacting gut-barrier function and immune response. For example, short-chain fatty acids produced by Bifidobacterium, Bacteroides, Enterobacter, Faecalibacterium, and Roseburia species impact host immune cell differentiation and metabolism as well as influence susceptibility to pathogens.
Studies have shown that sodium butyrate significantly improves epithelial-barrier function. Other experiments have used transplantation of the intestinal microbiota to show that introduction of certain microbial phenotypes can significantly increase gut permeability.
Practical advice for clinicians and patients
How do you advise patients to avoid gut-barrier disruption?
It is important to educate and counsel patients about the long list of risk factors, many of which are closely related to a Western diet and lifestyle, which can increase their risk for leaky gut.
Once one has it, can it be repaired? Can you share a bit about your protocols in general terms?
Many interventions have been shown to improve intestinal permeability. They include berberine, butyrate, caloric restriction and fasting, curcumin, dietary fiber (prebiotics), moderate exercise, fermented food, fish oil, glutamine, quercetin, probiotics, vagus nerve stimulation, vitamin D, and zinc.
Protocols have to be tailored to patients and their risk factors, diet, and lifestyle.
What are some tips from a nutrition and lifestyle standpoint that patients can follow to ensure a robust gut barrier?
It is important to emphasize a high-fiber diet with naturally fermented food, incorporating time-restricted eating, such as eating an early dinner and nothing else before bedtime, a moderate exercise routine, and gut-brain modulation with techniques such as acupuncture that can incorporate vagus nerve stimulation. Limited safe precision supplementation can be discussed on an individual basis based on the patient’s interest, additional testing, and other existing health conditions.
Dr. Akash Goel is a clinical assistant professor of medicine at Weill Cornell in gastroenterology and hepatology. He has disclosed no relevant financial relationships. His work has appeared on networks and publications such as CNN, The New York Times, Time Magazine, and Financial Times. He has a deep interest in nutrition, food as medicine, and the intersection between the gut microbiome and human health.
A version of this article appeared on Medscape.com.
An interview with Elena Ivanina, DO, MPH
An interview with Elena Ivanina, DO, MPH
From Ayurveda to the teachings of Hippocrates, medicine’s earliest traditions advanced a belief that the gut was the foundation of all health and disease. It wasn’t until recently, however, that Western medicine has adopted the notion of gut-barrier dysfunction as a pathologic phenomenon critical to not only digestive health but also chronic allergic, inflammatory, and autoimmune disease.
To learn more, Medscape contributor Akash Goel, MD, interviewed Elena Ivanina, DO, MPH, an integrative gastroenterologist, on the role of the gut barrier. Dr. Ivanina is the founder of the Center for Integrative Gut Health and the former director of Neurogastroenterology and Motility at Lenox Hill Hospital in New York. She runs the educational platform for all things gut health, gutlove.com.
What is the role of the gut barrier in overall health and disease?
The gut contains the human body’s largest interface between a person and their external environment. The actual interface is at the gut barrier, where there needs to be an ideal homeostasis and selectivity mechanism to allow the absorption of healthy nutrients, but on the other hand prevent the penetration of harmful microbes, food antigens, and other proinflammatory factors and toxins.
The gut barrier is made up of the mucus layer, gut microbiome, epithelial cells, and immune cells in the lamina propria. When this apparatus is disrupted by factors such as infection, low-fiber diet, antibiotics, and alcohol, then it cannot function normally to selectively keep out the harmful intraluminal substances.
Gut-barrier disruption leads to translocation of dangerous intraluminal components, such as bacteria and their components, into the gut wall and, most importantly, exposes the immune system to them. This causes improper immune activation and dysregulation, which has been shown to lead to various diseases, including gastrointestinal inflammatory disorders such as inflammatory bowel disease (IBD) and celiac disease, systemic autoimmune diseases such as multiple sclerosis and rheumatoid arthritis, and metabolic diseases such as obesity and diabetes.
Is disruption of this barrier what is usually referred to as “leaky gut”?
Leaky gut is a colloquial term for increased intestinal permeability or intestinal hyperpermeability. In a 2019 review article, Dr. Michael Camilleri exposes leaky gut as a term that can be misleading and confusing to the general population. It calls upon clinicians to have an increased awareness of the potential of barrier dysfunction in diseases, and to consider the barrier as a target for treatment.
Is leaky gut more of a mechanism of underlying chronic disease or is it a disease of its own?
Intestinal permeability is a pathophysiologic process in the gut with certain risk factors that in some conditions has been shown to precede chronic disease. There has not been any convincing evidence that it can be diagnosed and treated as its own entity, but research is ongoing.
In IBD, the Crohn’s and Colitis Canada Genetic, Environmental, Microbial Project research consortium has been studying individuals at increased risk for Crohn’s disease because of a first-degree family member with Crohn’s disease. They found an increased abundance of Ruminococcus torques in the microbiomes of at-risk individuals who went on to develop the disease. R. torques are mucin degraders that induce an increase in other mucin-using bacteria, which can contribute to gut-barrier compromise.
In other studies, patients have been found to have asymptomatic intestinal hyperpermeability years before their diagnosis of Crohn’s disease. This supports understanding more about the potential of intestinal hyperpermeability as its own diagnosis that, if addressed, could possibly prevent disease development.
The many possible sources of gut-barrier disruption
What causes leaky gut, and when should physicians and patients be suspicious if they have it?
There are many risk factors that have been associated with leaky gut in both human studies and animal studies, including acrolein (food toxin), aging, alcohol, antacid drugs, antibiotics, burn injury, chemotherapy, circadian rhythm disruption, corticosteroids, emulsifiers (food additives), strenuous exercise (≥ 2 hours) at 60% VO2 max, starvation, fructose, fructans, gliadin (wheat protein), high-fat diet, high-salt diet, high-sugar diet, hyperglycemia, low-fiber diet, nonsteroidal anti-inflammatory drugs, pesticide, proinflammatory cytokines, psychological stress, radiation, sleep deprivation, smoking, and sweeteners.
Patients may be completely asymptomatic with leaky gut. Physicians should be suspicious if there is a genetic predisposition to chronic disease or if any risk factors are unveiled after assessing diet and lifestyle exposures.
What is the role of the Western diet and processed food consumption in driving disruptions of the gut barrier?
The Western diet reduces gut-barrier mucus thickness, leading to increased gut permeability. People who consume a Western diet typically eat less than 15 grams of fiber per day, which is significantly less than many other cultures, including the hunter-gatherers of Tanzania (Hadza), who get 100 or more grams of fiber a day in their food.
With a fiber-depleted diet, gut microbiota that normally feed on fiber gradually disappear and other commensals shift their metabolism to degrade the gut-barrier mucus layer.
A low-fiber diet also decreases short-chain fatty acid production, which reduces production of mucus and affects tight junction regulation.
Emerging evidence on causality
New evidence is demonstrating that previous functional conditions of the gastrointestinal tract, like functional dyspepsia, are associated with abnormalities to the intestinal barrier. What is the association between conditions like functional dyspepsia and irritable bowel syndrome (IBS) with gut-barrier disruption?
Conditions such as functional dyspepsia and IBS are similar in that their pathophysiology is incompletely understood and likely attributable to contributions from many different underlying mechanisms. This makes it difficult for clinicians to explain the condition to patients and often to treat without specific therapeutic targets.
Emerging evidence with new diagnostic tools, such as confocal laser endomicroscopy, has demonstrated altered mucosal barrier function in both conditions.
In patients with IBS who have a suspected food intolerance, studies looking at exposure to the food antigens found that the food caused immediate breaks, increased intervillous spaces, and increased inflammatory cells in the gut mucosa. These changes were associated with patient responses to exclusion diets.
In functional dyspepsia, another study, using confocal laser endomicroscopy, has shown that affected patients have significantly greater epithelial gap density in the duodenum, compared with healthy controls. There was also impaired duodenal-epithelial barrier integrity and evidence of increased cellular pyroptosis in the duodenal mucosa.
These findings suggest that while IBS and functional dyspepsia are still likely multifactorial, there may be a common preclinical state that can be further investigated as far as preventing its development and using it as a therapeutic target.
What diagnostic testing are you using to determine whether patients have disruptions to the gut barrier? Are they validated or more experimental?
There are various testing strategies that have been used in research to diagnose intestinal hyperpermeability. In a 2021 analysis, Dr. Michael Camilleri found that the optimal probes for measuring small intestinal and colonic permeability are the mass excreted of 13C-mannitol at 0-2 hours and lactulose during 2-8 hours or sucralose during 8-24 hours. Studies looking at postinfectious IBS have incorporated elevated urinary lactulose/mannitol ratios. Dr. Alessio Fasano and others have looked at using zonulin as a biomarker of impaired gut-barrier function. These tests are still considered experimental.
Is there an association between alterations in the gut microbiome and gut-barrier disruption?
There is an integral relationship between the gut microbiome and gut-barrier function, and dysbiosis can disrupt gut-barrier functionality.
The microbiota produce a variety of metabolites in close proximity to the gut epithelium, impacting gut-barrier function and immune response. For example, short-chain fatty acids produced by Bifidobacterium, Bacteroides, Enterobacter, Faecalibacterium, and Roseburia species impact host immune cell differentiation and metabolism as well as influence susceptibility to pathogens.
Studies have shown that sodium butyrate significantly improves epithelial-barrier function. Other experiments have used transplantation of the intestinal microbiota to show that introduction of certain microbial phenotypes can significantly increase gut permeability.
Practical advice for clinicians and patients
How do you advise patients to avoid gut-barrier disruption?
It is important to educate and counsel patients about the long list of risk factors, many of which are closely related to a Western diet and lifestyle, which can increase their risk for leaky gut.
Once one has it, can it be repaired? Can you share a bit about your protocols in general terms?
Many interventions have been shown to improve intestinal permeability. They include berberine, butyrate, caloric restriction and fasting, curcumin, dietary fiber (prebiotics), moderate exercise, fermented food, fish oil, glutamine, quercetin, probiotics, vagus nerve stimulation, vitamin D, and zinc.
Protocols have to be tailored to patients and their risk factors, diet, and lifestyle.
What are some tips from a nutrition and lifestyle standpoint that patients can follow to ensure a robust gut barrier?
It is important to emphasize a high-fiber diet with naturally fermented food, incorporating time-restricted eating, such as eating an early dinner and nothing else before bedtime, a moderate exercise routine, and gut-brain modulation with techniques such as acupuncture that can incorporate vagus nerve stimulation. Limited safe precision supplementation can be discussed on an individual basis based on the patient’s interest, additional testing, and other existing health conditions.
Dr. Akash Goel is a clinical assistant professor of medicine at Weill Cornell in gastroenterology and hepatology. He has disclosed no relevant financial relationships. His work has appeared on networks and publications such as CNN, The New York Times, Time Magazine, and Financial Times. He has a deep interest in nutrition, food as medicine, and the intersection between the gut microbiome and human health.
A version of this article appeared on Medscape.com.
From Ayurveda to the teachings of Hippocrates, medicine’s earliest traditions advanced a belief that the gut was the foundation of all health and disease. It wasn’t until recently, however, that Western medicine has adopted the notion of gut-barrier dysfunction as a pathologic phenomenon critical to not only digestive health but also chronic allergic, inflammatory, and autoimmune disease.
To learn more, Medscape contributor Akash Goel, MD, interviewed Elena Ivanina, DO, MPH, an integrative gastroenterologist, on the role of the gut barrier. Dr. Ivanina is the founder of the Center for Integrative Gut Health and the former director of Neurogastroenterology and Motility at Lenox Hill Hospital in New York. She runs the educational platform for all things gut health, gutlove.com.
What is the role of the gut barrier in overall health and disease?
The gut contains the human body’s largest interface between a person and their external environment. The actual interface is at the gut barrier, where there needs to be an ideal homeostasis and selectivity mechanism to allow the absorption of healthy nutrients, but on the other hand prevent the penetration of harmful microbes, food antigens, and other proinflammatory factors and toxins.
The gut barrier is made up of the mucus layer, gut microbiome, epithelial cells, and immune cells in the lamina propria. When this apparatus is disrupted by factors such as infection, low-fiber diet, antibiotics, and alcohol, then it cannot function normally to selectively keep out the harmful intraluminal substances.
Gut-barrier disruption leads to translocation of dangerous intraluminal components, such as bacteria and their components, into the gut wall and, most importantly, exposes the immune system to them. This causes improper immune activation and dysregulation, which has been shown to lead to various diseases, including gastrointestinal inflammatory disorders such as inflammatory bowel disease (IBD) and celiac disease, systemic autoimmune diseases such as multiple sclerosis and rheumatoid arthritis, and metabolic diseases such as obesity and diabetes.
Is disruption of this barrier what is usually referred to as “leaky gut”?
Leaky gut is a colloquial term for increased intestinal permeability or intestinal hyperpermeability. In a 2019 review article, Dr. Michael Camilleri exposes leaky gut as a term that can be misleading and confusing to the general population. It calls upon clinicians to have an increased awareness of the potential of barrier dysfunction in diseases, and to consider the barrier as a target for treatment.
Is leaky gut more of a mechanism of underlying chronic disease or is it a disease of its own?
Intestinal permeability is a pathophysiologic process in the gut with certain risk factors that in some conditions has been shown to precede chronic disease. There has not been any convincing evidence that it can be diagnosed and treated as its own entity, but research is ongoing.
In IBD, the Crohn’s and Colitis Canada Genetic, Environmental, Microbial Project research consortium has been studying individuals at increased risk for Crohn’s disease because of a first-degree family member with Crohn’s disease. They found an increased abundance of Ruminococcus torques in the microbiomes of at-risk individuals who went on to develop the disease. R. torques are mucin degraders that induce an increase in other mucin-using bacteria, which can contribute to gut-barrier compromise.
In other studies, patients have been found to have asymptomatic intestinal hyperpermeability years before their diagnosis of Crohn’s disease. This supports understanding more about the potential of intestinal hyperpermeability as its own diagnosis that, if addressed, could possibly prevent disease development.
The many possible sources of gut-barrier disruption
What causes leaky gut, and when should physicians and patients be suspicious if they have it?
There are many risk factors that have been associated with leaky gut in both human studies and animal studies, including acrolein (food toxin), aging, alcohol, antacid drugs, antibiotics, burn injury, chemotherapy, circadian rhythm disruption, corticosteroids, emulsifiers (food additives), strenuous exercise (≥ 2 hours) at 60% VO2 max, starvation, fructose, fructans, gliadin (wheat protein), high-fat diet, high-salt diet, high-sugar diet, hyperglycemia, low-fiber diet, nonsteroidal anti-inflammatory drugs, pesticide, proinflammatory cytokines, psychological stress, radiation, sleep deprivation, smoking, and sweeteners.
Patients may be completely asymptomatic with leaky gut. Physicians should be suspicious if there is a genetic predisposition to chronic disease or if any risk factors are unveiled after assessing diet and lifestyle exposures.
What is the role of the Western diet and processed food consumption in driving disruptions of the gut barrier?
The Western diet reduces gut-barrier mucus thickness, leading to increased gut permeability. People who consume a Western diet typically eat less than 15 grams of fiber per day, which is significantly less than many other cultures, including the hunter-gatherers of Tanzania (Hadza), who get 100 or more grams of fiber a day in their food.
With a fiber-depleted diet, gut microbiota that normally feed on fiber gradually disappear and other commensals shift their metabolism to degrade the gut-barrier mucus layer.
A low-fiber diet also decreases short-chain fatty acid production, which reduces production of mucus and affects tight junction regulation.
Emerging evidence on causality
New evidence is demonstrating that previous functional conditions of the gastrointestinal tract, like functional dyspepsia, are associated with abnormalities to the intestinal barrier. What is the association between conditions like functional dyspepsia and irritable bowel syndrome (IBS) with gut-barrier disruption?
Conditions such as functional dyspepsia and IBS are similar in that their pathophysiology is incompletely understood and likely attributable to contributions from many different underlying mechanisms. This makes it difficult for clinicians to explain the condition to patients and often to treat without specific therapeutic targets.
Emerging evidence with new diagnostic tools, such as confocal laser endomicroscopy, has demonstrated altered mucosal barrier function in both conditions.
In patients with IBS who have a suspected food intolerance, studies looking at exposure to the food antigens found that the food caused immediate breaks, increased intervillous spaces, and increased inflammatory cells in the gut mucosa. These changes were associated with patient responses to exclusion diets.
In functional dyspepsia, another study, using confocal laser endomicroscopy, has shown that affected patients have significantly greater epithelial gap density in the duodenum, compared with healthy controls. There was also impaired duodenal-epithelial barrier integrity and evidence of increased cellular pyroptosis in the duodenal mucosa.
These findings suggest that while IBS and functional dyspepsia are still likely multifactorial, there may be a common preclinical state that can be further investigated as far as preventing its development and using it as a therapeutic target.
What diagnostic testing are you using to determine whether patients have disruptions to the gut barrier? Are they validated or more experimental?
There are various testing strategies that have been used in research to diagnose intestinal hyperpermeability. In a 2021 analysis, Dr. Michael Camilleri found that the optimal probes for measuring small intestinal and colonic permeability are the mass excreted of 13C-mannitol at 0-2 hours and lactulose during 2-8 hours or sucralose during 8-24 hours. Studies looking at postinfectious IBS have incorporated elevated urinary lactulose/mannitol ratios. Dr. Alessio Fasano and others have looked at using zonulin as a biomarker of impaired gut-barrier function. These tests are still considered experimental.
Is there an association between alterations in the gut microbiome and gut-barrier disruption?
There is an integral relationship between the gut microbiome and gut-barrier function, and dysbiosis can disrupt gut-barrier functionality.
The microbiota produce a variety of metabolites in close proximity to the gut epithelium, impacting gut-barrier function and immune response. For example, short-chain fatty acids produced by Bifidobacterium, Bacteroides, Enterobacter, Faecalibacterium, and Roseburia species impact host immune cell differentiation and metabolism as well as influence susceptibility to pathogens.
Studies have shown that sodium butyrate significantly improves epithelial-barrier function. Other experiments have used transplantation of the intestinal microbiota to show that introduction of certain microbial phenotypes can significantly increase gut permeability.
Practical advice for clinicians and patients
How do you advise patients to avoid gut-barrier disruption?
It is important to educate and counsel patients about the long list of risk factors, many of which are closely related to a Western diet and lifestyle, which can increase their risk for leaky gut.
Once one has it, can it be repaired? Can you share a bit about your protocols in general terms?
Many interventions have been shown to improve intestinal permeability. They include berberine, butyrate, caloric restriction and fasting, curcumin, dietary fiber (prebiotics), moderate exercise, fermented food, fish oil, glutamine, quercetin, probiotics, vagus nerve stimulation, vitamin D, and zinc.
Protocols have to be tailored to patients and their risk factors, diet, and lifestyle.
What are some tips from a nutrition and lifestyle standpoint that patients can follow to ensure a robust gut barrier?
It is important to emphasize a high-fiber diet with naturally fermented food, incorporating time-restricted eating, such as eating an early dinner and nothing else before bedtime, a moderate exercise routine, and gut-brain modulation with techniques such as acupuncture that can incorporate vagus nerve stimulation. Limited safe precision supplementation can be discussed on an individual basis based on the patient’s interest, additional testing, and other existing health conditions.
Dr. Akash Goel is a clinical assistant professor of medicine at Weill Cornell in gastroenterology and hepatology. He has disclosed no relevant financial relationships. His work has appeared on networks and publications such as CNN, The New York Times, Time Magazine, and Financial Times. He has a deep interest in nutrition, food as medicine, and the intersection between the gut microbiome and human health.
A version of this article appeared on Medscape.com.
An 88-year-old Black woman presented with 3 months duration of asymptomatic, violaceous patches on the left breast
Angiosarcomas are uncommon, high-grade malignant tumors of endothelial cell origin that can arise via the lymphatics or vasculature. They typically occur spontaneously; however, there have been cases reported of benign vascular transformation. These tumors are more commonly found in elderly men on the head and neck in sun-damaged skin.
. This is a late complication, typically occurring about 5-10 years after radiation. Stewart-Treves syndrome, chronic lymphedema occurring after breast cancer treatment with axillary node dissection, increases the risk of angiosarcoma. As a vascular tumor, angiosarcoma spreads hematogenously and carries a poor prognosis if not caught early. Differential diagnoses include other vascular tumors such as retiform hemangioendothelioma. In this specific patient, the differential diagnosis includes Paget’s disease, chronic radiation skin changes, and eczema.Histopathologically, angiosarcomas exhibit abnormal, pleomorphic, malignant endothelial cells. As the tumor progresses, the cell architecture becomes more distorted and cells form layers with papillary projections into the vascular lumen. Malignant cells may stain positive for CD31, CD34, the oncogene ERG and the proto-oncogene FLI-1. Histology in this patient revealed radiation changes in the dermis, as well as few vascular channels lined by large endothelial cells with marked nuclear atypia, in the form of large nucleoli and variably coarse chromatin. The cells were positive for MYC.
Treatment of angiosarcoma involves a multidisciplinary approach. Resection with wide margins is generally the treatment of choice. However, recurrence is relatively common, which may be a result of microsatellite deposits of the tumor. Perioperative radiation is recommended, and adjuvant chemotherapy often is recommended for metastatic disease. Specifically, paclitaxel has been found to promote survival in some cases of cutaneous angiosarcoma. Metastatic disease may be treated with cytotoxic drugs such as anthracyclines and taxanes. Additionally, targeted therapy including anti-VEGF drugs and tyrosine kinase inhibitors have been tested.
The case and photo were submitted by Mr. Shapiro of Nova Southeastern University College of Osteopathic Medicine, Fort Lauderdale, Fla., and Dr. Bilu Martin. The column was edited by Dr. Bilu Martin.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].
References
Cohen-Hallaleh RB et al. Clin Sarcoma Res. 2017 Aug 7:7:15.
Cozzi S et al. Rep Pract Oncol Radiother. 2021 Sep 30;26(5):827-32.
Spiker AM, Mangla A, Ramsey ML. Angiosarcoma. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island, Fla.: StatPearls Publishing; 2023 Jan-. Available from: www.ncbi.nlm.nih.gov/books/NBK441983/
Angiosarcomas are uncommon, high-grade malignant tumors of endothelial cell origin that can arise via the lymphatics or vasculature. They typically occur spontaneously; however, there have been cases reported of benign vascular transformation. These tumors are more commonly found in elderly men on the head and neck in sun-damaged skin.
. This is a late complication, typically occurring about 5-10 years after radiation. Stewart-Treves syndrome, chronic lymphedema occurring after breast cancer treatment with axillary node dissection, increases the risk of angiosarcoma. As a vascular tumor, angiosarcoma spreads hematogenously and carries a poor prognosis if not caught early. Differential diagnoses include other vascular tumors such as retiform hemangioendothelioma. In this specific patient, the differential diagnosis includes Paget’s disease, chronic radiation skin changes, and eczema.Histopathologically, angiosarcomas exhibit abnormal, pleomorphic, malignant endothelial cells. As the tumor progresses, the cell architecture becomes more distorted and cells form layers with papillary projections into the vascular lumen. Malignant cells may stain positive for CD31, CD34, the oncogene ERG and the proto-oncogene FLI-1. Histology in this patient revealed radiation changes in the dermis, as well as few vascular channels lined by large endothelial cells with marked nuclear atypia, in the form of large nucleoli and variably coarse chromatin. The cells were positive for MYC.
Treatment of angiosarcoma involves a multidisciplinary approach. Resection with wide margins is generally the treatment of choice. However, recurrence is relatively common, which may be a result of microsatellite deposits of the tumor. Perioperative radiation is recommended, and adjuvant chemotherapy often is recommended for metastatic disease. Specifically, paclitaxel has been found to promote survival in some cases of cutaneous angiosarcoma. Metastatic disease may be treated with cytotoxic drugs such as anthracyclines and taxanes. Additionally, targeted therapy including anti-VEGF drugs and tyrosine kinase inhibitors have been tested.
The case and photo were submitted by Mr. Shapiro of Nova Southeastern University College of Osteopathic Medicine, Fort Lauderdale, Fla., and Dr. Bilu Martin. The column was edited by Dr. Bilu Martin.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].
References
Cohen-Hallaleh RB et al. Clin Sarcoma Res. 2017 Aug 7:7:15.
Cozzi S et al. Rep Pract Oncol Radiother. 2021 Sep 30;26(5):827-32.
Spiker AM, Mangla A, Ramsey ML. Angiosarcoma. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island, Fla.: StatPearls Publishing; 2023 Jan-. Available from: www.ncbi.nlm.nih.gov/books/NBK441983/
Angiosarcomas are uncommon, high-grade malignant tumors of endothelial cell origin that can arise via the lymphatics or vasculature. They typically occur spontaneously; however, there have been cases reported of benign vascular transformation. These tumors are more commonly found in elderly men on the head and neck in sun-damaged skin.
. This is a late complication, typically occurring about 5-10 years after radiation. Stewart-Treves syndrome, chronic lymphedema occurring after breast cancer treatment with axillary node dissection, increases the risk of angiosarcoma. As a vascular tumor, angiosarcoma spreads hematogenously and carries a poor prognosis if not caught early. Differential diagnoses include other vascular tumors such as retiform hemangioendothelioma. In this specific patient, the differential diagnosis includes Paget’s disease, chronic radiation skin changes, and eczema.Histopathologically, angiosarcomas exhibit abnormal, pleomorphic, malignant endothelial cells. As the tumor progresses, the cell architecture becomes more distorted and cells form layers with papillary projections into the vascular lumen. Malignant cells may stain positive for CD31, CD34, the oncogene ERG and the proto-oncogene FLI-1. Histology in this patient revealed radiation changes in the dermis, as well as few vascular channels lined by large endothelial cells with marked nuclear atypia, in the form of large nucleoli and variably coarse chromatin. The cells were positive for MYC.
Treatment of angiosarcoma involves a multidisciplinary approach. Resection with wide margins is generally the treatment of choice. However, recurrence is relatively common, which may be a result of microsatellite deposits of the tumor. Perioperative radiation is recommended, and adjuvant chemotherapy often is recommended for metastatic disease. Specifically, paclitaxel has been found to promote survival in some cases of cutaneous angiosarcoma. Metastatic disease may be treated with cytotoxic drugs such as anthracyclines and taxanes. Additionally, targeted therapy including anti-VEGF drugs and tyrosine kinase inhibitors have been tested.
The case and photo were submitted by Mr. Shapiro of Nova Southeastern University College of Osteopathic Medicine, Fort Lauderdale, Fla., and Dr. Bilu Martin. The column was edited by Dr. Bilu Martin.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].
References
Cohen-Hallaleh RB et al. Clin Sarcoma Res. 2017 Aug 7:7:15.
Cozzi S et al. Rep Pract Oncol Radiother. 2021 Sep 30;26(5):827-32.
Spiker AM, Mangla A, Ramsey ML. Angiosarcoma. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island, Fla.: StatPearls Publishing; 2023 Jan-. Available from: www.ncbi.nlm.nih.gov/books/NBK441983/
What not to prescribe to older adults and what to use instead
This transcript has been edited for clarity.
These are important criteria because medications are metabolized differently in older adults and have different effects compared with younger patients. For the sake of these criteria, older adults are 65 years of age or older. That said, we know that everyone from 65 to 100 is not the same. As people age, they develop more comorbidities, they become more frail, and they are more sensitive to the effects and side effects of drugs.
The guidance covers potentially inappropriate medications for older adults. The word “potentially” is important because this is guidance. As clinicians, we make decisions involving individuals. This guidance should be used with judgment, integrating the clinical context of the individual patient.
There is a lot in this guidance. I am going to try to cover what I feel are the most important points.
Aspirin. Since the risk for major bleeding increases with age, for primary prevention of atherosclerotic cardiovascular disease, the harm can be greater than the benefit in older adults, so aspirin should not be used for primary prevention. Aspirin remains indicated for secondary prevention in individuals with established cardiovascular disease.
Warfarin. For treatment of atrial fibrillation or venous thromboembolism (deep vein thrombosis or pulmonary embolism), warfarin should be avoided if possible. Warfarin has a higher risk for major bleeding, particularly intracranial bleeding, than direct oral anticoagulants (DOACs); therefore the latter are preferred. Rivaroxaban should be avoided, as it has a higher risk for major bleeding in older adults than the other DOACs. Apixaban is preferred over dabigatran. If a patient is well controlled on warfarin, you can consider continuing that treatment.
Antipsychotics. These include first- and second-generation antipsychotics such as aripiprazole, haloperidol, olanzapine, quetiapine, risperidone, and others. The guidance says to avoid these agents except for FDA-approved indications such as schizophrenia, bipolar disorder, and adjuvant treatment of depression. Use of these antipsychotics can increase risk for stroke, heart attack, and mortality. Essentially, the guidance says do not use these medications lightly for the treatment of agitated dementia. For those of us with older patients, this can get tricky because agitated dementia is a difficult issue for which there are no good effective medications. The Beers guidance recognizes this in saying that these medications should be avoided unless behavioral interventions have failed. So, there are times where you may need to use these medicines, but use them judiciously.
For patients with dementia, anticholinergics, antipsychotics, and benzodiazepines should be avoided if possible.
Benzodiazepines. Benzodiazepines should also be avoided because older adults have increased sensitivity to their effects due to slower metabolism and clearance of these medications, which can lead to a much longer half-life and higher serum level. In older adults, benzodiazepines increase the risk for cognitive impairment, delirium, falls, fractures, and even motor accidents. The same concerns affect the group of non-benzodiazepine sleeping medicines known as “Z-drugs.”
Nonsteroidal anti-inflammatory drugs (NSAIDs). Used frequently in our practices, NSAIDs are nevertheless on the list. As we think through the risk-benefit ratio of using NSAIDs in older adults, we often underappreciate the risks of these agents. Upper gastrointestinal ulcers with bleeding occur in approximately 1% of patients treated for 3-6 months with an NSAID and in 2%-4% of patients treated for a year. NSAIDs also increase the risk for renal impairment and cardiovascular disease.
Other medications to avoid (if possible). These include:
Sulfonylureas, due to a high risk for hypoglycemia. A short-acting sulfonylurea, such as glipizide, should be used if one is needed.
Proton pump inhibitors should not be used long-term if it can be avoided.
Digoxin should not be first-line treatment for atrial fibrillation or heart failure. Decreased renal clearance in older adults can lead to toxic levels of digoxin, particularly during acute illnesses. Avoid doses > 0.125 mg/day.
Nitrofurantoin should be avoided when the patient’s creatinine clearance is < 30 or for long-term suppressive therapy.
Avoid combining medications that have high anticholinergic side effects, such as scopolamine, diphenhydramine, oxybutynin, cyclobenzaprine, and others.
It is always important to understand the benefits and the risks of the drugs we prescribe. It is also important to remember that older adults are a particularly vulnerable population. The Beers criteria provide important guidance, which we can then use to make decisions about medicines for individual patients.
Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director in the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed ties with AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly, GSK, Merck, Sanofi, Sanofi Pasteur, and Teva.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
These are important criteria because medications are metabolized differently in older adults and have different effects compared with younger patients. For the sake of these criteria, older adults are 65 years of age or older. That said, we know that everyone from 65 to 100 is not the same. As people age, they develop more comorbidities, they become more frail, and they are more sensitive to the effects and side effects of drugs.
The guidance covers potentially inappropriate medications for older adults. The word “potentially” is important because this is guidance. As clinicians, we make decisions involving individuals. This guidance should be used with judgment, integrating the clinical context of the individual patient.
There is a lot in this guidance. I am going to try to cover what I feel are the most important points.
Aspirin. Since the risk for major bleeding increases with age, for primary prevention of atherosclerotic cardiovascular disease, the harm can be greater than the benefit in older adults, so aspirin should not be used for primary prevention. Aspirin remains indicated for secondary prevention in individuals with established cardiovascular disease.
Warfarin. For treatment of atrial fibrillation or venous thromboembolism (deep vein thrombosis or pulmonary embolism), warfarin should be avoided if possible. Warfarin has a higher risk for major bleeding, particularly intracranial bleeding, than direct oral anticoagulants (DOACs); therefore the latter are preferred. Rivaroxaban should be avoided, as it has a higher risk for major bleeding in older adults than the other DOACs. Apixaban is preferred over dabigatran. If a patient is well controlled on warfarin, you can consider continuing that treatment.
Antipsychotics. These include first- and second-generation antipsychotics such as aripiprazole, haloperidol, olanzapine, quetiapine, risperidone, and others. The guidance says to avoid these agents except for FDA-approved indications such as schizophrenia, bipolar disorder, and adjuvant treatment of depression. Use of these antipsychotics can increase risk for stroke, heart attack, and mortality. Essentially, the guidance says do not use these medications lightly for the treatment of agitated dementia. For those of us with older patients, this can get tricky because agitated dementia is a difficult issue for which there are no good effective medications. The Beers guidance recognizes this in saying that these medications should be avoided unless behavioral interventions have failed. So, there are times where you may need to use these medicines, but use them judiciously.
For patients with dementia, anticholinergics, antipsychotics, and benzodiazepines should be avoided if possible.
Benzodiazepines. Benzodiazepines should also be avoided because older adults have increased sensitivity to their effects due to slower metabolism and clearance of these medications, which can lead to a much longer half-life and higher serum level. In older adults, benzodiazepines increase the risk for cognitive impairment, delirium, falls, fractures, and even motor accidents. The same concerns affect the group of non-benzodiazepine sleeping medicines known as “Z-drugs.”
Nonsteroidal anti-inflammatory drugs (NSAIDs). Used frequently in our practices, NSAIDs are nevertheless on the list. As we think through the risk-benefit ratio of using NSAIDs in older adults, we often underappreciate the risks of these agents. Upper gastrointestinal ulcers with bleeding occur in approximately 1% of patients treated for 3-6 months with an NSAID and in 2%-4% of patients treated for a year. NSAIDs also increase the risk for renal impairment and cardiovascular disease.
Other medications to avoid (if possible). These include:
Sulfonylureas, due to a high risk for hypoglycemia. A short-acting sulfonylurea, such as glipizide, should be used if one is needed.
Proton pump inhibitors should not be used long-term if it can be avoided.
Digoxin should not be first-line treatment for atrial fibrillation or heart failure. Decreased renal clearance in older adults can lead to toxic levels of digoxin, particularly during acute illnesses. Avoid doses > 0.125 mg/day.
Nitrofurantoin should be avoided when the patient’s creatinine clearance is < 30 or for long-term suppressive therapy.
Avoid combining medications that have high anticholinergic side effects, such as scopolamine, diphenhydramine, oxybutynin, cyclobenzaprine, and others.
It is always important to understand the benefits and the risks of the drugs we prescribe. It is also important to remember that older adults are a particularly vulnerable population. The Beers criteria provide important guidance, which we can then use to make decisions about medicines for individual patients.
Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director in the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed ties with AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly, GSK, Merck, Sanofi, Sanofi Pasteur, and Teva.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
These are important criteria because medications are metabolized differently in older adults and have different effects compared with younger patients. For the sake of these criteria, older adults are 65 years of age or older. That said, we know that everyone from 65 to 100 is not the same. As people age, they develop more comorbidities, they become more frail, and they are more sensitive to the effects and side effects of drugs.
The guidance covers potentially inappropriate medications for older adults. The word “potentially” is important because this is guidance. As clinicians, we make decisions involving individuals. This guidance should be used with judgment, integrating the clinical context of the individual patient.
There is a lot in this guidance. I am going to try to cover what I feel are the most important points.
Aspirin. Since the risk for major bleeding increases with age, for primary prevention of atherosclerotic cardiovascular disease, the harm can be greater than the benefit in older adults, so aspirin should not be used for primary prevention. Aspirin remains indicated for secondary prevention in individuals with established cardiovascular disease.
Warfarin. For treatment of atrial fibrillation or venous thromboembolism (deep vein thrombosis or pulmonary embolism), warfarin should be avoided if possible. Warfarin has a higher risk for major bleeding, particularly intracranial bleeding, than direct oral anticoagulants (DOACs); therefore the latter are preferred. Rivaroxaban should be avoided, as it has a higher risk for major bleeding in older adults than the other DOACs. Apixaban is preferred over dabigatran. If a patient is well controlled on warfarin, you can consider continuing that treatment.
Antipsychotics. These include first- and second-generation antipsychotics such as aripiprazole, haloperidol, olanzapine, quetiapine, risperidone, and others. The guidance says to avoid these agents except for FDA-approved indications such as schizophrenia, bipolar disorder, and adjuvant treatment of depression. Use of these antipsychotics can increase risk for stroke, heart attack, and mortality. Essentially, the guidance says do not use these medications lightly for the treatment of agitated dementia. For those of us with older patients, this can get tricky because agitated dementia is a difficult issue for which there are no good effective medications. The Beers guidance recognizes this in saying that these medications should be avoided unless behavioral interventions have failed. So, there are times where you may need to use these medicines, but use them judiciously.
For patients with dementia, anticholinergics, antipsychotics, and benzodiazepines should be avoided if possible.
Benzodiazepines. Benzodiazepines should also be avoided because older adults have increased sensitivity to their effects due to slower metabolism and clearance of these medications, which can lead to a much longer half-life and higher serum level. In older adults, benzodiazepines increase the risk for cognitive impairment, delirium, falls, fractures, and even motor accidents. The same concerns affect the group of non-benzodiazepine sleeping medicines known as “Z-drugs.”
Nonsteroidal anti-inflammatory drugs (NSAIDs). Used frequently in our practices, NSAIDs are nevertheless on the list. As we think through the risk-benefit ratio of using NSAIDs in older adults, we often underappreciate the risks of these agents. Upper gastrointestinal ulcers with bleeding occur in approximately 1% of patients treated for 3-6 months with an NSAID and in 2%-4% of patients treated for a year. NSAIDs also increase the risk for renal impairment and cardiovascular disease.
Other medications to avoid (if possible). These include:
Sulfonylureas, due to a high risk for hypoglycemia. A short-acting sulfonylurea, such as glipizide, should be used if one is needed.
Proton pump inhibitors should not be used long-term if it can be avoided.
Digoxin should not be first-line treatment for atrial fibrillation or heart failure. Decreased renal clearance in older adults can lead to toxic levels of digoxin, particularly during acute illnesses. Avoid doses > 0.125 mg/day.
Nitrofurantoin should be avoided when the patient’s creatinine clearance is < 30 or for long-term suppressive therapy.
Avoid combining medications that have high anticholinergic side effects, such as scopolamine, diphenhydramine, oxybutynin, cyclobenzaprine, and others.
It is always important to understand the benefits and the risks of the drugs we prescribe. It is also important to remember that older adults are a particularly vulnerable population. The Beers criteria provide important guidance, which we can then use to make decisions about medicines for individual patients.
Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director in the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed ties with AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly, GSK, Merck, Sanofi, Sanofi Pasteur, and Teva.
A version of this article appeared on Medscape.com.
MOC: An ‘insult to oncologists’ engaged in patient care
This transcript has been edited for clarity.
I am far from the only doctor, and certainly far from the only oncologist, to recently comment on the topic of Maintenance of Certification. Of course, this is happening in a wider debate about our relationship as subspecialists to the American Board of Internal Medicine, and what they deem acceptable for the recertification of doctors in practice.
For instance, 2011 was my first experience ever using a form of immunotherapy. It was an anti-CTLA4 agent, ipilimumab, and I was treating metastatic melanoma. I learned in that instance just how effective these drugs can be, but also how toxic they can be. Ever since then, I’ve been refining my use of immunotherapy. We do that iteratively. We do that as we encounter patients and as we try to meet their needs.
I do understand that the ABIM is saying they want an independent governing body to legislate that process. I think the reason this is stuck in the craw of so many oncologists is that we demonstrate our commitment to continuing medical education all the time.
I’m recording this in my office, which is separate from the space where I see patients. I see patients in a different group of exam rooms for their privacy and it’s a better setup for aspects of the physical encounter. Not a single patient has ever asked to come into my office and see my diplomas, and I sometimes wonder if I keep them here mostly as a visual cue to myself, sort of an antidote to ward off imposter syndrome and remind myself, Oh yeah – I earned these. I earned these through formal training.
Then something happens once you finish your training, whether it’s residency or fellowship, and you become an attending. I think you feel a weight of responsibility, the responsibility of independent learning. All of us are doing this. We have to do this. The field is moving along at such a rapid clip that it’s essentially built into what we do that we are going to keep up. In fact, channels such as the various aspects of social media are a way I curate my own information feed so I can stay up to speed and not feel like I’m drowning in a deluge of new data.
But what’s hard to demonstrate to the ABIM is that [this learning] is already happening. I think we can do it if we submit our records of CME credits that we formally accrue. The reason this is such an almost insult to oncologists in practice is because it is a necessary part of our day-to-day existence to keep apprised of developments so we can apply them to patient care.
One litmus test of attending a medical conference like the annual meeting of the American Society of Clinical Oncology is to ask oneself, When I go back to clinic, is this meeting going to change the way that I take care of patients? The answer almost invariably these days is yes. I go to multiple meetings per year, and I think it’s the exception, not the rule, that I return home and nothing changes in my management patterns. Again, this process is happening whether the ABIM recognizes it or not.
Lastly, I sat down in the fall of 2022 and I did my recertification. I looked at the span of all the things that had happened between 2012, when I first sat for my board examination in medical oncology, and 2022. It was staggering. I think the reason that it wasn’t such an overwhelming amount of information to review is that I had actually been accreting it slowly and gradually, month by month, year by year throughout that decade.
Again, it’s necessary that the ABIM hear us, hear oncologists, and know that of all the medical subspecialties they govern, it is basically already an essential task of our day-to-day professional existence that we engage in lifelong learning. To suggest otherwise really paints us as outdated. The reason that matters so much is that if we’re not up-to-date, then we are underserving our patients.
Mark A. Lewis, MD, is director of gastrointestinal oncology at Intermountain Healthcare in Salt Lake City. He reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
I am far from the only doctor, and certainly far from the only oncologist, to recently comment on the topic of Maintenance of Certification. Of course, this is happening in a wider debate about our relationship as subspecialists to the American Board of Internal Medicine, and what they deem acceptable for the recertification of doctors in practice.
For instance, 2011 was my first experience ever using a form of immunotherapy. It was an anti-CTLA4 agent, ipilimumab, and I was treating metastatic melanoma. I learned in that instance just how effective these drugs can be, but also how toxic they can be. Ever since then, I’ve been refining my use of immunotherapy. We do that iteratively. We do that as we encounter patients and as we try to meet their needs.
I do understand that the ABIM is saying they want an independent governing body to legislate that process. I think the reason this is stuck in the craw of so many oncologists is that we demonstrate our commitment to continuing medical education all the time.
I’m recording this in my office, which is separate from the space where I see patients. I see patients in a different group of exam rooms for their privacy and it’s a better setup for aspects of the physical encounter. Not a single patient has ever asked to come into my office and see my diplomas, and I sometimes wonder if I keep them here mostly as a visual cue to myself, sort of an antidote to ward off imposter syndrome and remind myself, Oh yeah – I earned these. I earned these through formal training.
Then something happens once you finish your training, whether it’s residency or fellowship, and you become an attending. I think you feel a weight of responsibility, the responsibility of independent learning. All of us are doing this. We have to do this. The field is moving along at such a rapid clip that it’s essentially built into what we do that we are going to keep up. In fact, channels such as the various aspects of social media are a way I curate my own information feed so I can stay up to speed and not feel like I’m drowning in a deluge of new data.
But what’s hard to demonstrate to the ABIM is that [this learning] is already happening. I think we can do it if we submit our records of CME credits that we formally accrue. The reason this is such an almost insult to oncologists in practice is because it is a necessary part of our day-to-day existence to keep apprised of developments so we can apply them to patient care.
One litmus test of attending a medical conference like the annual meeting of the American Society of Clinical Oncology is to ask oneself, When I go back to clinic, is this meeting going to change the way that I take care of patients? The answer almost invariably these days is yes. I go to multiple meetings per year, and I think it’s the exception, not the rule, that I return home and nothing changes in my management patterns. Again, this process is happening whether the ABIM recognizes it or not.
Lastly, I sat down in the fall of 2022 and I did my recertification. I looked at the span of all the things that had happened between 2012, when I first sat for my board examination in medical oncology, and 2022. It was staggering. I think the reason that it wasn’t such an overwhelming amount of information to review is that I had actually been accreting it slowly and gradually, month by month, year by year throughout that decade.
Again, it’s necessary that the ABIM hear us, hear oncologists, and know that of all the medical subspecialties they govern, it is basically already an essential task of our day-to-day professional existence that we engage in lifelong learning. To suggest otherwise really paints us as outdated. The reason that matters so much is that if we’re not up-to-date, then we are underserving our patients.
Mark A. Lewis, MD, is director of gastrointestinal oncology at Intermountain Healthcare in Salt Lake City. He reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
I am far from the only doctor, and certainly far from the only oncologist, to recently comment on the topic of Maintenance of Certification. Of course, this is happening in a wider debate about our relationship as subspecialists to the American Board of Internal Medicine, and what they deem acceptable for the recertification of doctors in practice.
For instance, 2011 was my first experience ever using a form of immunotherapy. It was an anti-CTLA4 agent, ipilimumab, and I was treating metastatic melanoma. I learned in that instance just how effective these drugs can be, but also how toxic they can be. Ever since then, I’ve been refining my use of immunotherapy. We do that iteratively. We do that as we encounter patients and as we try to meet their needs.
I do understand that the ABIM is saying they want an independent governing body to legislate that process. I think the reason this is stuck in the craw of so many oncologists is that we demonstrate our commitment to continuing medical education all the time.
I’m recording this in my office, which is separate from the space where I see patients. I see patients in a different group of exam rooms for their privacy and it’s a better setup for aspects of the physical encounter. Not a single patient has ever asked to come into my office and see my diplomas, and I sometimes wonder if I keep them here mostly as a visual cue to myself, sort of an antidote to ward off imposter syndrome and remind myself, Oh yeah – I earned these. I earned these through formal training.
Then something happens once you finish your training, whether it’s residency or fellowship, and you become an attending. I think you feel a weight of responsibility, the responsibility of independent learning. All of us are doing this. We have to do this. The field is moving along at such a rapid clip that it’s essentially built into what we do that we are going to keep up. In fact, channels such as the various aspects of social media are a way I curate my own information feed so I can stay up to speed and not feel like I’m drowning in a deluge of new data.
But what’s hard to demonstrate to the ABIM is that [this learning] is already happening. I think we can do it if we submit our records of CME credits that we formally accrue. The reason this is such an almost insult to oncologists in practice is because it is a necessary part of our day-to-day existence to keep apprised of developments so we can apply them to patient care.
One litmus test of attending a medical conference like the annual meeting of the American Society of Clinical Oncology is to ask oneself, When I go back to clinic, is this meeting going to change the way that I take care of patients? The answer almost invariably these days is yes. I go to multiple meetings per year, and I think it’s the exception, not the rule, that I return home and nothing changes in my management patterns. Again, this process is happening whether the ABIM recognizes it or not.
Lastly, I sat down in the fall of 2022 and I did my recertification. I looked at the span of all the things that had happened between 2012, when I first sat for my board examination in medical oncology, and 2022. It was staggering. I think the reason that it wasn’t such an overwhelming amount of information to review is that I had actually been accreting it slowly and gradually, month by month, year by year throughout that decade.
Again, it’s necessary that the ABIM hear us, hear oncologists, and know that of all the medical subspecialties they govern, it is basically already an essential task of our day-to-day professional existence that we engage in lifelong learning. To suggest otherwise really paints us as outdated. The reason that matters so much is that if we’re not up-to-date, then we are underserving our patients.
Mark A. Lewis, MD, is director of gastrointestinal oncology at Intermountain Healthcare in Salt Lake City. He reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
The multiple meanings of sex
Knowing the sex of a developing fetus is a common question many expectant parents ask at their prenatal appointments. While the sex of a fetus has minimal clinical significance to obstetrician/gynecologists, technology has made ascertaining the answer to this question much more accessible.
In addition to detecting certain genetic abnormalities, both noninvasive prenatal testing (NIPT) and preimplantation genetic testing (PGT) can discern the chromosomal sex of a fetus prior to birth. At the 20-week anatomy scan, the ultrasonographer can detect the presence of external genitalia to determine the sex. In fact, when a baby is first born, obstetrician/gynecologists are consistently asked “do I have a boy or a girl?” Assigning the sex of a newborn is one of the many tasks we complete in the delivery room. However, some of you reading this article would disagree.
“You cannot assign sex at birth.” “Sex is fixed, you cannot change biology.” These are examples of statements that frequent the comments section of my medical articles and plague professionals who treat gender diverse patients. I would argue, as would many biologists, scientists, and physicians, that these statements oversimplify biologic reality.
The term “sex” has multiple meanings: It can allude to the act of reproduction itself, but in the context of sexual determination and sexual differentiation, it can refer to the biologic and structural composition of a developing human. Within this paradigm, there exist three definitions for sex: chromosomal, gonadal, and phenotypic.
Chromosomal sex refers to the genetic makeup of a human, typically XX or XY chromosomes. There are also variations within this seemingly binary system. Embryos can have an extra sex chromosome, as seen in Klinefelter syndrome, which is characterized by XXY karyotype. Embryos can also be devoid of a sex chromosome, as observed in Turner’s syndrome, which is characterized by an XO karyotype. These variations can impact fertility and expression of secondary sexual characteristics as the type of sex chromosomes present results in primary sex determination, or the development of gonads.
Most often, individuals with a chromosomal makeup of XX are considered female and will subsequently develop ovaries that produce oocytes (eggs). Individuals with XY chromosomes are deemed male and will go on to develop testes, which are responsible for spermatogenesis (sperm production).
Gonadal sex is the presence of either testes or ovaries. The primary function of testes is to produce sperm for reproduction and to secrete testosterone, the primary male sex hormone. Similarly, ovaries produce oocytes and secrete estrogen as the primary female sex hormone. Gonads can be surgically removed either via orchiectomy (the removal of testes), or oophorectomy (the removal of ovaries) for a variety of reasons. There is no current medical technology that can replace the function of these structures, although patients can be placed on hormone replacement to counter the negative physiologic consequences resulting from their removal.
Secondary sex determination, or sexual differentiation, is the development of external genitalia and internal genital tracts because of the hormones produced from the gonads. At puberty, further differentiation occurs with the development of pubic and axillary hair and breast growth. This process determines phenotypic sex – the visible distinction between male and female.
When opponents of gender affirming care state that individuals cannot change sex, are they correct or false? The answer to this question is entirely dependent on which definition of sex they are using. Chromosomal? Gonadal? Phenotypic? It is an immutable fact that humans cannot change chromosomal sex. No one in the transgender community, either provider or patient, would dispute this. However, we can remove gonadal structures and alter phenotypic sex.
In fact, many cisgender individuals also revise their phenotypic sex when they undergo augmentation mammaplasty, penile enlargement, or vulvoplasty procedures for the exact same reason.
Circling back to the debate about whether we can “assign sex at birth,” it all depends on what definition of sex you are referencing. At birth, obstetrician/gynecologists most often look at the phenotypic sex and make assumptions about the genetic and gonadal sex based on the secondary sexual characteristics. So yes, we can, and we do assign sex at birth. However, in the case of intersex individuals, these physical characteristics may not align with their gonadal and chromosomal composition.
In the case of an infant that has a known XY karyotype prior to birth but a female phenotype at birth (as seen in a condition called complete androgen insensitivity syndrome), what sex should be assigned to that baby? Should the infant be raised male or female? A lot of unintended but significant harm has resulted from providers and parents trying to answer that very question. The mistreatment of intersex patients through forced and coercive medical and surgical treatments, often in infancy, should serve as a dark reminder that sex and gender are not as biologically binary as we would like to believe.
Dr. Brandt is an ob.gyn. and fellowship-trained gender-affirming surgeon in West Reading, Pa. She has no relevant disclosures.
References
Moore KL and Persaud TVN. The urogenital system. In: Before we are born: essentials of embryology and birth defects. 7th ed. Philadelphia: Saunders Elsevier;2008:163-89.
Standring S. Development of the urogenital system. In: Gray’s Anatomy, 42nd ed. Philadelphia: Elsevier;2021:341-64.
Escobar O et al. Pediatric endocrinology. In: Zitelli BJ, ed. Zitelli and Davis’ atlas of pediatric physical diagnosis 8th edition. Philadelphia: Elsevier;2023:342-81.
Knowing the sex of a developing fetus is a common question many expectant parents ask at their prenatal appointments. While the sex of a fetus has minimal clinical significance to obstetrician/gynecologists, technology has made ascertaining the answer to this question much more accessible.
In addition to detecting certain genetic abnormalities, both noninvasive prenatal testing (NIPT) and preimplantation genetic testing (PGT) can discern the chromosomal sex of a fetus prior to birth. At the 20-week anatomy scan, the ultrasonographer can detect the presence of external genitalia to determine the sex. In fact, when a baby is first born, obstetrician/gynecologists are consistently asked “do I have a boy or a girl?” Assigning the sex of a newborn is one of the many tasks we complete in the delivery room. However, some of you reading this article would disagree.
“You cannot assign sex at birth.” “Sex is fixed, you cannot change biology.” These are examples of statements that frequent the comments section of my medical articles and plague professionals who treat gender diverse patients. I would argue, as would many biologists, scientists, and physicians, that these statements oversimplify biologic reality.
The term “sex” has multiple meanings: It can allude to the act of reproduction itself, but in the context of sexual determination and sexual differentiation, it can refer to the biologic and structural composition of a developing human. Within this paradigm, there exist three definitions for sex: chromosomal, gonadal, and phenotypic.
Chromosomal sex refers to the genetic makeup of a human, typically XX or XY chromosomes. There are also variations within this seemingly binary system. Embryos can have an extra sex chromosome, as seen in Klinefelter syndrome, which is characterized by XXY karyotype. Embryos can also be devoid of a sex chromosome, as observed in Turner’s syndrome, which is characterized by an XO karyotype. These variations can impact fertility and expression of secondary sexual characteristics as the type of sex chromosomes present results in primary sex determination, or the development of gonads.
Most often, individuals with a chromosomal makeup of XX are considered female and will subsequently develop ovaries that produce oocytes (eggs). Individuals with XY chromosomes are deemed male and will go on to develop testes, which are responsible for spermatogenesis (sperm production).
Gonadal sex is the presence of either testes or ovaries. The primary function of testes is to produce sperm for reproduction and to secrete testosterone, the primary male sex hormone. Similarly, ovaries produce oocytes and secrete estrogen as the primary female sex hormone. Gonads can be surgically removed either via orchiectomy (the removal of testes), or oophorectomy (the removal of ovaries) for a variety of reasons. There is no current medical technology that can replace the function of these structures, although patients can be placed on hormone replacement to counter the negative physiologic consequences resulting from their removal.
Secondary sex determination, or sexual differentiation, is the development of external genitalia and internal genital tracts because of the hormones produced from the gonads. At puberty, further differentiation occurs with the development of pubic and axillary hair and breast growth. This process determines phenotypic sex – the visible distinction between male and female.
When opponents of gender affirming care state that individuals cannot change sex, are they correct or false? The answer to this question is entirely dependent on which definition of sex they are using. Chromosomal? Gonadal? Phenotypic? It is an immutable fact that humans cannot change chromosomal sex. No one in the transgender community, either provider or patient, would dispute this. However, we can remove gonadal structures and alter phenotypic sex.
In fact, many cisgender individuals also revise their phenotypic sex when they undergo augmentation mammaplasty, penile enlargement, or vulvoplasty procedures for the exact same reason.
Circling back to the debate about whether we can “assign sex at birth,” it all depends on what definition of sex you are referencing. At birth, obstetrician/gynecologists most often look at the phenotypic sex and make assumptions about the genetic and gonadal sex based on the secondary sexual characteristics. So yes, we can, and we do assign sex at birth. However, in the case of intersex individuals, these physical characteristics may not align with their gonadal and chromosomal composition.
In the case of an infant that has a known XY karyotype prior to birth but a female phenotype at birth (as seen in a condition called complete androgen insensitivity syndrome), what sex should be assigned to that baby? Should the infant be raised male or female? A lot of unintended but significant harm has resulted from providers and parents trying to answer that very question. The mistreatment of intersex patients through forced and coercive medical and surgical treatments, often in infancy, should serve as a dark reminder that sex and gender are not as biologically binary as we would like to believe.
Dr. Brandt is an ob.gyn. and fellowship-trained gender-affirming surgeon in West Reading, Pa. She has no relevant disclosures.
References
Moore KL and Persaud TVN. The urogenital system. In: Before we are born: essentials of embryology and birth defects. 7th ed. Philadelphia: Saunders Elsevier;2008:163-89.
Standring S. Development of the urogenital system. In: Gray’s Anatomy, 42nd ed. Philadelphia: Elsevier;2021:341-64.
Escobar O et al. Pediatric endocrinology. In: Zitelli BJ, ed. Zitelli and Davis’ atlas of pediatric physical diagnosis 8th edition. Philadelphia: Elsevier;2023:342-81.
Knowing the sex of a developing fetus is a common question many expectant parents ask at their prenatal appointments. While the sex of a fetus has minimal clinical significance to obstetrician/gynecologists, technology has made ascertaining the answer to this question much more accessible.
In addition to detecting certain genetic abnormalities, both noninvasive prenatal testing (NIPT) and preimplantation genetic testing (PGT) can discern the chromosomal sex of a fetus prior to birth. At the 20-week anatomy scan, the ultrasonographer can detect the presence of external genitalia to determine the sex. In fact, when a baby is first born, obstetrician/gynecologists are consistently asked “do I have a boy or a girl?” Assigning the sex of a newborn is one of the many tasks we complete in the delivery room. However, some of you reading this article would disagree.
“You cannot assign sex at birth.” “Sex is fixed, you cannot change biology.” These are examples of statements that frequent the comments section of my medical articles and plague professionals who treat gender diverse patients. I would argue, as would many biologists, scientists, and physicians, that these statements oversimplify biologic reality.
The term “sex” has multiple meanings: It can allude to the act of reproduction itself, but in the context of sexual determination and sexual differentiation, it can refer to the biologic and structural composition of a developing human. Within this paradigm, there exist three definitions for sex: chromosomal, gonadal, and phenotypic.
Chromosomal sex refers to the genetic makeup of a human, typically XX or XY chromosomes. There are also variations within this seemingly binary system. Embryos can have an extra sex chromosome, as seen in Klinefelter syndrome, which is characterized by XXY karyotype. Embryos can also be devoid of a sex chromosome, as observed in Turner’s syndrome, which is characterized by an XO karyotype. These variations can impact fertility and expression of secondary sexual characteristics as the type of sex chromosomes present results in primary sex determination, or the development of gonads.
Most often, individuals with a chromosomal makeup of XX are considered female and will subsequently develop ovaries that produce oocytes (eggs). Individuals with XY chromosomes are deemed male and will go on to develop testes, which are responsible for spermatogenesis (sperm production).
Gonadal sex is the presence of either testes or ovaries. The primary function of testes is to produce sperm for reproduction and to secrete testosterone, the primary male sex hormone. Similarly, ovaries produce oocytes and secrete estrogen as the primary female sex hormone. Gonads can be surgically removed either via orchiectomy (the removal of testes), or oophorectomy (the removal of ovaries) for a variety of reasons. There is no current medical technology that can replace the function of these structures, although patients can be placed on hormone replacement to counter the negative physiologic consequences resulting from their removal.
Secondary sex determination, or sexual differentiation, is the development of external genitalia and internal genital tracts because of the hormones produced from the gonads. At puberty, further differentiation occurs with the development of pubic and axillary hair and breast growth. This process determines phenotypic sex – the visible distinction between male and female.
When opponents of gender affirming care state that individuals cannot change sex, are they correct or false? The answer to this question is entirely dependent on which definition of sex they are using. Chromosomal? Gonadal? Phenotypic? It is an immutable fact that humans cannot change chromosomal sex. No one in the transgender community, either provider or patient, would dispute this. However, we can remove gonadal structures and alter phenotypic sex.
In fact, many cisgender individuals also revise their phenotypic sex when they undergo augmentation mammaplasty, penile enlargement, or vulvoplasty procedures for the exact same reason.
Circling back to the debate about whether we can “assign sex at birth,” it all depends on what definition of sex you are referencing. At birth, obstetrician/gynecologists most often look at the phenotypic sex and make assumptions about the genetic and gonadal sex based on the secondary sexual characteristics. So yes, we can, and we do assign sex at birth. However, in the case of intersex individuals, these physical characteristics may not align with their gonadal and chromosomal composition.
In the case of an infant that has a known XY karyotype prior to birth but a female phenotype at birth (as seen in a condition called complete androgen insensitivity syndrome), what sex should be assigned to that baby? Should the infant be raised male or female? A lot of unintended but significant harm has resulted from providers and parents trying to answer that very question. The mistreatment of intersex patients through forced and coercive medical and surgical treatments, often in infancy, should serve as a dark reminder that sex and gender are not as biologically binary as we would like to believe.
Dr. Brandt is an ob.gyn. and fellowship-trained gender-affirming surgeon in West Reading, Pa. She has no relevant disclosures.
References
Moore KL and Persaud TVN. The urogenital system. In: Before we are born: essentials of embryology and birth defects. 7th ed. Philadelphia: Saunders Elsevier;2008:163-89.
Standring S. Development of the urogenital system. In: Gray’s Anatomy, 42nd ed. Philadelphia: Elsevier;2021:341-64.
Escobar O et al. Pediatric endocrinology. In: Zitelli BJ, ed. Zitelli and Davis’ atlas of pediatric physical diagnosis 8th edition. Philadelphia: Elsevier;2023:342-81.
New evaluation and management of CPT codes for telemedicine in 2025
. The AMA says the new codes are designed to bring the coding system up to date with the changing landscape of health care and reflect the realities of modern medical practice.
The 17 new CPT codes will encompass a variety of telemedicine services. While the official language of the codes has not been released yet, codes for telemedicine visits using a real-time audio-visual platform could be organized similarly to existing office/outpatient E/M visits (99202-99205, 99212-99215). As part of these revisions, the current telephone E/M codes (99441-99443) will be deleted and replaced with new codes for audio-only E/M.
Implementation of so many codes will require health care providers and systems to adapt their documentation and coding practices. Typically, the exact language and code numbers for new and revised codes are not released to the public until fall of the preceding year, leaving only a few months for practices to educate their physicians and coding staff and prepare their internal systems for implementation starting Jan. 1, 2025. However, given the significant education and systems changes that will be necessary to prepare for so many new codes, we will advocate that the AMA release this information in early 2024.
Additionally, the reimbursement for telemedicine services may not ultimately be the same as for in-person E/M office visits. The AMA/Specialty Society RVS Update Committee (RUC) provides recommendations to the Centers for Medicare & Medicaid Services (CMS) for consideration in developing Relative Value Units (RVUs) for new procedures, including the telemedicine codes. The RUC’s recommendations for the telemedicine codes are not yet publicly available. However, it is important to note that regardless of the RUC recommendations, CMS makes all final decisions about Medicare payment. CMS could decide to set the payments for the telemedicine codes at parity with in-person office E/M visits or less than, more than, or some combination at the individual code level.
If payments for telemedicine visits are set at parity with or higher than office E/M visits, practices can focus primarily on physician and staff education and system implementation of the new codes. However, if telemedicine visit payments are less than in-person E/M office visits, it would have significant implications for practices, providers, and patients. Providers might be discouraged from offering virtual care, leading to a disparity in the availability of telehealth services, with patients in some areas or with certain conditions having limited access. Additionally, not all patients have access to a smartphone or stable internet. Research has shown increased use of audio-only visits among marginalized groups including African Americans, non-English speakers, older patients, those with public insurance as opposed to private insurance and patients living in rural communities and communities with low broadband access. For these patients, audio-only is a lifeline that allows them to access needed care.
Hughes HK, Hasselfeld BW, Greene JA. Health Care Access on the Line - Audio-Only Visits and Digitally Inclusive Care. N Engl J Med. 2022 Nov 17;387(20):1823-1826. doi: 10.1056/NEJMp2118292. Epub 2022 Nov 12. PMID: 36373819.
Chen J, Li KY, Andino J, Hill CE, Ng S, Steppe E, Ellimoottil C. Predictors of Audio-Only Versus Video Telehealth Visits During the COVID-19 Pandemic. J Gen Intern Med. 2022 Apr;37(5):1138-1144. doi: 10.1007/s11606-021-07172-y. Epub 2021 Nov 17. PMID: 34791589; PMCID: PMC8597874.
If payment for audio-only is significantly less than in-person office E/M payments, practices may not offer this option furthering health care inequities.
Beyond the extensive preparation needed and the financial implications, there could be impacts to coverage policies. Currently, telemedicine coverage is triggered by reporting the appropriate office E/M level visit with telemedicine modifier 95. If the new telemedicine codes are no longer tied to the in-person codes, laws requiring payers to provide coverage and parity may need to be adjusted accordingly or they could become less effective. If coverage parity is not maintained, that may lead to changes in practice that could also worsen access and health disparities. Some insurers have already started rolling back coverages. Recently, Aetna decided to stop covering telemedicine visits as of Dec. 1, 2023.
Other insurers may follow suit.
As practices prepare for 2024, tracking insurance coverage policies for telemedicine, staying alert for information from the AMA about the new telemedicine CPT codes, and monitoring the proposed payments for telemedicine that CMS will release in late June to early July in the 2025 Medicare Physician Fee Schedule proposed rule will be important. Participation in advocacy efforts will be critical once the full details are released by the AMA and CMS about the new telemedicine codes and their proposed values. The AGA is monitoring this issue and will continue to fight to reduce burden to physicians and practices, which includes fighting for payment parity with in-person office E/M visits and maintaining coverage benefits for patients.
The authors have reported no conflicts of interest.
. The AMA says the new codes are designed to bring the coding system up to date with the changing landscape of health care and reflect the realities of modern medical practice.
The 17 new CPT codes will encompass a variety of telemedicine services. While the official language of the codes has not been released yet, codes for telemedicine visits using a real-time audio-visual platform could be organized similarly to existing office/outpatient E/M visits (99202-99205, 99212-99215). As part of these revisions, the current telephone E/M codes (99441-99443) will be deleted and replaced with new codes for audio-only E/M.
Implementation of so many codes will require health care providers and systems to adapt their documentation and coding practices. Typically, the exact language and code numbers for new and revised codes are not released to the public until fall of the preceding year, leaving only a few months for practices to educate their physicians and coding staff and prepare their internal systems for implementation starting Jan. 1, 2025. However, given the significant education and systems changes that will be necessary to prepare for so many new codes, we will advocate that the AMA release this information in early 2024.
Additionally, the reimbursement for telemedicine services may not ultimately be the same as for in-person E/M office visits. The AMA/Specialty Society RVS Update Committee (RUC) provides recommendations to the Centers for Medicare & Medicaid Services (CMS) for consideration in developing Relative Value Units (RVUs) for new procedures, including the telemedicine codes. The RUC’s recommendations for the telemedicine codes are not yet publicly available. However, it is important to note that regardless of the RUC recommendations, CMS makes all final decisions about Medicare payment. CMS could decide to set the payments for the telemedicine codes at parity with in-person office E/M visits or less than, more than, or some combination at the individual code level.
If payments for telemedicine visits are set at parity with or higher than office E/M visits, practices can focus primarily on physician and staff education and system implementation of the new codes. However, if telemedicine visit payments are less than in-person E/M office visits, it would have significant implications for practices, providers, and patients. Providers might be discouraged from offering virtual care, leading to a disparity in the availability of telehealth services, with patients in some areas or with certain conditions having limited access. Additionally, not all patients have access to a smartphone or stable internet. Research has shown increased use of audio-only visits among marginalized groups including African Americans, non-English speakers, older patients, those with public insurance as opposed to private insurance and patients living in rural communities and communities with low broadband access. For these patients, audio-only is a lifeline that allows them to access needed care.
Hughes HK, Hasselfeld BW, Greene JA. Health Care Access on the Line - Audio-Only Visits and Digitally Inclusive Care. N Engl J Med. 2022 Nov 17;387(20):1823-1826. doi: 10.1056/NEJMp2118292. Epub 2022 Nov 12. PMID: 36373819.
Chen J, Li KY, Andino J, Hill CE, Ng S, Steppe E, Ellimoottil C. Predictors of Audio-Only Versus Video Telehealth Visits During the COVID-19 Pandemic. J Gen Intern Med. 2022 Apr;37(5):1138-1144. doi: 10.1007/s11606-021-07172-y. Epub 2021 Nov 17. PMID: 34791589; PMCID: PMC8597874.
If payment for audio-only is significantly less than in-person office E/M payments, practices may not offer this option furthering health care inequities.
Beyond the extensive preparation needed and the financial implications, there could be impacts to coverage policies. Currently, telemedicine coverage is triggered by reporting the appropriate office E/M level visit with telemedicine modifier 95. If the new telemedicine codes are no longer tied to the in-person codes, laws requiring payers to provide coverage and parity may need to be adjusted accordingly or they could become less effective. If coverage parity is not maintained, that may lead to changes in practice that could also worsen access and health disparities. Some insurers have already started rolling back coverages. Recently, Aetna decided to stop covering telemedicine visits as of Dec. 1, 2023.
Other insurers may follow suit.
As practices prepare for 2024, tracking insurance coverage policies for telemedicine, staying alert for information from the AMA about the new telemedicine CPT codes, and monitoring the proposed payments for telemedicine that CMS will release in late June to early July in the 2025 Medicare Physician Fee Schedule proposed rule will be important. Participation in advocacy efforts will be critical once the full details are released by the AMA and CMS about the new telemedicine codes and their proposed values. The AGA is monitoring this issue and will continue to fight to reduce burden to physicians and practices, which includes fighting for payment parity with in-person office E/M visits and maintaining coverage benefits for patients.
The authors have reported no conflicts of interest.
. The AMA says the new codes are designed to bring the coding system up to date with the changing landscape of health care and reflect the realities of modern medical practice.
The 17 new CPT codes will encompass a variety of telemedicine services. While the official language of the codes has not been released yet, codes for telemedicine visits using a real-time audio-visual platform could be organized similarly to existing office/outpatient E/M visits (99202-99205, 99212-99215). As part of these revisions, the current telephone E/M codes (99441-99443) will be deleted and replaced with new codes for audio-only E/M.
Implementation of so many codes will require health care providers and systems to adapt their documentation and coding practices. Typically, the exact language and code numbers for new and revised codes are not released to the public until fall of the preceding year, leaving only a few months for practices to educate their physicians and coding staff and prepare their internal systems for implementation starting Jan. 1, 2025. However, given the significant education and systems changes that will be necessary to prepare for so many new codes, we will advocate that the AMA release this information in early 2024.
Additionally, the reimbursement for telemedicine services may not ultimately be the same as for in-person E/M office visits. The AMA/Specialty Society RVS Update Committee (RUC) provides recommendations to the Centers for Medicare & Medicaid Services (CMS) for consideration in developing Relative Value Units (RVUs) for new procedures, including the telemedicine codes. The RUC’s recommendations for the telemedicine codes are not yet publicly available. However, it is important to note that regardless of the RUC recommendations, CMS makes all final decisions about Medicare payment. CMS could decide to set the payments for the telemedicine codes at parity with in-person office E/M visits or less than, more than, or some combination at the individual code level.
If payments for telemedicine visits are set at parity with or higher than office E/M visits, practices can focus primarily on physician and staff education and system implementation of the new codes. However, if telemedicine visit payments are less than in-person E/M office visits, it would have significant implications for practices, providers, and patients. Providers might be discouraged from offering virtual care, leading to a disparity in the availability of telehealth services, with patients in some areas or with certain conditions having limited access. Additionally, not all patients have access to a smartphone or stable internet. Research has shown increased use of audio-only visits among marginalized groups including African Americans, non-English speakers, older patients, those with public insurance as opposed to private insurance and patients living in rural communities and communities with low broadband access. For these patients, audio-only is a lifeline that allows them to access needed care.
Hughes HK, Hasselfeld BW, Greene JA. Health Care Access on the Line - Audio-Only Visits and Digitally Inclusive Care. N Engl J Med. 2022 Nov 17;387(20):1823-1826. doi: 10.1056/NEJMp2118292. Epub 2022 Nov 12. PMID: 36373819.
Chen J, Li KY, Andino J, Hill CE, Ng S, Steppe E, Ellimoottil C. Predictors of Audio-Only Versus Video Telehealth Visits During the COVID-19 Pandemic. J Gen Intern Med. 2022 Apr;37(5):1138-1144. doi: 10.1007/s11606-021-07172-y. Epub 2021 Nov 17. PMID: 34791589; PMCID: PMC8597874.
If payment for audio-only is significantly less than in-person office E/M payments, practices may not offer this option furthering health care inequities.
Beyond the extensive preparation needed and the financial implications, there could be impacts to coverage policies. Currently, telemedicine coverage is triggered by reporting the appropriate office E/M level visit with telemedicine modifier 95. If the new telemedicine codes are no longer tied to the in-person codes, laws requiring payers to provide coverage and parity may need to be adjusted accordingly or they could become less effective. If coverage parity is not maintained, that may lead to changes in practice that could also worsen access and health disparities. Some insurers have already started rolling back coverages. Recently, Aetna decided to stop covering telemedicine visits as of Dec. 1, 2023.
Other insurers may follow suit.
As practices prepare for 2024, tracking insurance coverage policies for telemedicine, staying alert for information from the AMA about the new telemedicine CPT codes, and monitoring the proposed payments for telemedicine that CMS will release in late June to early July in the 2025 Medicare Physician Fee Schedule proposed rule will be important. Participation in advocacy efforts will be critical once the full details are released by the AMA and CMS about the new telemedicine codes and their proposed values. The AGA is monitoring this issue and will continue to fight to reduce burden to physicians and practices, which includes fighting for payment parity with in-person office E/M visits and maintaining coverage benefits for patients.
The authors have reported no conflicts of interest.
Hypertensive disorders of pregnancy and high stroke risk in Black women
I’d like to talk with you about a recent report from the large-scale Black Women’s Health Study, published in the new journal NEJM Evidence.
This study looked at the association between hypertensive disorders of pregnancy, including preeclampsia and gestational hypertension, and the risk for stroke over the next 20 (median, 22) years. Previous studies have linked hypertensive disorders of pregnancy with an increased risk for stroke. However, most of these studies have been done in White women of European ancestry, and evidence in Black women has been very limited, despite a disproportionately high risk of having a hypertensive disorder of pregnancy and also of stroke.
We know that pregnancy itself can lead to some remodeling of the vascular system, but we don’t know whether a direct causal relationship exists between preeclampsia or gestational hypertension and subsequent stroke. Another potential explanation is that these complications of pregnancy serve as a window into a woman’s future cardiometabolic health and a marker of her cardiovascular risk.
Regardless, the clinical implications are the same. First, we would want to prevent these complications of pregnancy whenever possible. Some women will be candidates for the use of aspirin if they are at high risk for preeclampsia, and certainly for monitoring blood pressure very closely during pregnancy. It will also be important to maintain blood pressure control in the postpartum period and during the subsequent years of adulthood to minimize risk for stroke, because hypertension is such a powerful risk factor for stroke.
It will also be tremendously important to intensify lifestyle modifications such as increasing physical activity and having a heart-healthy diet. These complications of pregnancy have also been linked in other studies to an increased risk for subsequent coronary heart disease events and heart failure.
This transcript has been edited for clarity.
Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and chief of the division of preventive medicine, Brigham and Women’s Hospital, both in Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).
A version of this article appeared on Medscape.com.
I’d like to talk with you about a recent report from the large-scale Black Women’s Health Study, published in the new journal NEJM Evidence.
This study looked at the association between hypertensive disorders of pregnancy, including preeclampsia and gestational hypertension, and the risk for stroke over the next 20 (median, 22) years. Previous studies have linked hypertensive disorders of pregnancy with an increased risk for stroke. However, most of these studies have been done in White women of European ancestry, and evidence in Black women has been very limited, despite a disproportionately high risk of having a hypertensive disorder of pregnancy and also of stroke.
We know that pregnancy itself can lead to some remodeling of the vascular system, but we don’t know whether a direct causal relationship exists between preeclampsia or gestational hypertension and subsequent stroke. Another potential explanation is that these complications of pregnancy serve as a window into a woman’s future cardiometabolic health and a marker of her cardiovascular risk.
Regardless, the clinical implications are the same. First, we would want to prevent these complications of pregnancy whenever possible. Some women will be candidates for the use of aspirin if they are at high risk for preeclampsia, and certainly for monitoring blood pressure very closely during pregnancy. It will also be important to maintain blood pressure control in the postpartum period and during the subsequent years of adulthood to minimize risk for stroke, because hypertension is such a powerful risk factor for stroke.
It will also be tremendously important to intensify lifestyle modifications such as increasing physical activity and having a heart-healthy diet. These complications of pregnancy have also been linked in other studies to an increased risk for subsequent coronary heart disease events and heart failure.
This transcript has been edited for clarity.
Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and chief of the division of preventive medicine, Brigham and Women’s Hospital, both in Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).
A version of this article appeared on Medscape.com.
I’d like to talk with you about a recent report from the large-scale Black Women’s Health Study, published in the new journal NEJM Evidence.
This study looked at the association between hypertensive disorders of pregnancy, including preeclampsia and gestational hypertension, and the risk for stroke over the next 20 (median, 22) years. Previous studies have linked hypertensive disorders of pregnancy with an increased risk for stroke. However, most of these studies have been done in White women of European ancestry, and evidence in Black women has been very limited, despite a disproportionately high risk of having a hypertensive disorder of pregnancy and also of stroke.
We know that pregnancy itself can lead to some remodeling of the vascular system, but we don’t know whether a direct causal relationship exists between preeclampsia or gestational hypertension and subsequent stroke. Another potential explanation is that these complications of pregnancy serve as a window into a woman’s future cardiometabolic health and a marker of her cardiovascular risk.
Regardless, the clinical implications are the same. First, we would want to prevent these complications of pregnancy whenever possible. Some women will be candidates for the use of aspirin if they are at high risk for preeclampsia, and certainly for monitoring blood pressure very closely during pregnancy. It will also be important to maintain blood pressure control in the postpartum period and during the subsequent years of adulthood to minimize risk for stroke, because hypertension is such a powerful risk factor for stroke.
It will also be tremendously important to intensify lifestyle modifications such as increasing physical activity and having a heart-healthy diet. These complications of pregnancy have also been linked in other studies to an increased risk for subsequent coronary heart disease events and heart failure.
This transcript has been edited for clarity.
Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and chief of the division of preventive medicine, Brigham and Women’s Hospital, both in Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).
A version of this article appeared on Medscape.com.