Commentary

This transcript has been edited for clarity. 

Giving patients a beta-blocker after a myocardial infarction is standard of care. It’s in the guidelines. It’s one of the performance measures used by the American College of Cardiology (ACC) and the American Heart Association (AHA). If you aren’t putting your post–acute coronary syndrome (ACS) patients on a beta-blocker, the ACC and the AHA both think you suck. 

They are very disappointed in you, just like your mother was when you told her you didn’t want to become a surgeon because you don’t like waking up early, your hands shake when you get nervous, it’s not your fault, there’s nothing you can do about it, so just leave me alone!

The data on beta-blockers are decades old. In the time before stents, statins, angiotensin-converting enzyme inhibitors, and dual antiplatelet therapy, when patients either died or got better on their own, beta-blockers showed major benefits. Studies like the Norwegian Multicenter Study Group, the BHAT trial, and the ISIS-1 trial proved the benefits of beta blockade. These studies date back to the 1980s, when you could call a study ISIS without controversy. 

It was a simpler time, when all you had to worry about was the Cold War, apartheid, and the global AIDS pandemic. It was a time when doctors smoked in their offices, and patients had bigger infarcts that caused large scars and systolic dysfunction. That world is no longer our world, except for the war, the global pandemic, and the out-of-control gas prices. 

The reality is that, before troponins, we probably missed most small heart attacks. Now, most infarcts are small, and most patients walk away from their heart attacks with essentially normal hearts. Do beta-blockers still matter? If you’re a fan of Cochrane reviews, the answer is yes. 

In 2021, Cochrane published a review of beta-blockers in patients without heart failure after myocardial infarction (MI). The authors of that analysis concluded, after the usual caveats about heterogeneity, potential bias, and the whims of a random universe, that, yes, beta-blockers do reduce mortality. The risk ratio for max all-cause mortality was 0.81. 

What does that mean practically? The absolute risk was reduced from 10.9% to 8.7%, a 2.2–percentage point absolute decrease and about a 20% relative drop. A little math gives us a third number: 46. That’s the number needed to treat. If you think about how many patients you admit during a typical week of critical care unit with an MI, a number needed to treat of 46 is a pretty good trade-off for a fairly inexpensive medication with fairly minimal side effects. 

Of course, these are the same people who claim that masks don’t stop the spread of COVID-19. Sure, were they the only people who thought that handwashing was the best way to stop a respiratory virus? No. We all believed that fantasy for far longer than we should have. Not everybody can bat a thousand, if by batting a thousand, you mean reflecting on how your words will impact on a broader population primed to believe misinformation because of the increasingly toxic social media environment and worsening politicization and radicalization of our politics. 

By the way, if any of you want to come to Canada, you can stay with me. Things are incrementally better here. In this day and age, incrementally better is the best we can hope for. 

Here’s the wrinkle with the Cochrane beta-blocker review: Many of the studies took place before early revascularization became the norm and before our current armamentarium of drugs became standard of care. 

Back in the day, bed rest and the power of positive thinking were the mainstays of cardiac treatment. Also, many of these studies mixed together ST-segment MI (STEMI) and non-STEMI patients, so you’re obviously going to see more benefits in STEMI patients who are at higher risk. Some of them used intravenous (IV) beta-blockers right away, whereas some were looking only at oral beta-blockers started days after the infarct. 

We don’t use IV beta-blockers that much anymore because of the risk for shock. 

Also, some studies had short-term follow-up where the benefits were less pronounced, and some studies used doses and types of beta-blockers rarely used today. Some of the studies had a mix of coronary and heart failure patients, which muddies the water because the heart failure patients would clearly benefit from being on a beta-blocker. 

Basically, the data are not definitive because they are old and don’t reflect our current standard of care. The data contain a heterogeneous mix of patients that aren’t really relevant to the question that we’re asking. The question we’re asking is, should you put all your post-MI patients on a beta-blocker routinely, even if they don’t have heart failure? 

The REDUCE-AMI trial is the first of a few trials testing, or to be more accurate, retesting, whether beta-blockers are useful after an MI. BETAMI, REBOOT, DANBLOCK— you’ll be hearing these names in the next few years, either because the studies get published or because they’re the Twitter handles of people harassing you online. Either/or. (By the way, I’ll be cold in my grave before I call it X.) 

For now, REDUCE-AMI is the first across the finish line, and at least in cardiology, finishing first is a good thing. This study enrolled patients with ACS, both STEMI and non-STEMI, with a post-MI ejection fraction ≥ 50%, and the result was nothing. The risk ratio for all-cause mortality was 0.94 and was not statistically significant. 

In absolute terms, that’s a reduction from 4.1% to 3.9%, or a 0.2–percentage point decrease; this translates into a number needed to treat of 500, which is 10 times higher than what the Cochrane review found. That’s if you assume that there is, in fact, a small benefit amidst all the statistical noise, which there probably isn’t. 

Now, studies like this can never rule out small effects, either positive or negative, so maybe there is a small benefit from using beta-blockers. If it’s there, it’s really small. Do beta-blockers work? Well, yes, obviously, for heart failure and atrial fibrillation — which, let’s face it, are not exactly rare and often coexist in patients with heart disease. They probably aren’t that great as blood pressure pills, but that’s a story for another day and another video. 

Yes, beta-blockers are useful pills, and they are standard of care, just maybe not for post-MI patients with normal ejection fractions because they probably don’t really need them. They worked in the pre-stent, pre-aspirin, pre-anything era. 

That’s not our world anymore. Things change. It’s not the 1980s. That’s why I don’t have a mullet, and that’s why you need to update your kitchen. 
 

Dr. Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Giving patients a beta-blocker after a myocardial infarction is standard of care. It’s in the guidelines. It’s one of the performance measures used by the American College of Cardiology (ACC) and the American Heart Association (AHA). If you aren’t putting your post–acute coronary syndrome (ACS) patients on a beta-blocker, the ACC and the AHA both think you suck. 

They are very disappointed in you, just like your mother was when you told her you didn’t want to become a surgeon because you don’t like waking up early, your hands shake when you get nervous, it’s not your fault, there’s nothing you can do about it, so just leave me alone!

The data on beta-blockers are decades old. In the time before stents, statins, angiotensin-converting enzyme inhibitors, and dual antiplatelet therapy, when patients either died or got better on their own, beta-blockers showed major benefits. Studies like the Norwegian Multicenter Study Group, the BHAT trial, and the ISIS-1 trial proved the benefits of beta blockade. These studies date back to the 1980s, when you could call a study ISIS without controversy. 

It was a simpler time, when all you had to worry about was the Cold War, apartheid, and the global AIDS pandemic. It was a time when doctors smoked in their offices, and patients had bigger infarcts that caused large scars and systolic dysfunction. That world is no longer our world, except for the war, the global pandemic, and the out-of-control gas prices. 

The reality is that, before troponins, we probably missed most small heart attacks. Now, most infarcts are small, and most patients walk away from their heart attacks with essentially normal hearts. Do beta-blockers still matter? If you’re a fan of Cochrane reviews, the answer is yes. 

In 2021, Cochrane published a review of beta-blockers in patients without heart failure after myocardial infarction (MI). The authors of that analysis concluded, after the usual caveats about heterogeneity, potential bias, and the whims of a random universe, that, yes, beta-blockers do reduce mortality. The risk ratio for max all-cause mortality was 0.81. 

What does that mean practically? The absolute risk was reduced from 10.9% to 8.7%, a 2.2–percentage point absolute decrease and about a 20% relative drop. A little math gives us a third number: 46. That’s the number needed to treat. If you think about how many patients you admit during a typical week of critical care unit with an MI, a number needed to treat of 46 is a pretty good trade-off for a fairly inexpensive medication with fairly minimal side effects. 

Of course, these are the same people who claim that masks don’t stop the spread of COVID-19. Sure, were they the only people who thought that handwashing was the best way to stop a respiratory virus? No. We all believed that fantasy for far longer than we should have. Not everybody can bat a thousand, if by batting a thousand, you mean reflecting on how your words will impact on a broader population primed to believe misinformation because of the increasingly toxic social media environment and worsening politicization and radicalization of our politics. 

By the way, if any of you want to come to Canada, you can stay with me. Things are incrementally better here. In this day and age, incrementally better is the best we can hope for. 

Here’s the wrinkle with the Cochrane beta-blocker review: Many of the studies took place before early revascularization became the norm and before our current armamentarium of drugs became standard of care. 

Back in the day, bed rest and the power of positive thinking were the mainstays of cardiac treatment. Also, many of these studies mixed together ST-segment MI (STEMI) and non-STEMI patients, so you’re obviously going to see more benefits in STEMI patients who are at higher risk. Some of them used intravenous (IV) beta-blockers right away, whereas some were looking only at oral beta-blockers started days after the infarct. 

We don’t use IV beta-blockers that much anymore because of the risk for shock. 

Also, some studies had short-term follow-up where the benefits were less pronounced, and some studies used doses and types of beta-blockers rarely used today. Some of the studies had a mix of coronary and heart failure patients, which muddies the water because the heart failure patients would clearly benefit from being on a beta-blocker. 

Basically, the data are not definitive because they are old and don’t reflect our current standard of care. The data contain a heterogeneous mix of patients that aren’t really relevant to the question that we’re asking. The question we’re asking is, should you put all your post-MI patients on a beta-blocker routinely, even if they don’t have heart failure? 

The REDUCE-AMI trial is the first of a few trials testing, or to be more accurate, retesting, whether beta-blockers are useful after an MI. BETAMI, REBOOT, DANBLOCK— you’ll be hearing these names in the next few years, either because the studies get published or because they’re the Twitter handles of people harassing you online. Either/or. (By the way, I’ll be cold in my grave before I call it X.) 

For now, REDUCE-AMI is the first across the finish line, and at least in cardiology, finishing first is a good thing. This study enrolled patients with ACS, both STEMI and non-STEMI, with a post-MI ejection fraction ≥ 50%, and the result was nothing. The risk ratio for all-cause mortality was 0.94 and was not statistically significant. 

In absolute terms, that’s a reduction from 4.1% to 3.9%, or a 0.2–percentage point decrease; this translates into a number needed to treat of 500, which is 10 times higher than what the Cochrane review found. That’s if you assume that there is, in fact, a small benefit amidst all the statistical noise, which there probably isn’t. 

Now, studies like this can never rule out small effects, either positive or negative, so maybe there is a small benefit from using beta-blockers. If it’s there, it’s really small. Do beta-blockers work? Well, yes, obviously, for heart failure and atrial fibrillation — which, let’s face it, are not exactly rare and often coexist in patients with heart disease. They probably aren’t that great as blood pressure pills, but that’s a story for another day and another video. 

Yes, beta-blockers are useful pills, and they are standard of care, just maybe not for post-MI patients with normal ejection fractions because they probably don’t really need them. They worked in the pre-stent, pre-aspirin, pre-anything era. 

That’s not our world anymore. Things change. It’s not the 1980s. That’s why I don’t have a mullet, and that’s why you need to update your kitchen. 
 

Dr. Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Giving patients a beta-blocker after a myocardial infarction is standard of care. It’s in the guidelines. It’s one of the performance measures used by the American College of Cardiology (ACC) and the American Heart Association (AHA). If you aren’t putting your post–acute coronary syndrome (ACS) patients on a beta-blocker, the ACC and the AHA both think you suck. 

They are very disappointed in you, just like your mother was when you told her you didn’t want to become a surgeon because you don’t like waking up early, your hands shake when you get nervous, it’s not your fault, there’s nothing you can do about it, so just leave me alone!

The data on beta-blockers are decades old. In the time before stents, statins, angiotensin-converting enzyme inhibitors, and dual antiplatelet therapy, when patients either died or got better on their own, beta-blockers showed major benefits. Studies like the Norwegian Multicenter Study Group, the BHAT trial, and the ISIS-1 trial proved the benefits of beta blockade. These studies date back to the 1980s, when you could call a study ISIS without controversy. 

It was a simpler time, when all you had to worry about was the Cold War, apartheid, and the global AIDS pandemic. It was a time when doctors smoked in their offices, and patients had bigger infarcts that caused large scars and systolic dysfunction. That world is no longer our world, except for the war, the global pandemic, and the out-of-control gas prices. 

The reality is that, before troponins, we probably missed most small heart attacks. Now, most infarcts are small, and most patients walk away from their heart attacks with essentially normal hearts. Do beta-blockers still matter? If you’re a fan of Cochrane reviews, the answer is yes. 

In 2021, Cochrane published a review of beta-blockers in patients without heart failure after myocardial infarction (MI). The authors of that analysis concluded, after the usual caveats about heterogeneity, potential bias, and the whims of a random universe, that, yes, beta-blockers do reduce mortality. The risk ratio for max all-cause mortality was 0.81. 

What does that mean practically? The absolute risk was reduced from 10.9% to 8.7%, a 2.2–percentage point absolute decrease and about a 20% relative drop. A little math gives us a third number: 46. That’s the number needed to treat. If you think about how many patients you admit during a typical week of critical care unit with an MI, a number needed to treat of 46 is a pretty good trade-off for a fairly inexpensive medication with fairly minimal side effects. 

Of course, these are the same people who claim that masks don’t stop the spread of COVID-19. Sure, were they the only people who thought that handwashing was the best way to stop a respiratory virus? No. We all believed that fantasy for far longer than we should have. Not everybody can bat a thousand, if by batting a thousand, you mean reflecting on how your words will impact on a broader population primed to believe misinformation because of the increasingly toxic social media environment and worsening politicization and radicalization of our politics. 

By the way, if any of you want to come to Canada, you can stay with me. Things are incrementally better here. In this day and age, incrementally better is the best we can hope for. 

Here’s the wrinkle with the Cochrane beta-blocker review: Many of the studies took place before early revascularization became the norm and before our current armamentarium of drugs became standard of care. 

Back in the day, bed rest and the power of positive thinking were the mainstays of cardiac treatment. Also, many of these studies mixed together ST-segment MI (STEMI) and non-STEMI patients, so you’re obviously going to see more benefits in STEMI patients who are at higher risk. Some of them used intravenous (IV) beta-blockers right away, whereas some were looking only at oral beta-blockers started days after the infarct. 

We don’t use IV beta-blockers that much anymore because of the risk for shock. 

Also, some studies had short-term follow-up where the benefits were less pronounced, and some studies used doses and types of beta-blockers rarely used today. Some of the studies had a mix of coronary and heart failure patients, which muddies the water because the heart failure patients would clearly benefit from being on a beta-blocker. 

Basically, the data are not definitive because they are old and don’t reflect our current standard of care. The data contain a heterogeneous mix of patients that aren’t really relevant to the question that we’re asking. The question we’re asking is, should you put all your post-MI patients on a beta-blocker routinely, even if they don’t have heart failure? 

The REDUCE-AMI trial is the first of a few trials testing, or to be more accurate, retesting, whether beta-blockers are useful after an MI. BETAMI, REBOOT, DANBLOCK— you’ll be hearing these names in the next few years, either because the studies get published or because they’re the Twitter handles of people harassing you online. Either/or. (By the way, I’ll be cold in my grave before I call it X.) 

For now, REDUCE-AMI is the first across the finish line, and at least in cardiology, finishing first is a good thing. This study enrolled patients with ACS, both STEMI and non-STEMI, with a post-MI ejection fraction ≥ 50%, and the result was nothing. The risk ratio for all-cause mortality was 0.94 and was not statistically significant. 

In absolute terms, that’s a reduction from 4.1% to 3.9%, or a 0.2–percentage point decrease; this translates into a number needed to treat of 500, which is 10 times higher than what the Cochrane review found. That’s if you assume that there is, in fact, a small benefit amidst all the statistical noise, which there probably isn’t. 

Now, studies like this can never rule out small effects, either positive or negative, so maybe there is a small benefit from using beta-blockers. If it’s there, it’s really small. Do beta-blockers work? Well, yes, obviously, for heart failure and atrial fibrillation — which, let’s face it, are not exactly rare and often coexist in patients with heart disease. They probably aren’t that great as blood pressure pills, but that’s a story for another day and another video. 

Yes, beta-blockers are useful pills, and they are standard of care, just maybe not for post-MI patients with normal ejection fractions because they probably don’t really need them. They worked in the pre-stent, pre-aspirin, pre-anything era. 

That’s not our world anymore. Things change. It’s not the 1980s. That’s why I don’t have a mullet, and that’s why you need to update your kitchen. 
 

Dr. Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The field of GI is rapidly evolving, fueled by new scientific discoveries leading to improved understanding of disease mechanisms and more effective treatment approaches for patients with digestive and liver diseases. But there are many challenges confronting the pipeline of early-career investigators essential to future discovery, most notably a constrained funding environment leading to decreased protected time for research during these critical early years.

Foundation awards, such as those funded by the AGA Research Foundation, play a pivotal role in supporting the career development of promising young investigators in basic, translational, clinical, and health services research and ensure that we have a strong pipeline of independent investigators to stimulate ongoing discovery and innovation in our field. This year, the AGA Research Foundation distributed $2.6 million in funding to 76 investigators, including six coveted Research Scholar Awards awarded to early-career investigators. These promising young researchers represent the best and the brightest in our field — I hope you enjoy learning more about them in the pages of this issue and will join me in continuing to support the Foundation and its work under the leadership of Dr. Michael Camilleri.

University of Michigan

Also in our August issue, we bring you continued coverage from DDW and June’s EASL Congress, and report on innovative science published in AGA’s flagship journals, including a study investigating the impact of H pylori eradication on esophageal cancer risk. We also highlight several important studies relating to eosinophilic esophagitis, including a recent RCT published in The New England Journal of Medicine demonstrating the effectiveness of dupilumab in treatment of PPI-refractory pediatric EoE. Our August Member Spotlight features Dr. Neelendu Dey of Fred Hutchinson Cancer Center, who shares his perspectives on pursuing a career as a physician-scientist and chronicles his research focused on harnessing the microbiome for cancer prevention.

Finally, our quarterly In Focus column from The New Gastroenterologist provides practical advice regarding how best to evaluate patients with chronic bloating symptoms, a frequent presentation in our GI clinics. As always, thanks for reading and please don’t hesitate to reach out with suggestions for future coverage.
 

Megan A. Adams, MD, JD, MSc

Editor in Chief

The field of GI is rapidly evolving, fueled by new scientific discoveries leading to improved understanding of disease mechanisms and more effective treatment approaches for patients with digestive and liver diseases. But there are many challenges confronting the pipeline of early-career investigators essential to future discovery, most notably a constrained funding environment leading to decreased protected time for research during these critical early years.

Foundation awards, such as those funded by the AGA Research Foundation, play a pivotal role in supporting the career development of promising young investigators in basic, translational, clinical, and health services research and ensure that we have a strong pipeline of independent investigators to stimulate ongoing discovery and innovation in our field. This year, the AGA Research Foundation distributed $2.6 million in funding to 76 investigators, including six coveted Research Scholar Awards awarded to early-career investigators. These promising young researchers represent the best and the brightest in our field — I hope you enjoy learning more about them in the pages of this issue and will join me in continuing to support the Foundation and its work under the leadership of Dr. Michael Camilleri.

University of Michigan

Also in our August issue, we bring you continued coverage from DDW and June’s EASL Congress, and report on innovative science published in AGA’s flagship journals, including a study investigating the impact of H pylori eradication on esophageal cancer risk. We also highlight several important studies relating to eosinophilic esophagitis, including a recent RCT published in The New England Journal of Medicine demonstrating the effectiveness of dupilumab in treatment of PPI-refractory pediatric EoE. Our August Member Spotlight features Dr. Neelendu Dey of Fred Hutchinson Cancer Center, who shares his perspectives on pursuing a career as a physician-scientist and chronicles his research focused on harnessing the microbiome for cancer prevention.

Finally, our quarterly In Focus column from The New Gastroenterologist provides practical advice regarding how best to evaluate patients with chronic bloating symptoms, a frequent presentation in our GI clinics. As always, thanks for reading and please don’t hesitate to reach out with suggestions for future coverage.
 

Megan A. Adams, MD, JD, MSc

Editor in Chief

The field of GI is rapidly evolving, fueled by new scientific discoveries leading to improved understanding of disease mechanisms and more effective treatment approaches for patients with digestive and liver diseases. But there are many challenges confronting the pipeline of early-career investigators essential to future discovery, most notably a constrained funding environment leading to decreased protected time for research during these critical early years.

Foundation awards, such as those funded by the AGA Research Foundation, play a pivotal role in supporting the career development of promising young investigators in basic, translational, clinical, and health services research and ensure that we have a strong pipeline of independent investigators to stimulate ongoing discovery and innovation in our field. This year, the AGA Research Foundation distributed $2.6 million in funding to 76 investigators, including six coveted Research Scholar Awards awarded to early-career investigators. These promising young researchers represent the best and the brightest in our field — I hope you enjoy learning more about them in the pages of this issue and will join me in continuing to support the Foundation and its work under the leadership of Dr. Michael Camilleri.

University of Michigan

Also in our August issue, we bring you continued coverage from DDW and June’s EASL Congress, and report on innovative science published in AGA’s flagship journals, including a study investigating the impact of H pylori eradication on esophageal cancer risk. We also highlight several important studies relating to eosinophilic esophagitis, including a recent RCT published in The New England Journal of Medicine demonstrating the effectiveness of dupilumab in treatment of PPI-refractory pediatric EoE. Our August Member Spotlight features Dr. Neelendu Dey of Fred Hutchinson Cancer Center, who shares his perspectives on pursuing a career as a physician-scientist and chronicles his research focused on harnessing the microbiome for cancer prevention.

Finally, our quarterly In Focus column from The New Gastroenterologist provides practical advice regarding how best to evaluate patients with chronic bloating symptoms, a frequent presentation in our GI clinics. As always, thanks for reading and please don’t hesitate to reach out with suggestions for future coverage.
 

Megan A. Adams, MD, JD, MSc

Editor in Chief

This transcript has been edited for clarity.

We need more diverse students — more students from disadvantaged and underrepresented backgrounds in medical school. That is not a controversial take. That’s not even a new thought.

What is a hot take, however, is that free medical school alone is not going to accomplish this goal. In fact, based on data and what people think and are saying, that’s just reality.

I recently chatted about whether or not free medical school would motivate more students to pursue primary care. That was New York University’s (NYU’s) goal. If you haven’t seen that video, check it out. Now I want to explore whether free medical school would actually create a more diverse medical student body.

This topic is especially important now because, in 2023, the Supreme Court ended affirmative action for college admissions, and this naturally has a downstream effect when it comes to getting into medical school. Right now, about 6% of US physicians are Black or Hispanic/Latina, and around 0.1%-0.3% identify as Indigenous Americans, Native Hawaiians, or Pacific Islanders.

Is free medical school the answer? Well, that’s based on a huge assumption that the cost of medical school — incoming debt — is the single greatest barrier for students from diverse backgrounds, as if every single student from every background had the same level of resources in the same opportunity and were all equally competitive prior to applying, and just the prospect of debt is what caused the disparity. I don’t know if that’s reality. Let’s take a look at NYU.

After the free tuition announcement, total applications to the medical school went up nearly 50%. And from underrepresented groups, it was 100%. In 2019, the associate dean for admissions said, “A key driver was to remove a financial disincentive that dissuades people from pursuing a path in medicine.” But the acceptance rate stayed under 3%, and the average Medical College Admission Test (MCAT) and grade point average (GPA) to get in went up. Basically, the school just became more competitive.

I will always commend anyone, anywhere, who is making medical school more affordable and more accessible. With NYU, it seems a tuition gift just made it harder for students from disadvantaged backgrounds to actually get in. I mean, congratulations, you got more applications. This probably helped in ratings, and you got mentioned in news headlines, but are you actually achieving your mission?

At NYU, over the last few years, Black students made up about 11% of the medical school class, which is actually down from 2017 before the tuition gift. Students from low-income backgrounds, whom this would really benefit, used to make up around 12% of the class prior to the free tuition announcement, and now it’s around 3%-7%.

According to students from underrepresented backgrounds, the outreach and the equal opportunity need to start way earlier. The K-12 process needs to be addressed, as do mentorship opportunities and guidance throughout college, MCAT prep, resources for interviews, research opportunities, and so much more.

The following quote is from an interview with an interventional cardiology fellow who came here as a refugee: “For me, growing up, basic necessities like a quiet study space, high-speed internet, healthy meals and proper sleep were luxuries of which I could only dream. After resettling in the US as a political refugee, I lived in circumstances where such comforts were out of reach, and my path to medical school seemed insurmountable.” 

I also spoke to a friend in pediatric cancer, Michael Galvez, MD, who was outspoken about the need to improve representation in medicine, about what he thought would actually work to diversify medical schools. He mentioned adversity scores or looking at the distance traveled for applicants, as well as efforts to recruit from local, state, and community colleges, which often reflect local underserved populations. 

Dr. Galvez also agreed that although such metrics as GPA and MCAT are important, medical schools should also consider the impact applicants may have had for local, underserved communities and life experiences that may represent significant potential contributions applicants can make for public health.

The effort needs to start early. If we take a look at one of the most diverse medical schools in the country, UC Davis, we can see how this makes a difference. At UC Davis, in the class of 2026, about half of the 133 students come from underrepresented backgrounds in medicine. I’m taking a look at their website from the Office of Student and Resident Diversity, and it lists:

• K-12 outreach programs
• Undergraduate and community college programs
• Specific plans for postbaccalaureate students
• Support systems
• Resources for students that extend far beyond just premedical students

My home institution, Stanford School of Medicine, has similar programs as well, with similar ways for students from underrepresented backgrounds to find support and mentorship. This all makes a huge difference.

Regarding the actual admissions process for medical school, I’ll highlight the Johns Hopkins School of Medicine and the adaptions they’ve made to create a more fair and holistic process. It includes:

• A clear mission statement about diversity enhancement
• Anonymous voting
• A larger group to avoid bias
• Not showing academic metrics to interviewers
• Implicit association tests and trainings
• Removing photos from applications
• Appointing women, minorities, and young people with less implicit bias to the committees

Does this seem like a lot? It is, because a comprehensive approach is what it takes to build a more diverse US physician workforce, which will provide more culturally competent care, empower future generations, break down barriers and disparities in health care, and ultimately improve public health. Free tuition is awesome. I’m jealous. But on its own to solve these problems? This all feels like a misguided attempt.
 

Dr. Patel is clinical instructor, Department of Pediatrics, Columbia University College of Physicians and Surgeons, and pediatric hospitalist at Morgan Stanley Children’s Hospital of NewYork-Presbyterian, New York, and Benioff Children’s Hospital, University of California, San Francisco. He disclosed ties with Medumo Inc.

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

This transcript has been edited for clarity.

We need more diverse students — more students from disadvantaged and underrepresented backgrounds in medical school. That is not a controversial take. That’s not even a new thought.

What is a hot take, however, is that free medical school alone is not going to accomplish this goal. In fact, based on data and what people think and are saying, that’s just reality.

I recently chatted about whether or not free medical school would motivate more students to pursue primary care. That was New York University’s (NYU’s) goal. If you haven’t seen that video, check it out. Now I want to explore whether free medical school would actually create a more diverse medical student body.

This topic is especially important now because, in 2023, the Supreme Court ended affirmative action for college admissions, and this naturally has a downstream effect when it comes to getting into medical school. Right now, about 6% of US physicians are Black or Hispanic/Latina, and around 0.1%-0.3% identify as Indigenous Americans, Native Hawaiians, or Pacific Islanders.

Is free medical school the answer? Well, that’s based on a huge assumption that the cost of medical school — incoming debt — is the single greatest barrier for students from diverse backgrounds, as if every single student from every background had the same level of resources in the same opportunity and were all equally competitive prior to applying, and just the prospect of debt is what caused the disparity. I don’t know if that’s reality. Let’s take a look at NYU.

After the free tuition announcement, total applications to the medical school went up nearly 50%. And from underrepresented groups, it was 100%. In 2019, the associate dean for admissions said, “A key driver was to remove a financial disincentive that dissuades people from pursuing a path in medicine.” But the acceptance rate stayed under 3%, and the average Medical College Admission Test (MCAT) and grade point average (GPA) to get in went up. Basically, the school just became more competitive.

I will always commend anyone, anywhere, who is making medical school more affordable and more accessible. With NYU, it seems a tuition gift just made it harder for students from disadvantaged backgrounds to actually get in. I mean, congratulations, you got more applications. This probably helped in ratings, and you got mentioned in news headlines, but are you actually achieving your mission?

At NYU, over the last few years, Black students made up about 11% of the medical school class, which is actually down from 2017 before the tuition gift. Students from low-income backgrounds, whom this would really benefit, used to make up around 12% of the class prior to the free tuition announcement, and now it’s around 3%-7%.

According to students from underrepresented backgrounds, the outreach and the equal opportunity need to start way earlier. The K-12 process needs to be addressed, as do mentorship opportunities and guidance throughout college, MCAT prep, resources for interviews, research opportunities, and so much more.

The following quote is from an interview with an interventional cardiology fellow who came here as a refugee: “For me, growing up, basic necessities like a quiet study space, high-speed internet, healthy meals and proper sleep were luxuries of which I could only dream. After resettling in the US as a political refugee, I lived in circumstances where such comforts were out of reach, and my path to medical school seemed insurmountable.” 

I also spoke to a friend in pediatric cancer, Michael Galvez, MD, who was outspoken about the need to improve representation in medicine, about what he thought would actually work to diversify medical schools. He mentioned adversity scores or looking at the distance traveled for applicants, as well as efforts to recruit from local, state, and community colleges, which often reflect local underserved populations. 

Dr. Galvez also agreed that although such metrics as GPA and MCAT are important, medical schools should also consider the impact applicants may have had for local, underserved communities and life experiences that may represent significant potential contributions applicants can make for public health.

The effort needs to start early. If we take a look at one of the most diverse medical schools in the country, UC Davis, we can see how this makes a difference. At UC Davis, in the class of 2026, about half of the 133 students come from underrepresented backgrounds in medicine. I’m taking a look at their website from the Office of Student and Resident Diversity, and it lists:

• K-12 outreach programs
• Undergraduate and community college programs
• Specific plans for postbaccalaureate students
• Support systems
• Resources for students that extend far beyond just premedical students

My home institution, Stanford School of Medicine, has similar programs as well, with similar ways for students from underrepresented backgrounds to find support and mentorship. This all makes a huge difference.

Regarding the actual admissions process for medical school, I’ll highlight the Johns Hopkins School of Medicine and the adaptions they’ve made to create a more fair and holistic process. It includes:

• A clear mission statement about diversity enhancement
• Anonymous voting
• A larger group to avoid bias
• Not showing academic metrics to interviewers
• Implicit association tests and trainings
• Removing photos from applications
• Appointing women, minorities, and young people with less implicit bias to the committees

Does this seem like a lot? It is, because a comprehensive approach is what it takes to build a more diverse US physician workforce, which will provide more culturally competent care, empower future generations, break down barriers and disparities in health care, and ultimately improve public health. Free tuition is awesome. I’m jealous. But on its own to solve these problems? This all feels like a misguided attempt.
 

Dr. Patel is clinical instructor, Department of Pediatrics, Columbia University College of Physicians and Surgeons, and pediatric hospitalist at Morgan Stanley Children’s Hospital of NewYork-Presbyterian, New York, and Benioff Children’s Hospital, University of California, San Francisco. He disclosed ties with Medumo Inc.

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

This transcript has been edited for clarity.

We need more diverse students — more students from disadvantaged and underrepresented backgrounds in medical school. That is not a controversial take. That’s not even a new thought.

What is a hot take, however, is that free medical school alone is not going to accomplish this goal. In fact, based on data and what people think and are saying, that’s just reality.

I recently chatted about whether or not free medical school would motivate more students to pursue primary care. That was New York University’s (NYU’s) goal. If you haven’t seen that video, check it out. Now I want to explore whether free medical school would actually create a more diverse medical student body.

This topic is especially important now because, in 2023, the Supreme Court ended affirmative action for college admissions, and this naturally has a downstream effect when it comes to getting into medical school. Right now, about 6% of US physicians are Black or Hispanic/Latina, and around 0.1%-0.3% identify as Indigenous Americans, Native Hawaiians, or Pacific Islanders.

Is free medical school the answer? Well, that’s based on a huge assumption that the cost of medical school — incoming debt — is the single greatest barrier for students from diverse backgrounds, as if every single student from every background had the same level of resources in the same opportunity and were all equally competitive prior to applying, and just the prospect of debt is what caused the disparity. I don’t know if that’s reality. Let’s take a look at NYU.

After the free tuition announcement, total applications to the medical school went up nearly 50%. And from underrepresented groups, it was 100%. In 2019, the associate dean for admissions said, “A key driver was to remove a financial disincentive that dissuades people from pursuing a path in medicine.” But the acceptance rate stayed under 3%, and the average Medical College Admission Test (MCAT) and grade point average (GPA) to get in went up. Basically, the school just became more competitive.

I will always commend anyone, anywhere, who is making medical school more affordable and more accessible. With NYU, it seems a tuition gift just made it harder for students from disadvantaged backgrounds to actually get in. I mean, congratulations, you got more applications. This probably helped in ratings, and you got mentioned in news headlines, but are you actually achieving your mission?

At NYU, over the last few years, Black students made up about 11% of the medical school class, which is actually down from 2017 before the tuition gift. Students from low-income backgrounds, whom this would really benefit, used to make up around 12% of the class prior to the free tuition announcement, and now it’s around 3%-7%.

According to students from underrepresented backgrounds, the outreach and the equal opportunity need to start way earlier. The K-12 process needs to be addressed, as do mentorship opportunities and guidance throughout college, MCAT prep, resources for interviews, research opportunities, and so much more.

The following quote is from an interview with an interventional cardiology fellow who came here as a refugee: “For me, growing up, basic necessities like a quiet study space, high-speed internet, healthy meals and proper sleep were luxuries of which I could only dream. After resettling in the US as a political refugee, I lived in circumstances where such comforts were out of reach, and my path to medical school seemed insurmountable.” 

I also spoke to a friend in pediatric cancer, Michael Galvez, MD, who was outspoken about the need to improve representation in medicine, about what he thought would actually work to diversify medical schools. He mentioned adversity scores or looking at the distance traveled for applicants, as well as efforts to recruit from local, state, and community colleges, which often reflect local underserved populations. 

Dr. Galvez also agreed that although such metrics as GPA and MCAT are important, medical schools should also consider the impact applicants may have had for local, underserved communities and life experiences that may represent significant potential contributions applicants can make for public health.

The effort needs to start early. If we take a look at one of the most diverse medical schools in the country, UC Davis, we can see how this makes a difference. At UC Davis, in the class of 2026, about half of the 133 students come from underrepresented backgrounds in medicine. I’m taking a look at their website from the Office of Student and Resident Diversity, and it lists:

• K-12 outreach programs
• Undergraduate and community college programs
• Specific plans for postbaccalaureate students
• Support systems
• Resources for students that extend far beyond just premedical students

My home institution, Stanford School of Medicine, has similar programs as well, with similar ways for students from underrepresented backgrounds to find support and mentorship. This all makes a huge difference.

Regarding the actual admissions process for medical school, I’ll highlight the Johns Hopkins School of Medicine and the adaptions they’ve made to create a more fair and holistic process. It includes:

• A clear mission statement about diversity enhancement
• Anonymous voting
• A larger group to avoid bias
• Not showing academic metrics to interviewers
• Implicit association tests and trainings
• Removing photos from applications
• Appointing women, minorities, and young people with less implicit bias to the committees

Does this seem like a lot? It is, because a comprehensive approach is what it takes to build a more diverse US physician workforce, which will provide more culturally competent care, empower future generations, break down barriers and disparities in health care, and ultimately improve public health. Free tuition is awesome. I’m jealous. But on its own to solve these problems? This all feels like a misguided attempt.
 

Dr. Patel is clinical instructor, Department of Pediatrics, Columbia University College of Physicians and Surgeons, and pediatric hospitalist at Morgan Stanley Children’s Hospital of NewYork-Presbyterian, New York, and Benioff Children’s Hospital, University of California, San Francisco. He disclosed ties with Medumo Inc.

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

This transcript has been edited for clarity. 

Lawyers have the saying, “Bad facts make for bad cases; bad cases make for bad laws.” What we’re seeing, I fear, all too often in discussions about reproductive rights, reproductive behavior, and attempts to regulate and legislate with respect to abortion and contraception are many bad facts.

I do think it’s important that science and medicine speak up in local settings and every opportunity they have, not so much to say what government should do or to say whether they think a particular law is good or bad, but certainly to get the facts straight in their role as doctors, sometimes as scientists, and as caregivers.

Bad facts are making many bad policies in the reproductive behavior space. For example, there are many people, mainly on the conservative side, who are saying things like intrauterine devices, emergency contraception, and even birth control cause abortions. That is simply not true.

There are interventions that prevent fertilization from occurring. There are also interventions that prevent implantation from occurring. Neither of those are abortions. If an embryo has not implanted into a womb, it is not, by any biological definition, a pregnancy. 

In situations where a barrier method or something else prevents sperm and egg from meeting or if there is an agent that prevents an egg from implanting, these are facts that legislators, the public, and even your patients need to understand if they’re going to make sound policy about access to methods used to control reproduction.

Similarly, you can see debates about whether embryos are deserving of rights. An Alabama court has ruled that embryos are tiny children. A court can say what it wishes in terms of legal status, but it shouldn’t be deviating from the facts. 

The facts are clear. Embryos outside of a uterus implanted are not babies. They are not children. At most, an embryo in a dish might be considered, let’s say, a possible person. Once it implants in a uterus, it may become a potential person because it then still has a failure rate, postimplantation, of not becoming a baby that’s very high. Approximately 40%-50% of such embryos are genetically flawed and aren’t going to be able to turn into a child.

The notion that every embryo, whether it’s stored in a tank or sitting in a dish, is somehow a tiny child, factually is just not true. You can’t make good policy if you ignore the facts. People may wish to protect embryos. They may wish to restrict in vitro fertilization. They may wish to have people implant any embryo that is created and mandate that it has to happen because they don’t want any tiny children not to be brought to term.

Factually, they’re operating outside the realm of what biology and medicine know. There’s no tiny baby, no homunculus, or no preformed baby inside an embryo. An egg that simply fails to implant is not technically even a pregnancy. 

I think all of us have an obligation when we’re in disputes, wherever they occur, whether we’re fighting about laws, having an argument with the neighbors, or speaking to younger high school students or even patients, we need to try to make clear the facts about what we know about eggs, how birth control works, and embryos and their failure rate. 

We also have to be clear about the significance of saying the facts have to guide public policy. I think the facts should, but unfortunately, I don’t think that’s always been true in recent years. As efforts heat up to intervene more with things like contraception, getting the facts straight becomes even more important and more of a duty for those who know best.

Dr. Caplan is director, Division of Medical Ethics, New York University Langone Medical Center, New York. He served as a director, officer, partner, employee, adviser, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position). He is a contributing author and adviser for Medscape.

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

This transcript has been edited for clarity. 

Lawyers have the saying, “Bad facts make for bad cases; bad cases make for bad laws.” What we’re seeing, I fear, all too often in discussions about reproductive rights, reproductive behavior, and attempts to regulate and legislate with respect to abortion and contraception are many bad facts.

I do think it’s important that science and medicine speak up in local settings and every opportunity they have, not so much to say what government should do or to say whether they think a particular law is good or bad, but certainly to get the facts straight in their role as doctors, sometimes as scientists, and as caregivers.

Bad facts are making many bad policies in the reproductive behavior space. For example, there are many people, mainly on the conservative side, who are saying things like intrauterine devices, emergency contraception, and even birth control cause abortions. That is simply not true.

There are interventions that prevent fertilization from occurring. There are also interventions that prevent implantation from occurring. Neither of those are abortions. If an embryo has not implanted into a womb, it is not, by any biological definition, a pregnancy. 

In situations where a barrier method or something else prevents sperm and egg from meeting or if there is an agent that prevents an egg from implanting, these are facts that legislators, the public, and even your patients need to understand if they’re going to make sound policy about access to methods used to control reproduction.

Similarly, you can see debates about whether embryos are deserving of rights. An Alabama court has ruled that embryos are tiny children. A court can say what it wishes in terms of legal status, but it shouldn’t be deviating from the facts. 

The facts are clear. Embryos outside of a uterus implanted are not babies. They are not children. At most, an embryo in a dish might be considered, let’s say, a possible person. Once it implants in a uterus, it may become a potential person because it then still has a failure rate, postimplantation, of not becoming a baby that’s very high. Approximately 40%-50% of such embryos are genetically flawed and aren’t going to be able to turn into a child.

The notion that every embryo, whether it’s stored in a tank or sitting in a dish, is somehow a tiny child, factually is just not true. You can’t make good policy if you ignore the facts. People may wish to protect embryos. They may wish to restrict in vitro fertilization. They may wish to have people implant any embryo that is created and mandate that it has to happen because they don’t want any tiny children not to be brought to term.

Factually, they’re operating outside the realm of what biology and medicine know. There’s no tiny baby, no homunculus, or no preformed baby inside an embryo. An egg that simply fails to implant is not technically even a pregnancy. 

I think all of us have an obligation when we’re in disputes, wherever they occur, whether we’re fighting about laws, having an argument with the neighbors, or speaking to younger high school students or even patients, we need to try to make clear the facts about what we know about eggs, how birth control works, and embryos and their failure rate. 

We also have to be clear about the significance of saying the facts have to guide public policy. I think the facts should, but unfortunately, I don’t think that’s always been true in recent years. As efforts heat up to intervene more with things like contraception, getting the facts straight becomes even more important and more of a duty for those who know best.

Dr. Caplan is director, Division of Medical Ethics, New York University Langone Medical Center, New York. He served as a director, officer, partner, employee, adviser, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position). He is a contributing author and adviser for Medscape.

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

This transcript has been edited for clarity. 

Lawyers have the saying, “Bad facts make for bad cases; bad cases make for bad laws.” What we’re seeing, I fear, all too often in discussions about reproductive rights, reproductive behavior, and attempts to regulate and legislate with respect to abortion and contraception are many bad facts.

I do think it’s important that science and medicine speak up in local settings and every opportunity they have, not so much to say what government should do or to say whether they think a particular law is good or bad, but certainly to get the facts straight in their role as doctors, sometimes as scientists, and as caregivers.

Bad facts are making many bad policies in the reproductive behavior space. For example, there are many people, mainly on the conservative side, who are saying things like intrauterine devices, emergency contraception, and even birth control cause abortions. That is simply not true.

There are interventions that prevent fertilization from occurring. There are also interventions that prevent implantation from occurring. Neither of those are abortions. If an embryo has not implanted into a womb, it is not, by any biological definition, a pregnancy. 

In situations where a barrier method or something else prevents sperm and egg from meeting or if there is an agent that prevents an egg from implanting, these are facts that legislators, the public, and even your patients need to understand if they’re going to make sound policy about access to methods used to control reproduction.

Similarly, you can see debates about whether embryos are deserving of rights. An Alabama court has ruled that embryos are tiny children. A court can say what it wishes in terms of legal status, but it shouldn’t be deviating from the facts. 

The facts are clear. Embryos outside of a uterus implanted are not babies. They are not children. At most, an embryo in a dish might be considered, let’s say, a possible person. Once it implants in a uterus, it may become a potential person because it then still has a failure rate, postimplantation, of not becoming a baby that’s very high. Approximately 40%-50% of such embryos are genetically flawed and aren’t going to be able to turn into a child.

The notion that every embryo, whether it’s stored in a tank or sitting in a dish, is somehow a tiny child, factually is just not true. You can’t make good policy if you ignore the facts. People may wish to protect embryos. They may wish to restrict in vitro fertilization. They may wish to have people implant any embryo that is created and mandate that it has to happen because they don’t want any tiny children not to be brought to term.

Factually, they’re operating outside the realm of what biology and medicine know. There’s no tiny baby, no homunculus, or no preformed baby inside an embryo. An egg that simply fails to implant is not technically even a pregnancy. 

I think all of us have an obligation when we’re in disputes, wherever they occur, whether we’re fighting about laws, having an argument with the neighbors, or speaking to younger high school students or even patients, we need to try to make clear the facts about what we know about eggs, how birth control works, and embryos and their failure rate. 

We also have to be clear about the significance of saying the facts have to guide public policy. I think the facts should, but unfortunately, I don’t think that’s always been true in recent years. As efforts heat up to intervene more with things like contraception, getting the facts straight becomes even more important and more of a duty for those who know best.

Dr. Caplan is director, Division of Medical Ethics, New York University Langone Medical Center, New York. He served as a director, officer, partner, employee, adviser, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position). He is a contributing author and adviser for Medscape.

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

A 25-year-old man comes in with a pulled muscle. You ask if he has anything else to discuss. Sheepishly, he says he is concerned about his use of pornography. 

A 45-year-old woman struggling with depression finds herself persistently seeking sex outside the bounds of her long-term relationship. Her partner is threatening to leave. She is devastated and tells you she doesn’t understand her own behavior. 

Do these patients have some form of sex addiction? How should a primary care clinician intervene? Is a referral to a 12-step program for sex addiction the right choice? What other options exist? Is a diagnosis — let alone treatment — possible or appropriate? 
 

‘Who Are You Calling “Abnormal” ’?

Normal is not a meaningful concept in human sexual behavior. To quote the sex therapist Marty Klein, PhD: “Normal is just a setting on the dryer.” 

The same goes among partners: What is “normal” for one person in a sexual relationship may discomfit another. In partnerships, we have differences around all sorts of issues, from finances to parenting to how to load the dishwasher. Why should sex, sexual desire, and sexual frequency be different? 

Remember: Shame, fear, and secrecy often play a role in perpetuating behaviors that cause distress. Helping our patients accept and embrace their whole selves can provide important healing, relief from anxiety, and may even help them regulate their actions. Feeling less shame, fear, and secrecy may facilitate safer choices about sex, as well as testing and treatment for sexually transmitted infections.

The International Classification of Diseases-11 includes compulsive sexual behavior disorder (CSBD)as an attempt to create consensus around a complicated, and hotly debated, problem to facilitate diagnosis and research. Syndromes similar to CSBD have had many names: “hypersexual disorder,” “sexual addiction,” “sexual compulsivity,” and “out-of-control sexual behavior.” A sizable cohort of the sexuality research community casts doubt on whether CSBD is even a discrete diagnosis. 

According to the ICD-11, CSBD is characterized by “intense, repetitive sexual impulses or urges that are experienced as irresistible or uncontrollable” and result in significant distress or functional impairment.

This diagnosis has several important rule-outs. First, paraphilias, defined as a set of nonconsensual sexual behaviors and interests, are excluded. Another is that distress exclusively related to moral judgment or social disapproval is not sufficient for a diagnosis of CSBD. Finally, the diagnosis hinges on distress and does not rely on frequency of any type of sexual behavior. Some people experience significant distress over behaviors in which they engage infrequently, whereas others may have no distress from activities in which they engage quite frequently. 

In one study from Germany, 5% of men and 3% of women met criteria for CSBD. A small US study found the number to be 10% and 7%, respectively. The diagnosis is not simple. Compulsive sexual behavior can be secondary to other mental health or medical conditions. Behaviors sometimes confused with CSBD can result from neurologic diseases, such as frontal brain lesions or frontotemporal dementia, as well as the use of substances and medications that enhance dopaminergic activity. 

Impaired control over sexual impulses occurs in manic and hypomanic episodes. Compulsive sexual behavior frequently co-occurs with mood disorders, obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, and substance use disorders. Those meeting criteria for CSBD may engage in sexual behaviors as a way of coping with depression, anxiety, boredom, loneliness, or other negative affective states.  

The diagnosis of CSBD may be useful for clinicians. However, many, perhaps most, patients who present with concerns about their sexual behavior will fail to meet most criteria for CSBD. Their problem is of shorter duration, related to morality, external disapproval, lack of sexual health information, and anxiety about diverse erotic interests. It may be helpful for them to understand that they are not in the grip of a lifelong disorder but are experiencing common life challenges. 

Societal concerns about sexually explicit media, often called pornography, are complex, conflicting, and catastrophizing. Some studies indicate that sexually explicit media are positive for both individual and relational sexual satisfaction; other studies have found negative effects on sexual function. Concerns about pornography often are conflated with taboos about solo sexual activity. Ironically, use of pornography is associated with fear of addiction to pornography, creating a spiral of negative self-perception. 

Consequences of sexual behavior may induce distress, even if a person doesn’t meet criteria for CSBD, such as potential dissolution of a marriage, loss of a job, excessive spending, sexually transmitted infections, other health concerns, and even legal problems. Sexual behavior might not be the central issue but rather an offshoot of relational distress, a mental health disorder, or a dysfunctional coping style. 

Guilt and shame can act as potent contributors to maintaining the behaviors as well as promoting secrecy around them. Sexual medicine experts recommend avoiding interventions that increase the experience of discrimination and stigma and avoiding the pathologization of the behaviors of sexually diverse individuals. As in so many aspects of medical care, we must walk in our patients’ shoes and avoid imposing on them our own moral or religious values. 
 

What Can a Primary Care Provider Do?  

When a patient is concerned about sexual behavior that feels out of control, primary care providers have an important role in evaluating for neurologic disease or side effects related to the use of medication or other substances, and facilitating psychiatric assessment to evaluate for mental health comorbidities, past trauma, and associated attachment disorders. 

Our patients need resources to tease out the individual and relational problems that may arise. Seek out well-trained sex therapy colleagues in your community. The American Association of Sexuality Educators, Counselors, and Therapists (AASECT) is one certifying body in the United States for sex therapy. 

Because of the heterogeneity of those who present with out-of-control sexual behavior, no one treatment fits all. Twelve-step programs, especially those with a focus on sexual “abstinence,” may not be the best choice. Many psychotherapeutic modalities are effective and often focus on addressing underlying or unrecognized mental health concerns, provide training on self-regulation and urge management, and relationship skills. Most important, the therapist needs to be sexologically informed and aware of their own biases around sexuality. Medical treatments are not recommended without concurrent psychological intervention. 

Relational sex therapy can help couples create clear relational agreements that work for both parties (or, in polyamorous relationships, everyone involved). Relational distress also may be a stimulus for individual psychotherapy. 

Back to these two patients. 

The 25-year-old could be counseled that use of sexually explicit media and solo sex are not inherently bad or damaging. When used for pleasure and enjoyment, they do not lead to problems with partnered sex or cause sexual dysfunction. Counseling him to move toward social engagement and life goals, rather than away from pornography, may be all that is necessary. 

Our second patient probably will need more intensive treatment, including medication management for her mood and referral to a certified sex therapist who has expertise in working with out-of-control sexual behavior. When she returns to see you in follow-up, she ideally expresses reduced shame, more autonomy, and renewed connection to her values, and she is keeping her relational agreements without sacrificing her sexual needs. 
 

Dr. Kranz is medical director, Rochester Center for Sexual Wellness; assistant professor of Clinical Family Medicine and Obstetrics and Gynecology, University of Rochester Medical Center, Rochester, New York. Dr. Kranz has disclosed no relevant financial relationships. Dr. Rosen is director of Behavioral Health, Rochester Center for Sexual Wellness, Rochester, New York. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

A 25-year-old man comes in with a pulled muscle. You ask if he has anything else to discuss. Sheepishly, he says he is concerned about his use of pornography. 

A 45-year-old woman struggling with depression finds herself persistently seeking sex outside the bounds of her long-term relationship. Her partner is threatening to leave. She is devastated and tells you she doesn’t understand her own behavior. 

Do these patients have some form of sex addiction? How should a primary care clinician intervene? Is a referral to a 12-step program for sex addiction the right choice? What other options exist? Is a diagnosis — let alone treatment — possible or appropriate? 
 

‘Who Are You Calling “Abnormal” ’?

Normal is not a meaningful concept in human sexual behavior. To quote the sex therapist Marty Klein, PhD: “Normal is just a setting on the dryer.” 

The same goes among partners: What is “normal” for one person in a sexual relationship may discomfit another. In partnerships, we have differences around all sorts of issues, from finances to parenting to how to load the dishwasher. Why should sex, sexual desire, and sexual frequency be different? 

Remember: Shame, fear, and secrecy often play a role in perpetuating behaviors that cause distress. Helping our patients accept and embrace their whole selves can provide important healing, relief from anxiety, and may even help them regulate their actions. Feeling less shame, fear, and secrecy may facilitate safer choices about sex, as well as testing and treatment for sexually transmitted infections.

The International Classification of Diseases-11 includes compulsive sexual behavior disorder (CSBD)as an attempt to create consensus around a complicated, and hotly debated, problem to facilitate diagnosis and research. Syndromes similar to CSBD have had many names: “hypersexual disorder,” “sexual addiction,” “sexual compulsivity,” and “out-of-control sexual behavior.” A sizable cohort of the sexuality research community casts doubt on whether CSBD is even a discrete diagnosis. 

According to the ICD-11, CSBD is characterized by “intense, repetitive sexual impulses or urges that are experienced as irresistible or uncontrollable” and result in significant distress or functional impairment.

This diagnosis has several important rule-outs. First, paraphilias, defined as a set of nonconsensual sexual behaviors and interests, are excluded. Another is that distress exclusively related to moral judgment or social disapproval is not sufficient for a diagnosis of CSBD. Finally, the diagnosis hinges on distress and does not rely on frequency of any type of sexual behavior. Some people experience significant distress over behaviors in which they engage infrequently, whereas others may have no distress from activities in which they engage quite frequently. 

In one study from Germany, 5% of men and 3% of women met criteria for CSBD. A small US study found the number to be 10% and 7%, respectively. The diagnosis is not simple. Compulsive sexual behavior can be secondary to other mental health or medical conditions. Behaviors sometimes confused with CSBD can result from neurologic diseases, such as frontal brain lesions or frontotemporal dementia, as well as the use of substances and medications that enhance dopaminergic activity. 

Impaired control over sexual impulses occurs in manic and hypomanic episodes. Compulsive sexual behavior frequently co-occurs with mood disorders, obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, and substance use disorders. Those meeting criteria for CSBD may engage in sexual behaviors as a way of coping with depression, anxiety, boredom, loneliness, or other negative affective states.  

The diagnosis of CSBD may be useful for clinicians. However, many, perhaps most, patients who present with concerns about their sexual behavior will fail to meet most criteria for CSBD. Their problem is of shorter duration, related to morality, external disapproval, lack of sexual health information, and anxiety about diverse erotic interests. It may be helpful for them to understand that they are not in the grip of a lifelong disorder but are experiencing common life challenges. 

Societal concerns about sexually explicit media, often called pornography, are complex, conflicting, and catastrophizing. Some studies indicate that sexually explicit media are positive for both individual and relational sexual satisfaction; other studies have found negative effects on sexual function. Concerns about pornography often are conflated with taboos about solo sexual activity. Ironically, use of pornography is associated with fear of addiction to pornography, creating a spiral of negative self-perception. 

Consequences of sexual behavior may induce distress, even if a person doesn’t meet criteria for CSBD, such as potential dissolution of a marriage, loss of a job, excessive spending, sexually transmitted infections, other health concerns, and even legal problems. Sexual behavior might not be the central issue but rather an offshoot of relational distress, a mental health disorder, or a dysfunctional coping style. 

Guilt and shame can act as potent contributors to maintaining the behaviors as well as promoting secrecy around them. Sexual medicine experts recommend avoiding interventions that increase the experience of discrimination and stigma and avoiding the pathologization of the behaviors of sexually diverse individuals. As in so many aspects of medical care, we must walk in our patients’ shoes and avoid imposing on them our own moral or religious values. 
 

What Can a Primary Care Provider Do?  

When a patient is concerned about sexual behavior that feels out of control, primary care providers have an important role in evaluating for neurologic disease or side effects related to the use of medication or other substances, and facilitating psychiatric assessment to evaluate for mental health comorbidities, past trauma, and associated attachment disorders. 

Our patients need resources to tease out the individual and relational problems that may arise. Seek out well-trained sex therapy colleagues in your community. The American Association of Sexuality Educators, Counselors, and Therapists (AASECT) is one certifying body in the United States for sex therapy. 

Because of the heterogeneity of those who present with out-of-control sexual behavior, no one treatment fits all. Twelve-step programs, especially those with a focus on sexual “abstinence,” may not be the best choice. Many psychotherapeutic modalities are effective and often focus on addressing underlying or unrecognized mental health concerns, provide training on self-regulation and urge management, and relationship skills. Most important, the therapist needs to be sexologically informed and aware of their own biases around sexuality. Medical treatments are not recommended without concurrent psychological intervention. 

Relational sex therapy can help couples create clear relational agreements that work for both parties (or, in polyamorous relationships, everyone involved). Relational distress also may be a stimulus for individual psychotherapy. 

Back to these two patients. 

The 25-year-old could be counseled that use of sexually explicit media and solo sex are not inherently bad or damaging. When used for pleasure and enjoyment, they do not lead to problems with partnered sex or cause sexual dysfunction. Counseling him to move toward social engagement and life goals, rather than away from pornography, may be all that is necessary. 

Our second patient probably will need more intensive treatment, including medication management for her mood and referral to a certified sex therapist who has expertise in working with out-of-control sexual behavior. When she returns to see you in follow-up, she ideally expresses reduced shame, more autonomy, and renewed connection to her values, and she is keeping her relational agreements without sacrificing her sexual needs. 
 

Dr. Kranz is medical director, Rochester Center for Sexual Wellness; assistant professor of Clinical Family Medicine and Obstetrics and Gynecology, University of Rochester Medical Center, Rochester, New York. Dr. Kranz has disclosed no relevant financial relationships. Dr. Rosen is director of Behavioral Health, Rochester Center for Sexual Wellness, Rochester, New York. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

A 25-year-old man comes in with a pulled muscle. You ask if he has anything else to discuss. Sheepishly, he says he is concerned about his use of pornography. 

A 45-year-old woman struggling with depression finds herself persistently seeking sex outside the bounds of her long-term relationship. Her partner is threatening to leave. She is devastated and tells you she doesn’t understand her own behavior. 

Do these patients have some form of sex addiction? How should a primary care clinician intervene? Is a referral to a 12-step program for sex addiction the right choice? What other options exist? Is a diagnosis — let alone treatment — possible or appropriate? 
 

‘Who Are You Calling “Abnormal” ’?

Normal is not a meaningful concept in human sexual behavior. To quote the sex therapist Marty Klein, PhD: “Normal is just a setting on the dryer.” 

The same goes among partners: What is “normal” for one person in a sexual relationship may discomfit another. In partnerships, we have differences around all sorts of issues, from finances to parenting to how to load the dishwasher. Why should sex, sexual desire, and sexual frequency be different? 

Remember: Shame, fear, and secrecy often play a role in perpetuating behaviors that cause distress. Helping our patients accept and embrace their whole selves can provide important healing, relief from anxiety, and may even help them regulate their actions. Feeling less shame, fear, and secrecy may facilitate safer choices about sex, as well as testing and treatment for sexually transmitted infections.

The International Classification of Diseases-11 includes compulsive sexual behavior disorder (CSBD)as an attempt to create consensus around a complicated, and hotly debated, problem to facilitate diagnosis and research. Syndromes similar to CSBD have had many names: “hypersexual disorder,” “sexual addiction,” “sexual compulsivity,” and “out-of-control sexual behavior.” A sizable cohort of the sexuality research community casts doubt on whether CSBD is even a discrete diagnosis. 

According to the ICD-11, CSBD is characterized by “intense, repetitive sexual impulses or urges that are experienced as irresistible or uncontrollable” and result in significant distress or functional impairment.

This diagnosis has several important rule-outs. First, paraphilias, defined as a set of nonconsensual sexual behaviors and interests, are excluded. Another is that distress exclusively related to moral judgment or social disapproval is not sufficient for a diagnosis of CSBD. Finally, the diagnosis hinges on distress and does not rely on frequency of any type of sexual behavior. Some people experience significant distress over behaviors in which they engage infrequently, whereas others may have no distress from activities in which they engage quite frequently. 

In one study from Germany, 5% of men and 3% of women met criteria for CSBD. A small US study found the number to be 10% and 7%, respectively. The diagnosis is not simple. Compulsive sexual behavior can be secondary to other mental health or medical conditions. Behaviors sometimes confused with CSBD can result from neurologic diseases, such as frontal brain lesions or frontotemporal dementia, as well as the use of substances and medications that enhance dopaminergic activity. 

Impaired control over sexual impulses occurs in manic and hypomanic episodes. Compulsive sexual behavior frequently co-occurs with mood disorders, obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, and substance use disorders. Those meeting criteria for CSBD may engage in sexual behaviors as a way of coping with depression, anxiety, boredom, loneliness, or other negative affective states.  

The diagnosis of CSBD may be useful for clinicians. However, many, perhaps most, patients who present with concerns about their sexual behavior will fail to meet most criteria for CSBD. Their problem is of shorter duration, related to morality, external disapproval, lack of sexual health information, and anxiety about diverse erotic interests. It may be helpful for them to understand that they are not in the grip of a lifelong disorder but are experiencing common life challenges. 

Societal concerns about sexually explicit media, often called pornography, are complex, conflicting, and catastrophizing. Some studies indicate that sexually explicit media are positive for both individual and relational sexual satisfaction; other studies have found negative effects on sexual function. Concerns about pornography often are conflated with taboos about solo sexual activity. Ironically, use of pornography is associated with fear of addiction to pornography, creating a spiral of negative self-perception. 

Consequences of sexual behavior may induce distress, even if a person doesn’t meet criteria for CSBD, such as potential dissolution of a marriage, loss of a job, excessive spending, sexually transmitted infections, other health concerns, and even legal problems. Sexual behavior might not be the central issue but rather an offshoot of relational distress, a mental health disorder, or a dysfunctional coping style. 

Guilt and shame can act as potent contributors to maintaining the behaviors as well as promoting secrecy around them. Sexual medicine experts recommend avoiding interventions that increase the experience of discrimination and stigma and avoiding the pathologization of the behaviors of sexually diverse individuals. As in so many aspects of medical care, we must walk in our patients’ shoes and avoid imposing on them our own moral or religious values. 
 

What Can a Primary Care Provider Do?  

When a patient is concerned about sexual behavior that feels out of control, primary care providers have an important role in evaluating for neurologic disease or side effects related to the use of medication or other substances, and facilitating psychiatric assessment to evaluate for mental health comorbidities, past trauma, and associated attachment disorders. 

Our patients need resources to tease out the individual and relational problems that may arise. Seek out well-trained sex therapy colleagues in your community. The American Association of Sexuality Educators, Counselors, and Therapists (AASECT) is one certifying body in the United States for sex therapy. 

Because of the heterogeneity of those who present with out-of-control sexual behavior, no one treatment fits all. Twelve-step programs, especially those with a focus on sexual “abstinence,” may not be the best choice. Many psychotherapeutic modalities are effective and often focus on addressing underlying or unrecognized mental health concerns, provide training on self-regulation and urge management, and relationship skills. Most important, the therapist needs to be sexologically informed and aware of their own biases around sexuality. Medical treatments are not recommended without concurrent psychological intervention. 

Relational sex therapy can help couples create clear relational agreements that work for both parties (or, in polyamorous relationships, everyone involved). Relational distress also may be a stimulus for individual psychotherapy. 

Back to these two patients. 

The 25-year-old could be counseled that use of sexually explicit media and solo sex are not inherently bad or damaging. When used for pleasure and enjoyment, they do not lead to problems with partnered sex or cause sexual dysfunction. Counseling him to move toward social engagement and life goals, rather than away from pornography, may be all that is necessary. 

Our second patient probably will need more intensive treatment, including medication management for her mood and referral to a certified sex therapist who has expertise in working with out-of-control sexual behavior. When she returns to see you in follow-up, she ideally expresses reduced shame, more autonomy, and renewed connection to her values, and she is keeping her relational agreements without sacrificing her sexual needs. 
 

Dr. Kranz is medical director, Rochester Center for Sexual Wellness; assistant professor of Clinical Family Medicine and Obstetrics and Gynecology, University of Rochester Medical Center, Rochester, New York. Dr. Kranz has disclosed no relevant financial relationships. Dr. Rosen is director of Behavioral Health, Rochester Center for Sexual Wellness, Rochester, New York. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Hi. I’m Art Caplan. I’m at the Division of Medical Ethics at New York University Grossman School of Medicine in New York City. 

There are many things screwy with our healthcare system. Many of you [reading] this are dealing with bureaucracy, paperwork, all sorts of constraints, restraints, and requirements that sometimes make the practice of medicine, or even nursing, difficult.

I don’t think I’ve seen anything screwier, from a moral point of view, than the system we have that allows for preauthorization by third-party payers, or insurers, in order to give care to patients. It’s pretty clear that a third-party payer has a conflict of interest. It’s simple: They don’t want to spend money.

Their goal as profit-making companies is to reduce what it is that they’re going to authorize. That clearly is driving how the preauthorization process works. We’re not getting a neutral review by third parties of the appropriateness of treatment recommendations or somebody saying, this is the standard of care and this is what ought to happen.

We’re letting the people who have the pocketbooks and the wallets have prior approval of what the doctor thinks is correct. That is really not the way to practice medicine. 

We now have more evidence about what really is going on. A doctor was recently interviewed by ProPublica and said that she had worked for Cigna as a reviewer. Basically, the message she got from that insurer was to speed it up, go fast, and basically “deny, deny, deny” when she got requests. Those are her words, not mine.

We get a peek under the tent of how this works, and Dr. Day is basically saying she had to leave because she just didn’t feel that it was evidence-driven. It was driven by concerns about who’s going to lose money or make money.

If you want to check to see whether something is appropriate, the question becomes, who ought to do prior review? 

Who does it now? Sometimes doctors. Sometimes nurses who aren’t in the specialty where the request is coming in for preapproval. I’ve even seen situations where some companies use nurses in other countries, such as the Philippines, to do preapproval. They send them information, like a clip, to use to deny things that basically is boilerplate language, whatever the request is.

Looming up now, some insurers are starting to think, well, maybe artificial intelligence could do it. Just review the written request, trigger certain responses on the part of the artificial intelligence — it can deny the claims just as well as a human — and maybe it’s even cheaper to set up that system for the insurer.

This is ethically nuts. We need to have a system where doctors’ judgments drive what patients get. You listen to doctors, as I do, about preapproval access and they say patients sometimes give up trying to get what they think is needed. Continuity of care is interrupted if they have to keep making requests all the time.

There are adverse events when the thing that the doctor thought was most appropriate isn’t approved and something else is used that is less safe or less efficacious. It isn’t in patient interest to have the person with the wallet saying, this is what we think you need, and then having unqualified people or even automated intelligence with no accountability and no transparency get involved in preauthorization.

This system costs us money because middlemen are doing all this work. It basically becomes one of the huge scandals, in my view, of our health system, that doctors don’t ultimately decide what the patient needs. A preauthorizing third party or robot, without transparency, without accountability, and behind closed doors second-guesses what’s going on.

I’m Art Caplan at the Division of Medical Ethics at the New York University Grossman School of Medicine.

Arthur L. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York, New York, has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position). Serves as a contributing author and advisor for Medscape.

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

This transcript has been edited for clarity. 

Hi. I’m Art Caplan. I’m at the Division of Medical Ethics at New York University Grossman School of Medicine in New York City. 

There are many things screwy with our healthcare system. Many of you [reading] this are dealing with bureaucracy, paperwork, all sorts of constraints, restraints, and requirements that sometimes make the practice of medicine, or even nursing, difficult.

I don’t think I’ve seen anything screwier, from a moral point of view, than the system we have that allows for preauthorization by third-party payers, or insurers, in order to give care to patients. It’s pretty clear that a third-party payer has a conflict of interest. It’s simple: They don’t want to spend money.

Their goal as profit-making companies is to reduce what it is that they’re going to authorize. That clearly is driving how the preauthorization process works. We’re not getting a neutral review by third parties of the appropriateness of treatment recommendations or somebody saying, this is the standard of care and this is what ought to happen.

We’re letting the people who have the pocketbooks and the wallets have prior approval of what the doctor thinks is correct. That is really not the way to practice medicine. 

We now have more evidence about what really is going on. A doctor was recently interviewed by ProPublica and said that she had worked for Cigna as a reviewer. Basically, the message she got from that insurer was to speed it up, go fast, and basically “deny, deny, deny” when she got requests. Those are her words, not mine.

We get a peek under the tent of how this works, and Dr. Day is basically saying she had to leave because she just didn’t feel that it was evidence-driven. It was driven by concerns about who’s going to lose money or make money.

If you want to check to see whether something is appropriate, the question becomes, who ought to do prior review? 

Who does it now? Sometimes doctors. Sometimes nurses who aren’t in the specialty where the request is coming in for preapproval. I’ve even seen situations where some companies use nurses in other countries, such as the Philippines, to do preapproval. They send them information, like a clip, to use to deny things that basically is boilerplate language, whatever the request is.

Looming up now, some insurers are starting to think, well, maybe artificial intelligence could do it. Just review the written request, trigger certain responses on the part of the artificial intelligence — it can deny the claims just as well as a human — and maybe it’s even cheaper to set up that system for the insurer.

This is ethically nuts. We need to have a system where doctors’ judgments drive what patients get. You listen to doctors, as I do, about preapproval access and they say patients sometimes give up trying to get what they think is needed. Continuity of care is interrupted if they have to keep making requests all the time.

There are adverse events when the thing that the doctor thought was most appropriate isn’t approved and something else is used that is less safe or less efficacious. It isn’t in patient interest to have the person with the wallet saying, this is what we think you need, and then having unqualified people or even automated intelligence with no accountability and no transparency get involved in preauthorization.

This system costs us money because middlemen are doing all this work. It basically becomes one of the huge scandals, in my view, of our health system, that doctors don’t ultimately decide what the patient needs. A preauthorizing third party or robot, without transparency, without accountability, and behind closed doors second-guesses what’s going on.

I’m Art Caplan at the Division of Medical Ethics at the New York University Grossman School of Medicine.

Arthur L. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York, New York, has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position). Serves as a contributing author and advisor for Medscape.

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

This transcript has been edited for clarity. 

Hi. I’m Art Caplan. I’m at the Division of Medical Ethics at New York University Grossman School of Medicine in New York City. 

There are many things screwy with our healthcare system. Many of you [reading] this are dealing with bureaucracy, paperwork, all sorts of constraints, restraints, and requirements that sometimes make the practice of medicine, or even nursing, difficult.

I don’t think I’ve seen anything screwier, from a moral point of view, than the system we have that allows for preauthorization by third-party payers, or insurers, in order to give care to patients. It’s pretty clear that a third-party payer has a conflict of interest. It’s simple: They don’t want to spend money.

Their goal as profit-making companies is to reduce what it is that they’re going to authorize. That clearly is driving how the preauthorization process works. We’re not getting a neutral review by third parties of the appropriateness of treatment recommendations or somebody saying, this is the standard of care and this is what ought to happen.

We’re letting the people who have the pocketbooks and the wallets have prior approval of what the doctor thinks is correct. That is really not the way to practice medicine. 

We now have more evidence about what really is going on. A doctor was recently interviewed by ProPublica and said that she had worked for Cigna as a reviewer. Basically, the message she got from that insurer was to speed it up, go fast, and basically “deny, deny, deny” when she got requests. Those are her words, not mine.

We get a peek under the tent of how this works, and Dr. Day is basically saying she had to leave because she just didn’t feel that it was evidence-driven. It was driven by concerns about who’s going to lose money or make money.

If you want to check to see whether something is appropriate, the question becomes, who ought to do prior review? 

Who does it now? Sometimes doctors. Sometimes nurses who aren’t in the specialty where the request is coming in for preapproval. I’ve even seen situations where some companies use nurses in other countries, such as the Philippines, to do preapproval. They send them information, like a clip, to use to deny things that basically is boilerplate language, whatever the request is.

Looming up now, some insurers are starting to think, well, maybe artificial intelligence could do it. Just review the written request, trigger certain responses on the part of the artificial intelligence — it can deny the claims just as well as a human — and maybe it’s even cheaper to set up that system for the insurer.

This is ethically nuts. We need to have a system where doctors’ judgments drive what patients get. You listen to doctors, as I do, about preapproval access and they say patients sometimes give up trying to get what they think is needed. Continuity of care is interrupted if they have to keep making requests all the time.

There are adverse events when the thing that the doctor thought was most appropriate isn’t approved and something else is used that is less safe or less efficacious. It isn’t in patient interest to have the person with the wallet saying, this is what we think you need, and then having unqualified people or even automated intelligence with no accountability and no transparency get involved in preauthorization.

This system costs us money because middlemen are doing all this work. It basically becomes one of the huge scandals, in my view, of our health system, that doctors don’t ultimately decide what the patient needs. A preauthorizing third party or robot, without transparency, without accountability, and behind closed doors second-guesses what’s going on.

I’m Art Caplan at the Division of Medical Ethics at the New York University Grossman School of Medicine.

Arthur L. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York, New York, has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position). Serves as a contributing author and advisor for Medscape.

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

Recently, a patient of mine was hospitalized with chest pain. She was diagnosed with an acute coronary syndrome and started on a statin in addition to a beta-blocker, aspirin, and clopidogrel. After discharge, she had symptoms of dizziness and recurrent chest pain and her first thought was to stop the statin because she believed that her symptoms were statin-related side effects. I will cover a few areas where I think that there are some misunderstandings about statins.

Statins Are Not Bad For the Liver

When lovastatin first became available for prescription in the 1980s, frequent monitoring of transaminases was recommended. Patients and healthcare professionals became accustomed to frequent liver tests to monitor for statin toxicity, and to this day, some healthcare professionals still obtain liver function tests for this purpose.

But is there a reason to do this? Pfeffer and colleagues reported on the results of over 112,000 people enrolled in the West of Scotland Coronary Protection trial and found that the percentage of patients with any abnormal liver function test was similar (> 3 times the upper limit of normal for ALT) for patients taking pravastatin (1.4%) and for patients taking placebo (1.4%).¹ A panel of liver experts concurred that statin-associated transaminase elevations were not indicative of liver damage or dysfunction.² Furthermore, they noted that chronic liver disease and compensated cirrhosis were not contraindications to statin use.

In a small study, use of low-dose atorvastatin in patients with nonalcoholic steatohepatitis improved transaminase values in 75% of patients and liver steatosis and nonalcoholic fatty liver disease activity scores were significantly improved on biopsy in most of the patients.³ The US Food and Drug Administration (FDA) removed the recommendation for routine regular monitoring of liver function for patients on statins in 2012.⁴

Statins Do Not Cause Muscle Pain in Most Patients

Most muscle pain occurring in patients on statins is not due to the statin although patient concerns about muscle pain are common. In a meta-analysis of 19 large statin trials, 27.1% of participants treated with a statin reported at least one episode of muscle pain or weakness during a median of 4.3 years, compared with 26.6% of participants treated with placebo.⁵ Muscle pain for any reason is common, and patients on statins may stop therapy because of the symptoms.

Cohen and colleagues performed a survey of past and current statin users, asking about muscle symptoms.⁶ Muscle-related side effects were reported by 60% of former statin users and 25% of current users.

Herrett and colleagues performed an extensive series of n-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.⁷ Participants received either 2-month blocks of atorvastatin 20 mg or 2-month blocks of placebo, six times. They rated their muscle symptoms on a visual analogue scale at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.

Wood and colleagues took it a step further when they planned an n-of-1 trial that included statin, placebo, and no treatment.⁸ Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on a random sequence and reported daily symptom scores. The mean symptom intensity score was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
 

Statins Are Likely Helpful In the Very Elderly

Should we be using statins for primary prevention in our very old patients? For many years the answer was generally “no” on the basis of a lack of evidence. Patients in their 80s often were not included in clinical trials. The much used American Heart Association risk calculator stops at age 79. Given the prevalence of coronary artery disease in patients as they reach their 80s, wouldn’t primary prevention really be secondary prevention? Xu and colleagues in a recent study compared outcomes for patients who were treated with statins for primary prevention with a group who were not. In the patients aged 75-84 there was a risk reduction for major cardiovascular events of 1.2% over 5 years, and for those 85 and older the risk reduction was 4.4%. Importantly, there were no significantly increased risks for myopathies and liver dysfunction in either age group.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Pfeffer MA et al. Circulation. 2002;105(20):2341-6.

2. Cohen DE et al. Am J Cardiol. 2006;97(8A):77C-81C.

3. Hyogo H et al. Metabolism. 2008;57(12):1711-8.

4. FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs. 2012 Feb 28.

5. Cholesterol Treatment Trialists’ Collaboration. Lancet. 2022;400(10355):832-45.

6. Cohen JD et al. J Clin Lipidol. 2012;6(3):208-15.

7. Herrett E et al. BMJ. 2021 Feb 24;372:n1355.

8. Wood FA et al. N Engl J Med. 2020;383(22):2182-4.

9. Xu W et al. Ann Intern Med. 2024;177(6):701-10.

Recently, a patient of mine was hospitalized with chest pain. She was diagnosed with an acute coronary syndrome and started on a statin in addition to a beta-blocker, aspirin, and clopidogrel. After discharge, she had symptoms of dizziness and recurrent chest pain and her first thought was to stop the statin because she believed that her symptoms were statin-related side effects. I will cover a few areas where I think that there are some misunderstandings about statins.

Statins Are Not Bad For the Liver

When lovastatin first became available for prescription in the 1980s, frequent monitoring of transaminases was recommended. Patients and healthcare professionals became accustomed to frequent liver tests to monitor for statin toxicity, and to this day, some healthcare professionals still obtain liver function tests for this purpose.

But is there a reason to do this? Pfeffer and colleagues reported on the results of over 112,000 people enrolled in the West of Scotland Coronary Protection trial and found that the percentage of patients with any abnormal liver function test was similar (> 3 times the upper limit of normal for ALT) for patients taking pravastatin (1.4%) and for patients taking placebo (1.4%).¹ A panel of liver experts concurred that statin-associated transaminase elevations were not indicative of liver damage or dysfunction.² Furthermore, they noted that chronic liver disease and compensated cirrhosis were not contraindications to statin use.

In a small study, use of low-dose atorvastatin in patients with nonalcoholic steatohepatitis improved transaminase values in 75% of patients and liver steatosis and nonalcoholic fatty liver disease activity scores were significantly improved on biopsy in most of the patients.³ The US Food and Drug Administration (FDA) removed the recommendation for routine regular monitoring of liver function for patients on statins in 2012.⁴

Statins Do Not Cause Muscle Pain in Most Patients

Most muscle pain occurring in patients on statins is not due to the statin although patient concerns about muscle pain are common. In a meta-analysis of 19 large statin trials, 27.1% of participants treated with a statin reported at least one episode of muscle pain or weakness during a median of 4.3 years, compared with 26.6% of participants treated with placebo.⁵ Muscle pain for any reason is common, and patients on statins may stop therapy because of the symptoms.

Cohen and colleagues performed a survey of past and current statin users, asking about muscle symptoms.⁶ Muscle-related side effects were reported by 60% of former statin users and 25% of current users.

Herrett and colleagues performed an extensive series of n-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.⁷ Participants received either 2-month blocks of atorvastatin 20 mg or 2-month blocks of placebo, six times. They rated their muscle symptoms on a visual analogue scale at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.

Wood and colleagues took it a step further when they planned an n-of-1 trial that included statin, placebo, and no treatment.⁸ Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on a random sequence and reported daily symptom scores. The mean symptom intensity score was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
 

Statins Are Likely Helpful In the Very Elderly

Should we be using statins for primary prevention in our very old patients? For many years the answer was generally “no” on the basis of a lack of evidence. Patients in their 80s often were not included in clinical trials. The much used American Heart Association risk calculator stops at age 79. Given the prevalence of coronary artery disease in patients as they reach their 80s, wouldn’t primary prevention really be secondary prevention? Xu and colleagues in a recent study compared outcomes for patients who were treated with statins for primary prevention with a group who were not. In the patients aged 75-84 there was a risk reduction for major cardiovascular events of 1.2% over 5 years, and for those 85 and older the risk reduction was 4.4%. Importantly, there were no significantly increased risks for myopathies and liver dysfunction in either age group.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Pfeffer MA et al. Circulation. 2002;105(20):2341-6.

2. Cohen DE et al. Am J Cardiol. 2006;97(8A):77C-81C.

3. Hyogo H et al. Metabolism. 2008;57(12):1711-8.

4. FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs. 2012 Feb 28.

5. Cholesterol Treatment Trialists’ Collaboration. Lancet. 2022;400(10355):832-45.

6. Cohen JD et al. J Clin Lipidol. 2012;6(3):208-15.

7. Herrett E et al. BMJ. 2021 Feb 24;372:n1355.

8. Wood FA et al. N Engl J Med. 2020;383(22):2182-4.

9. Xu W et al. Ann Intern Med. 2024;177(6):701-10.

Recently, a patient of mine was hospitalized with chest pain. She was diagnosed with an acute coronary syndrome and started on a statin in addition to a beta-blocker, aspirin, and clopidogrel. After discharge, she had symptoms of dizziness and recurrent chest pain and her first thought was to stop the statin because she believed that her symptoms were statin-related side effects. I will cover a few areas where I think that there are some misunderstandings about statins.

Statins Are Not Bad For the Liver

When lovastatin first became available for prescription in the 1980s, frequent monitoring of transaminases was recommended. Patients and healthcare professionals became accustomed to frequent liver tests to monitor for statin toxicity, and to this day, some healthcare professionals still obtain liver function tests for this purpose.

But is there a reason to do this? Pfeffer and colleagues reported on the results of over 112,000 people enrolled in the West of Scotland Coronary Protection trial and found that the percentage of patients with any abnormal liver function test was similar (> 3 times the upper limit of normal for ALT) for patients taking pravastatin (1.4%) and for patients taking placebo (1.4%).¹ A panel of liver experts concurred that statin-associated transaminase elevations were not indicative of liver damage or dysfunction.² Furthermore, they noted that chronic liver disease and compensated cirrhosis were not contraindications to statin use.

In a small study, use of low-dose atorvastatin in patients with nonalcoholic steatohepatitis improved transaminase values in 75% of patients and liver steatosis and nonalcoholic fatty liver disease activity scores were significantly improved on biopsy in most of the patients.³ The US Food and Drug Administration (FDA) removed the recommendation for routine regular monitoring of liver function for patients on statins in 2012.⁴

Statins Do Not Cause Muscle Pain in Most Patients

Most muscle pain occurring in patients on statins is not due to the statin although patient concerns about muscle pain are common. In a meta-analysis of 19 large statin trials, 27.1% of participants treated with a statin reported at least one episode of muscle pain or weakness during a median of 4.3 years, compared with 26.6% of participants treated with placebo.⁵ Muscle pain for any reason is common, and patients on statins may stop therapy because of the symptoms.

Cohen and colleagues performed a survey of past and current statin users, asking about muscle symptoms.⁶ Muscle-related side effects were reported by 60% of former statin users and 25% of current users.

Herrett and colleagues performed an extensive series of n-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.⁷ Participants received either 2-month blocks of atorvastatin 20 mg or 2-month blocks of placebo, six times. They rated their muscle symptoms on a visual analogue scale at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.

Wood and colleagues took it a step further when they planned an n-of-1 trial that included statin, placebo, and no treatment.⁸ Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on a random sequence and reported daily symptom scores. The mean symptom intensity score was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
 

Statins Are Likely Helpful In the Very Elderly

Should we be using statins for primary prevention in our very old patients? For many years the answer was generally “no” on the basis of a lack of evidence. Patients in their 80s often were not included in clinical trials. The much used American Heart Association risk calculator stops at age 79. Given the prevalence of coronary artery disease in patients as they reach their 80s, wouldn’t primary prevention really be secondary prevention? Xu and colleagues in a recent study compared outcomes for patients who were treated with statins for primary prevention with a group who were not. In the patients aged 75-84 there was a risk reduction for major cardiovascular events of 1.2% over 5 years, and for those 85 and older the risk reduction was 4.4%. Importantly, there were no significantly increased risks for myopathies and liver dysfunction in either age group.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Pfeffer MA et al. Circulation. 2002;105(20):2341-6.

2. Cohen DE et al. Am J Cardiol. 2006;97(8A):77C-81C.

3. Hyogo H et al. Metabolism. 2008;57(12):1711-8.

4. FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs. 2012 Feb 28.

5. Cholesterol Treatment Trialists’ Collaboration. Lancet. 2022;400(10355):832-45.

6. Cohen JD et al. J Clin Lipidol. 2012;6(3):208-15.

7. Herrett E et al. BMJ. 2021 Feb 24;372:n1355.

8. Wood FA et al. N Engl J Med. 2020;383(22):2182-4.

9. Xu W et al. Ann Intern Med. 2024;177(6):701-10.

To the Editor:

We read with interest the Case Letter from Wang et al¹ (Cutis. 2023;112:E13-E15) of a 60-year-old man whose metastatic salivary duct adenocarcinoma manifested with the shield sign as well as carcinoma hemorrhagiectoides. Cutaneous metastases have seldom been described in association with salivary duct carcinoma.^2-7 In addition, carcinoma hemorrhagiectoides–associated shield sign has not been commonly reported.^5,8-12

Salivary duct carcinoma—an uncommon head and neck malignancy characterized by androgen receptor expression—rarely is associated with cutaneous metastases. Based on a PubMed search of articles indexed for MEDLINE using the terms cutaneous, metastatic, salivary duct carcinoma, and/or skin, including the patient described by Wang et al,¹ there have been 8 individuals with cutaneous metastases from this cancer. The morphology of the cutaneous metastases has varied from angiomatous to angiokeratomalike (black and keratotic) papules, bullae, macules (red), papules and nodules (erythematous and scaly), plaques (cellulitislike and confluent that were purpuric, hemorrhagic, and violaceous), pseudovesicles, purpuric papules, subcutaneous nodules, and an ulcer (superficial and mimicked a basal cell carcinoma).^1-7 Remarkably, 4 of 8 patients (50%) with salivary duct carcinoma cutaneous metastases presented with a shield sign,^5,7 including the case reported by Wang et al.¹

The shield sign is a distinctive clinical manifestation of cutaneous metastasis.¹⁰ It was named to describe the skin metastases located predominantly on the chest area that would be covered by a medieval knight’s shield^5,10,12; metastatic lesions also have been noted on the proximal arm and/or the upper back in a similar distribution.^8,9 To date, based on a PubMed search of articles indexed for MEDLINE using the search terms breast cancer, carcinoma, hemorrhagiectoides, metastases, salivary duct carcinoma, shield, and/or sign, the shield sign has been described in 6 patients with cutaneous metastases either from salivary duct carcinoma (4 patients)^1,5,7 or breast cancer (2 patients).^8,9 The shield sign pathologically corresponds to carcinoma hemorrhagiectoides, an inflammatory pattern of cutaneous metastases.^5,11

Inflammatory cutaneous metastatic carcinoma has 3 distinctive clinical and pathologic manifestations.¹¹ Carcinoma erysipelatoides and carcinoma telangiectoides were the earlier described variants.¹¹ In 2012, carcinoma hemorrhagiectoides was described as the third pattern of inflammatory cutaneous metastasis.⁵

Carcinoma erysipelatoides, which clinically mimics cutaneous streptococcal cellulitis, appears as a well-defined erythematous patch or plaque; the tumor cells can be found in the lymphatic vessels and either are absent or minimally present in the dermis. Carcinoma telangiectoides, which clinically mimics idiopathic telangiectases, appears as an erythematous patch with prominent telangiectases; the tumor cells can be found in the blood vessels and are either absent or minimally present in the dermis. Carcinoma hemorrhagiectoides appears as purpuric or violaceous indurated plaques; the tumor cells are not only found in the blood vessels, in the lymphatic vessels, or both, but also can be mildly to extensively present in the dermis.^5,10,11

In conclusion, the shield sign is a unique presentation of inflammatory cutaneous metastatic carcinoma, which is associated with carcinoma hemorrhagiectoides. The clinical features of the infiltrated plaques correspond to the presence of tumor cells in the blood vessels, lymphatic vessels, and the dermis; in addition, the purpuric and violaceous appearance correlates with the presence of extravasated erythrocytes or hemorrhage in the dermis. To date, half of the patients with skin metastases from salivary duct carcinoma have presented with carcinoma hemorrhagiectoides–associated shield sign.

Authors’ Response

We appreciate and welcome the comments provided by the authors. Drawing attention to unusual pathologic manifestations of cutaneous metastatic salivary duct carcinoma manifesting with the shield sign, the authors present a comprehensive review of 3 distinctive presentations: carcinoma erysipelatoides, carcinoma telangiectoides, and carcinoma hemorrhagiectoides. The inclusion of these variants enriches the discussion and makes this letter a valuable addition to the literature on cutaneous metastatic carcinoma, particularly metastatic salivary duct carcinoma.

Xintong Wang, MD; William H. Westra, MD

From the Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York.

The authors report no conflict of interest.

To the Editor:

We read with interest the Case Letter from Wang et al¹ (Cutis. 2023;112:E13-E15) of a 60-year-old man whose metastatic salivary duct adenocarcinoma manifested with the shield sign as well as carcinoma hemorrhagiectoides. Cutaneous metastases have seldom been described in association with salivary duct carcinoma.^2-7 In addition, carcinoma hemorrhagiectoides–associated shield sign has not been commonly reported.^5,8-12

Salivary duct carcinoma—an uncommon head and neck malignancy characterized by androgen receptor expression—rarely is associated with cutaneous metastases. Based on a PubMed search of articles indexed for MEDLINE using the terms cutaneous, metastatic, salivary duct carcinoma, and/or skin, including the patient described by Wang et al,¹ there have been 8 individuals with cutaneous metastases from this cancer. The morphology of the cutaneous metastases has varied from angiomatous to angiokeratomalike (black and keratotic) papules, bullae, macules (red), papules and nodules (erythematous and scaly), plaques (cellulitislike and confluent that were purpuric, hemorrhagic, and violaceous), pseudovesicles, purpuric papules, subcutaneous nodules, and an ulcer (superficial and mimicked a basal cell carcinoma).^1-7 Remarkably, 4 of 8 patients (50%) with salivary duct carcinoma cutaneous metastases presented with a shield sign,^5,7 including the case reported by Wang et al.¹

The shield sign is a distinctive clinical manifestation of cutaneous metastasis.¹⁰ It was named to describe the skin metastases located predominantly on the chest area that would be covered by a medieval knight’s shield^5,10,12; metastatic lesions also have been noted on the proximal arm and/or the upper back in a similar distribution.^8,9 To date, based on a PubMed search of articles indexed for MEDLINE using the search terms breast cancer, carcinoma, hemorrhagiectoides, metastases, salivary duct carcinoma, shield, and/or sign, the shield sign has been described in 6 patients with cutaneous metastases either from salivary duct carcinoma (4 patients)^1,5,7 or breast cancer (2 patients).^8,9 The shield sign pathologically corresponds to carcinoma hemorrhagiectoides, an inflammatory pattern of cutaneous metastases.^5,11

Inflammatory cutaneous metastatic carcinoma has 3 distinctive clinical and pathologic manifestations.¹¹ Carcinoma erysipelatoides and carcinoma telangiectoides were the earlier described variants.¹¹ In 2012, carcinoma hemorrhagiectoides was described as the third pattern of inflammatory cutaneous metastasis.⁵

Carcinoma erysipelatoides, which clinically mimics cutaneous streptococcal cellulitis, appears as a well-defined erythematous patch or plaque; the tumor cells can be found in the lymphatic vessels and either are absent or minimally present in the dermis. Carcinoma telangiectoides, which clinically mimics idiopathic telangiectases, appears as an erythematous patch with prominent telangiectases; the tumor cells can be found in the blood vessels and are either absent or minimally present in the dermis. Carcinoma hemorrhagiectoides appears as purpuric or violaceous indurated plaques; the tumor cells are not only found in the blood vessels, in the lymphatic vessels, or both, but also can be mildly to extensively present in the dermis.^5,10,11

In conclusion, the shield sign is a unique presentation of inflammatory cutaneous metastatic carcinoma, which is associated with carcinoma hemorrhagiectoides. The clinical features of the infiltrated plaques correspond to the presence of tumor cells in the blood vessels, lymphatic vessels, and the dermis; in addition, the purpuric and violaceous appearance correlates with the presence of extravasated erythrocytes or hemorrhage in the dermis. To date, half of the patients with skin metastases from salivary duct carcinoma have presented with carcinoma hemorrhagiectoides–associated shield sign.

Authors’ Response

We appreciate and welcome the comments provided by the authors. Drawing attention to unusual pathologic manifestations of cutaneous metastatic salivary duct carcinoma manifesting with the shield sign, the authors present a comprehensive review of 3 distinctive presentations: carcinoma erysipelatoides, carcinoma telangiectoides, and carcinoma hemorrhagiectoides. The inclusion of these variants enriches the discussion and makes this letter a valuable addition to the literature on cutaneous metastatic carcinoma, particularly metastatic salivary duct carcinoma.

Xintong Wang, MD; William H. Westra, MD

From the Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York.

The authors report no conflict of interest.

To the Editor:

We read with interest the Case Letter from Wang et al¹ (Cutis. 2023;112:E13-E15) of a 60-year-old man whose metastatic salivary duct adenocarcinoma manifested with the shield sign as well as carcinoma hemorrhagiectoides. Cutaneous metastases have seldom been described in association with salivary duct carcinoma.^2-7 In addition, carcinoma hemorrhagiectoides–associated shield sign has not been commonly reported.^5,8-12

Salivary duct carcinoma—an uncommon head and neck malignancy characterized by androgen receptor expression—rarely is associated with cutaneous metastases. Based on a PubMed search of articles indexed for MEDLINE using the terms cutaneous, metastatic, salivary duct carcinoma, and/or skin, including the patient described by Wang et al,¹ there have been 8 individuals with cutaneous metastases from this cancer. The morphology of the cutaneous metastases has varied from angiomatous to angiokeratomalike (black and keratotic) papules, bullae, macules (red), papules and nodules (erythematous and scaly), plaques (cellulitislike and confluent that were purpuric, hemorrhagic, and violaceous), pseudovesicles, purpuric papules, subcutaneous nodules, and an ulcer (superficial and mimicked a basal cell carcinoma).^1-7 Remarkably, 4 of 8 patients (50%) with salivary duct carcinoma cutaneous metastases presented with a shield sign,^5,7 including the case reported by Wang et al.¹

The shield sign is a distinctive clinical manifestation of cutaneous metastasis.¹⁰ It was named to describe the skin metastases located predominantly on the chest area that would be covered by a medieval knight’s shield^5,10,12; metastatic lesions also have been noted on the proximal arm and/or the upper back in a similar distribution.^8,9 To date, based on a PubMed search of articles indexed for MEDLINE using the search terms breast cancer, carcinoma, hemorrhagiectoides, metastases, salivary duct carcinoma, shield, and/or sign, the shield sign has been described in 6 patients with cutaneous metastases either from salivary duct carcinoma (4 patients)^1,5,7 or breast cancer (2 patients).^8,9 The shield sign pathologically corresponds to carcinoma hemorrhagiectoides, an inflammatory pattern of cutaneous metastases.^5,11

Inflammatory cutaneous metastatic carcinoma has 3 distinctive clinical and pathologic manifestations.¹¹ Carcinoma erysipelatoides and carcinoma telangiectoides were the earlier described variants.¹¹ In 2012, carcinoma hemorrhagiectoides was described as the third pattern of inflammatory cutaneous metastasis.⁵

Carcinoma erysipelatoides, which clinically mimics cutaneous streptococcal cellulitis, appears as a well-defined erythematous patch or plaque; the tumor cells can be found in the lymphatic vessels and either are absent or minimally present in the dermis. Carcinoma telangiectoides, which clinically mimics idiopathic telangiectases, appears as an erythematous patch with prominent telangiectases; the tumor cells can be found in the blood vessels and are either absent or minimally present in the dermis. Carcinoma hemorrhagiectoides appears as purpuric or violaceous indurated plaques; the tumor cells are not only found in the blood vessels, in the lymphatic vessels, or both, but also can be mildly to extensively present in the dermis.^5,10,11

In conclusion, the shield sign is a unique presentation of inflammatory cutaneous metastatic carcinoma, which is associated with carcinoma hemorrhagiectoides. The clinical features of the infiltrated plaques correspond to the presence of tumor cells in the blood vessels, lymphatic vessels, and the dermis; in addition, the purpuric and violaceous appearance correlates with the presence of extravasated erythrocytes or hemorrhage in the dermis. To date, half of the patients with skin metastases from salivary duct carcinoma have presented with carcinoma hemorrhagiectoides–associated shield sign.

Authors’ Response

We appreciate and welcome the comments provided by the authors. Drawing attention to unusual pathologic manifestations of cutaneous metastatic salivary duct carcinoma manifesting with the shield sign, the authors present a comprehensive review of 3 distinctive presentations: carcinoma erysipelatoides, carcinoma telangiectoides, and carcinoma hemorrhagiectoides. The inclusion of these variants enriches the discussion and makes this letter a valuable addition to the literature on cutaneous metastatic carcinoma, particularly metastatic salivary duct carcinoma.

Xintong Wang, MD; William H. Westra, MD

From the Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York.

The authors report no conflict of interest.