MDedge Internal Medicine

This transcript has been edited for clarity. 

Aspirin. Once upon a time, everybody over age 50 years was supposed to take a baby aspirin. Now we make it a point to tell people to stop. What is going on?  

Our recommendations vis-à-vis aspirin have evolved at a dizzying pace. The young’uns watching us right now don’t know what things were like in the 1980s. The Reagan era was a wild, heady time where nuclear war was imminent and we didn’t prescribe aspirin to patients. 

That only started in 1988, which was a banner year in human history. Not because a number of doves were incinerated by the lighting of the Olympic torch at the Seoul Olympics — look it up if you don’t know what I’m talking about — but because 1988 saw the publication of the ISIS-2 trial, which first showed a mortality benefit to prescribing aspirin post–myocardial infarction (MI).

Giving patients aspirin during or after a heart attack is not controversial. It’s one of the few things in this business that isn’t, but that’s secondary prevention — treating somebody after they develop a disease. Primary prevention, treating them before they have their incident event, is a very different ballgame. Here, things are messy. 

For one thing, the doses used have been very inconsistent. We should point out that the reason for 81 mg of aspirin is very arbitrary and is rooted in the old apothecary system of weights and measurements. A standard dose of aspirin was 5 grains, where 20 grains made 1 scruple, 3 scruples made 1 dram, 8 drams made 1 oz, and 12 oz made 1 lb - because screw you, metric system. Therefore, 5 grains was 325 mg of aspirin, and 1 quarter of the standard dose became 81 mg if you rounded out the decimal. 

People have tried all kinds of dosing structures with aspirin prophylaxis. The Physicians’ Health Study used a full-dose aspirin, 325 mg every 2 days, while the Hypertension Optimal Treatment (HOT) trial tested 75 mg daily and the Women’s Health Study tested 100 mg, but every other day. 

Ironically, almost no one has studied 81 mg every day, which is weird if you think about it. The bigger problem here is not the variability of doses used, but the discrepancy when you look at older vs newer studies.

Older studies, like the Physicians’ Health Study, did show a benefit, at least in the subgroup of patients over age 50 years, which is probably where the “everybody over 50 should be taking an aspirin” idea comes from, at least as near as I can tell. 

More recent studies, like the Women’s Health Study, ASPREE, or ASPIRE, didn’t show a benefit. I know what you’re thinking: Newer stuff is always better. That’s why you should never trust anybody over age 40 years. The context of primary prevention studies has changed. In the ‘80s and ‘90s, people smoked more and we didn’t have the same medications that we have today. We talked about all this in the beta-blocker video to explain why beta-blockers don’t seem to have a benefit post MI.

We have a similar issue here. The magnitude of the benefit with aspirin primary prevention has decreased because we’re all just healthier overall. So, yay! Progress! Here’s where the numbers matter. No one is saying that aspirin doesn’t help. It does. 

If we look at the 2019 meta-analysis published in JAMA, there is a cardiovascular benefit. The numbers bear that out. I know you’re all here for the math, so here we go. Aspirin reduced the composite cardiovascular endpoint from 65.2 to 60.2 events per 10,000 patient-years; or to put it more meaningfully in absolute risk reduction terms, because that’s my jam, an absolute risk reduction of 0.41%, which means a number needed to treat of 241, which is okay-ish. It’s not super-great, but it may be justifiable for something that costs next to nothing. 

The tradeoff is bleeding. Major bleeding increased from 16.4 to 23.1 bleeds per 10,000 patient-years, or an absolute risk increase of 0.47%, which is a number needed to harm of 210. That’s the problem. Aspirin does prevent heart disease. The benefit is small, for sure, but the real problem is that it’s outweighed by the risk of bleeding, so you’re not really coming out ahead. 

The real tragedy here is that the public is locked into this idea of everyone over age 50 years should be taking an aspirin. Even today, even though guidelines have recommended against aspirin for primary prevention for some time, data from the National Health Interview Survey sample found that nearly one in three older adults take aspirin for primary prevention when they shouldn’t be. That’s a large number of people. That’s millions of Americans — and Canadians, but nobody cares about us. It’s fine. 

That’s the point. We’re not debunking aspirin. It does work. The benefits are just really small in a primary prevention population and offset by the admittedly also really small risks of bleeding. It’s a tradeoff that doesn’t really work in your favor.

But that’s aspirin for cardiovascular disease. When it comes to cancer or DVT prophylaxis, that’s another really interesting story. We might have to save that for another time. Do I know how to tease a sequel or what?

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. 

Aspirin. Once upon a time, everybody over age 50 years was supposed to take a baby aspirin. Now we make it a point to tell people to stop. What is going on?  

Our recommendations vis-à-vis aspirin have evolved at a dizzying pace. The young’uns watching us right now don’t know what things were like in the 1980s. The Reagan era was a wild, heady time where nuclear war was imminent and we didn’t prescribe aspirin to patients. 

That only started in 1988, which was a banner year in human history. Not because a number of doves were incinerated by the lighting of the Olympic torch at the Seoul Olympics — look it up if you don’t know what I’m talking about — but because 1988 saw the publication of the ISIS-2 trial, which first showed a mortality benefit to prescribing aspirin post–myocardial infarction (MI).

Giving patients aspirin during or after a heart attack is not controversial. It’s one of the few things in this business that isn’t, but that’s secondary prevention — treating somebody after they develop a disease. Primary prevention, treating them before they have their incident event, is a very different ballgame. Here, things are messy. 

For one thing, the doses used have been very inconsistent. We should point out that the reason for 81 mg of aspirin is very arbitrary and is rooted in the old apothecary system of weights and measurements. A standard dose of aspirin was 5 grains, where 20 grains made 1 scruple, 3 scruples made 1 dram, 8 drams made 1 oz, and 12 oz made 1 lb - because screw you, metric system. Therefore, 5 grains was 325 mg of aspirin, and 1 quarter of the standard dose became 81 mg if you rounded out the decimal. 

People have tried all kinds of dosing structures with aspirin prophylaxis. The Physicians’ Health Study used a full-dose aspirin, 325 mg every 2 days, while the Hypertension Optimal Treatment (HOT) trial tested 75 mg daily and the Women’s Health Study tested 100 mg, but every other day. 

Ironically, almost no one has studied 81 mg every day, which is weird if you think about it. The bigger problem here is not the variability of doses used, but the discrepancy when you look at older vs newer studies.

Older studies, like the Physicians’ Health Study, did show a benefit, at least in the subgroup of patients over age 50 years, which is probably where the “everybody over 50 should be taking an aspirin” idea comes from, at least as near as I can tell. 

More recent studies, like the Women’s Health Study, ASPREE, or ASPIRE, didn’t show a benefit. I know what you’re thinking: Newer stuff is always better. That’s why you should never trust anybody over age 40 years. The context of primary prevention studies has changed. In the ‘80s and ‘90s, people smoked more and we didn’t have the same medications that we have today. We talked about all this in the beta-blocker video to explain why beta-blockers don’t seem to have a benefit post MI.

We have a similar issue here. The magnitude of the benefit with aspirin primary prevention has decreased because we’re all just healthier overall. So, yay! Progress! Here’s where the numbers matter. No one is saying that aspirin doesn’t help. It does. 

If we look at the 2019 meta-analysis published in JAMA, there is a cardiovascular benefit. The numbers bear that out. I know you’re all here for the math, so here we go. Aspirin reduced the composite cardiovascular endpoint from 65.2 to 60.2 events per 10,000 patient-years; or to put it more meaningfully in absolute risk reduction terms, because that’s my jam, an absolute risk reduction of 0.41%, which means a number needed to treat of 241, which is okay-ish. It’s not super-great, but it may be justifiable for something that costs next to nothing. 

The tradeoff is bleeding. Major bleeding increased from 16.4 to 23.1 bleeds per 10,000 patient-years, or an absolute risk increase of 0.47%, which is a number needed to harm of 210. That’s the problem. Aspirin does prevent heart disease. The benefit is small, for sure, but the real problem is that it’s outweighed by the risk of bleeding, so you’re not really coming out ahead. 

The real tragedy here is that the public is locked into this idea of everyone over age 50 years should be taking an aspirin. Even today, even though guidelines have recommended against aspirin for primary prevention for some time, data from the National Health Interview Survey sample found that nearly one in three older adults take aspirin for primary prevention when they shouldn’t be. That’s a large number of people. That’s millions of Americans — and Canadians, but nobody cares about us. It’s fine. 

That’s the point. We’re not debunking aspirin. It does work. The benefits are just really small in a primary prevention population and offset by the admittedly also really small risks of bleeding. It’s a tradeoff that doesn’t really work in your favor.

But that’s aspirin for cardiovascular disease. When it comes to cancer or DVT prophylaxis, that’s another really interesting story. We might have to save that for another time. Do I know how to tease a sequel or what?

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. 

Aspirin. Once upon a time, everybody over age 50 years was supposed to take a baby aspirin. Now we make it a point to tell people to stop. What is going on?  

Our recommendations vis-à-vis aspirin have evolved at a dizzying pace. The young’uns watching us right now don’t know what things were like in the 1980s. The Reagan era was a wild, heady time where nuclear war was imminent and we didn’t prescribe aspirin to patients. 

That only started in 1988, which was a banner year in human history. Not because a number of doves were incinerated by the lighting of the Olympic torch at the Seoul Olympics — look it up if you don’t know what I’m talking about — but because 1988 saw the publication of the ISIS-2 trial, which first showed a mortality benefit to prescribing aspirin post–myocardial infarction (MI).

Giving patients aspirin during or after a heart attack is not controversial. It’s one of the few things in this business that isn’t, but that’s secondary prevention — treating somebody after they develop a disease. Primary prevention, treating them before they have their incident event, is a very different ballgame. Here, things are messy. 

For one thing, the doses used have been very inconsistent. We should point out that the reason for 81 mg of aspirin is very arbitrary and is rooted in the old apothecary system of weights and measurements. A standard dose of aspirin was 5 grains, where 20 grains made 1 scruple, 3 scruples made 1 dram, 8 drams made 1 oz, and 12 oz made 1 lb - because screw you, metric system. Therefore, 5 grains was 325 mg of aspirin, and 1 quarter of the standard dose became 81 mg if you rounded out the decimal. 

People have tried all kinds of dosing structures with aspirin prophylaxis. The Physicians’ Health Study used a full-dose aspirin, 325 mg every 2 days, while the Hypertension Optimal Treatment (HOT) trial tested 75 mg daily and the Women’s Health Study tested 100 mg, but every other day. 

Ironically, almost no one has studied 81 mg every day, which is weird if you think about it. The bigger problem here is not the variability of doses used, but the discrepancy when you look at older vs newer studies.

Older studies, like the Physicians’ Health Study, did show a benefit, at least in the subgroup of patients over age 50 years, which is probably where the “everybody over 50 should be taking an aspirin” idea comes from, at least as near as I can tell. 

More recent studies, like the Women’s Health Study, ASPREE, or ASPIRE, didn’t show a benefit. I know what you’re thinking: Newer stuff is always better. That’s why you should never trust anybody over age 40 years. The context of primary prevention studies has changed. In the ‘80s and ‘90s, people smoked more and we didn’t have the same medications that we have today. We talked about all this in the beta-blocker video to explain why beta-blockers don’t seem to have a benefit post MI.

We have a similar issue here. The magnitude of the benefit with aspirin primary prevention has decreased because we’re all just healthier overall. So, yay! Progress! Here’s where the numbers matter. No one is saying that aspirin doesn’t help. It does. 

If we look at the 2019 meta-analysis published in JAMA, there is a cardiovascular benefit. The numbers bear that out. I know you’re all here for the math, so here we go. Aspirin reduced the composite cardiovascular endpoint from 65.2 to 60.2 events per 10,000 patient-years; or to put it more meaningfully in absolute risk reduction terms, because that’s my jam, an absolute risk reduction of 0.41%, which means a number needed to treat of 241, which is okay-ish. It’s not super-great, but it may be justifiable for something that costs next to nothing. 

The tradeoff is bleeding. Major bleeding increased from 16.4 to 23.1 bleeds per 10,000 patient-years, or an absolute risk increase of 0.47%, which is a number needed to harm of 210. That’s the problem. Aspirin does prevent heart disease. The benefit is small, for sure, but the real problem is that it’s outweighed by the risk of bleeding, so you’re not really coming out ahead. 

The real tragedy here is that the public is locked into this idea of everyone over age 50 years should be taking an aspirin. Even today, even though guidelines have recommended against aspirin for primary prevention for some time, data from the National Health Interview Survey sample found that nearly one in three older adults take aspirin for primary prevention when they shouldn’t be. That’s a large number of people. That’s millions of Americans — and Canadians, but nobody cares about us. It’s fine. 

That’s the point. We’re not debunking aspirin. It does work. The benefits are just really small in a primary prevention population and offset by the admittedly also really small risks of bleeding. It’s a tradeoff that doesn’t really work in your favor.

But that’s aspirin for cardiovascular disease. When it comes to cancer or DVT prophylaxis, that’s another really interesting story. We might have to save that for another time. Do I know how to tease a sequel or what?

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.

TOPLINE:

An estimated 72 million ambulatory visits for superficial cutaneous fungal infections (SCFIs) in the United States were recorded during 2005-2016, with an increasing trend over the years. Tinea unguium, tinea pedis, and tinea corporis were among the most common infections.

METHODOLOGY:

• Researchers analyzed data from the National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey from 2005 to 2016, to evaluate trends in the prevalence of SCFIs during this period.
• The analysis included over 13 billion ambulatory visits to nonfederally funded community, office-based physician practices, and emergency or outpatient departments in the United States, with an estimated 1,104,258,333 annual average.
• The Jonckheere-Terpstra nonparametric test for trend was used to determine the pattern of SCFI prevalence over the 12-year period.

TAKEAWAY:

• SCFIs constituted approximately 0.54% of all annual ambulatory visits, with an estimated 6,001,852 visits for SCFIs per year and over 72 million total visits for the infections during the study period.
• Tinea unguium, tinea pedis, and tinea corporis were the most common infections, comprising 20.5%, 12.2%, and 12.0% of the total visits, respectively.
• Researchers noted an increasing trend in annual SCFIs (P = .03).

IN PRACTICE:

“We observed a high burden of SCFIs among outpatient visits in the United States and an increasing trend in their prevalence,” the authors wrote. These results, they added, “highlight the importance of healthcare providers being able to identify, treat, and, when necessary, refer patients with SCFIs, as a high burden of disease is associated with a significant negative impact on the individual and population levels.”

SOURCE:

The study was co-led by Sarah L. Spaulding, BS, and A. Mitchel Wride, BA, from the Yale School of Medicine, New Haven, Connecticut, and was published online October 30 in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The authors did not list any study limitations.

DISCLOSURES:

The lead authors were supported by Yale School of Medicine Medical Student Research Fellowships. Two other authors declared receiving consulting fees, research funding, and licensing fees outside the submitted work and also served on a data and safety monitoring board for Advarra Inc.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

An estimated 72 million ambulatory visits for superficial cutaneous fungal infections (SCFIs) in the United States were recorded during 2005-2016, with an increasing trend over the years. Tinea unguium, tinea pedis, and tinea corporis were among the most common infections.

METHODOLOGY:

• Researchers analyzed data from the National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey from 2005 to 2016, to evaluate trends in the prevalence of SCFIs during this period.
• The analysis included over 13 billion ambulatory visits to nonfederally funded community, office-based physician practices, and emergency or outpatient departments in the United States, with an estimated 1,104,258,333 annual average.
• The Jonckheere-Terpstra nonparametric test for trend was used to determine the pattern of SCFI prevalence over the 12-year period.

TAKEAWAY:

• SCFIs constituted approximately 0.54% of all annual ambulatory visits, with an estimated 6,001,852 visits for SCFIs per year and over 72 million total visits for the infections during the study period.
• Tinea unguium, tinea pedis, and tinea corporis were the most common infections, comprising 20.5%, 12.2%, and 12.0% of the total visits, respectively.
• Researchers noted an increasing trend in annual SCFIs (P = .03).

IN PRACTICE:

“We observed a high burden of SCFIs among outpatient visits in the United States and an increasing trend in their prevalence,” the authors wrote. These results, they added, “highlight the importance of healthcare providers being able to identify, treat, and, when necessary, refer patients with SCFIs, as a high burden of disease is associated with a significant negative impact on the individual and population levels.”

SOURCE:

The study was co-led by Sarah L. Spaulding, BS, and A. Mitchel Wride, BA, from the Yale School of Medicine, New Haven, Connecticut, and was published online October 30 in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The authors did not list any study limitations.

DISCLOSURES:

The lead authors were supported by Yale School of Medicine Medical Student Research Fellowships. Two other authors declared receiving consulting fees, research funding, and licensing fees outside the submitted work and also served on a data and safety monitoring board for Advarra Inc.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

An estimated 72 million ambulatory visits for superficial cutaneous fungal infections (SCFIs) in the United States were recorded during 2005-2016, with an increasing trend over the years. Tinea unguium, tinea pedis, and tinea corporis were among the most common infections.

METHODOLOGY:

• Researchers analyzed data from the National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey from 2005 to 2016, to evaluate trends in the prevalence of SCFIs during this period.
• The analysis included over 13 billion ambulatory visits to nonfederally funded community, office-based physician practices, and emergency or outpatient departments in the United States, with an estimated 1,104,258,333 annual average.
• The Jonckheere-Terpstra nonparametric test for trend was used to determine the pattern of SCFI prevalence over the 12-year period.

TAKEAWAY:

• SCFIs constituted approximately 0.54% of all annual ambulatory visits, with an estimated 6,001,852 visits for SCFIs per year and over 72 million total visits for the infections during the study period.
• Tinea unguium, tinea pedis, and tinea corporis were the most common infections, comprising 20.5%, 12.2%, and 12.0% of the total visits, respectively.
• Researchers noted an increasing trend in annual SCFIs (P = .03).

IN PRACTICE:

“We observed a high burden of SCFIs among outpatient visits in the United States and an increasing trend in their prevalence,” the authors wrote. These results, they added, “highlight the importance of healthcare providers being able to identify, treat, and, when necessary, refer patients with SCFIs, as a high burden of disease is associated with a significant negative impact on the individual and population levels.”

SOURCE:

The study was co-led by Sarah L. Spaulding, BS, and A. Mitchel Wride, BA, from the Yale School of Medicine, New Haven, Connecticut, and was published online October 30 in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The authors did not list any study limitations.

DISCLOSURES:

The lead authors were supported by Yale School of Medicine Medical Student Research Fellowships. Two other authors declared receiving consulting fees, research funding, and licensing fees outside the submitted work and also served on a data and safety monitoring board for Advarra Inc.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Individuals with hidradenitis suppurativa (HS) face a significantly increased risk for bulimia nervosa and binge eating disorder, an analysis of national data showed.

“Clinicians should actively screen for eating disorders,” particularly bulimia nervosa and binge eating disorder, in patients with HS,” lead study author Christopher Guirguis, DMD, a student at Georgetown University School of Medicine, Washington, DC, told this news organization in advance of the annual Symposium on Hidradenitis Suppurative Advances, where the study was presented during an oral abstract session. “The significant psychological burden in these patients requires a holistic approach that integrates both dermatologic and psychosocial care. Addressing their mental health needs is essential for improving overall patient outcomes and quality of life,” he added.

Chrisopher Guirguis

In collaboration with fellow Georgetown medical student and first author Lauren Chin and Mikael Horissian, MD, a dermatologist and director of the HS Clinic at Gesinger Health System, Danville, Pennsylvania, Guirguis drew from the National Institutes of Health’s All of Us Research Program to identify 1653 individuals with a diagnosis of HS and a control group of 8265 individuals without a diagnosis of HS. They used the Observational Medical Outcomes Partnership to identify anorexia nervosa, bulimia nervosa, body dysmorphic disorder, binge eating disorder, and eating disorder, unspecified. Obsessive-compulsive disorder (OCD) was also included because of its association with bulimia. They used statistical models to compare cohorts and comorbidities. “What makes this work unique is its focus on the link between HS and eating disorders, a relationship previously underexplored,” he said.

The mean age of the overall study cohort was 46.8 years, and 78.6% were female. Univariate analysis revealed that, compared with controls, individuals in the HS cohort showed significantly increased diagnoses of bulimia, binge eating disorder, OCD, and eating disorder, unspecified, by 2.6, 5.48, 2.50, and 2.43 times, respectively (P < .05 for all associations). After adjusting for age, race, sex, and ethnicity, the researchers observed that patients with HS were 4.46 times as likely to have a diagnosis of binge eating disorder and 3.51 times as likely to have a diagnosis of bulimia as those who did not have HS (P < .05 for both associations).

Guirguis said that the absence of body dysmorphic disorder diagnoses in the HS cohort was unexpected. “Given HS’s known association with body image issues, we anticipated a higher prevalence of BDD,” he said. “This discrepancy may reflect underreporting or diagnostic overshadowing, where the physical symptoms of HS dominate clinical attention, potentially masking or complicating the identification of psychological conditions like BDD.”

He acknowledged certain limitations of the study, including the potential for variations in documentation practices in the database. “Additionally, there may be bias due to underrepresentation of certain demographic groups or underreporting of psychological comorbidities, which could influence the findings.”

Patricia M. Richey, MD, assistant professor of dermatology, at Boston University School of Medicine in Massachusetts, who was asked to comment on the study, said the results “should affect how physicians discuss lifestyle recommendations in those already at increased risk of psychiatric disease and disrupted body image.” The findings should also “prompt physicians to screen this patient population more thoroughly for eating disorders as we know they are an underrecognized and often undertreated entity,” she added.

Neither the study authors nor Richey reported having relevant disclosures.

A version of this article appeared on Medscape.com.

Individuals with hidradenitis suppurativa (HS) face a significantly increased risk for bulimia nervosa and binge eating disorder, an analysis of national data showed.

“Clinicians should actively screen for eating disorders,” particularly bulimia nervosa and binge eating disorder, in patients with HS,” lead study author Christopher Guirguis, DMD, a student at Georgetown University School of Medicine, Washington, DC, told this news organization in advance of the annual Symposium on Hidradenitis Suppurative Advances, where the study was presented during an oral abstract session. “The significant psychological burden in these patients requires a holistic approach that integrates both dermatologic and psychosocial care. Addressing their mental health needs is essential for improving overall patient outcomes and quality of life,” he added.

Chrisopher Guirguis

In collaboration with fellow Georgetown medical student and first author Lauren Chin and Mikael Horissian, MD, a dermatologist and director of the HS Clinic at Gesinger Health System, Danville, Pennsylvania, Guirguis drew from the National Institutes of Health’s All of Us Research Program to identify 1653 individuals with a diagnosis of HS and a control group of 8265 individuals without a diagnosis of HS. They used the Observational Medical Outcomes Partnership to identify anorexia nervosa, bulimia nervosa, body dysmorphic disorder, binge eating disorder, and eating disorder, unspecified. Obsessive-compulsive disorder (OCD) was also included because of its association with bulimia. They used statistical models to compare cohorts and comorbidities. “What makes this work unique is its focus on the link between HS and eating disorders, a relationship previously underexplored,” he said.

The mean age of the overall study cohort was 46.8 years, and 78.6% were female. Univariate analysis revealed that, compared with controls, individuals in the HS cohort showed significantly increased diagnoses of bulimia, binge eating disorder, OCD, and eating disorder, unspecified, by 2.6, 5.48, 2.50, and 2.43 times, respectively (P < .05 for all associations). After adjusting for age, race, sex, and ethnicity, the researchers observed that patients with HS were 4.46 times as likely to have a diagnosis of binge eating disorder and 3.51 times as likely to have a diagnosis of bulimia as those who did not have HS (P < .05 for both associations).

Guirguis said that the absence of body dysmorphic disorder diagnoses in the HS cohort was unexpected. “Given HS’s known association with body image issues, we anticipated a higher prevalence of BDD,” he said. “This discrepancy may reflect underreporting or diagnostic overshadowing, where the physical symptoms of HS dominate clinical attention, potentially masking or complicating the identification of psychological conditions like BDD.”

He acknowledged certain limitations of the study, including the potential for variations in documentation practices in the database. “Additionally, there may be bias due to underrepresentation of certain demographic groups or underreporting of psychological comorbidities, which could influence the findings.”

Patricia M. Richey, MD, assistant professor of dermatology, at Boston University School of Medicine in Massachusetts, who was asked to comment on the study, said the results “should affect how physicians discuss lifestyle recommendations in those already at increased risk of psychiatric disease and disrupted body image.” The findings should also “prompt physicians to screen this patient population more thoroughly for eating disorders as we know they are an underrecognized and often undertreated entity,” she added.

Neither the study authors nor Richey reported having relevant disclosures.

A version of this article appeared on Medscape.com.

Individuals with hidradenitis suppurativa (HS) face a significantly increased risk for bulimia nervosa and binge eating disorder, an analysis of national data showed.

“Clinicians should actively screen for eating disorders,” particularly bulimia nervosa and binge eating disorder, in patients with HS,” lead study author Christopher Guirguis, DMD, a student at Georgetown University School of Medicine, Washington, DC, told this news organization in advance of the annual Symposium on Hidradenitis Suppurative Advances, where the study was presented during an oral abstract session. “The significant psychological burden in these patients requires a holistic approach that integrates both dermatologic and psychosocial care. Addressing their mental health needs is essential for improving overall patient outcomes and quality of life,” he added.

Chrisopher Guirguis

In collaboration with fellow Georgetown medical student and first author Lauren Chin and Mikael Horissian, MD, a dermatologist and director of the HS Clinic at Gesinger Health System, Danville, Pennsylvania, Guirguis drew from the National Institutes of Health’s All of Us Research Program to identify 1653 individuals with a diagnosis of HS and a control group of 8265 individuals without a diagnosis of HS. They used the Observational Medical Outcomes Partnership to identify anorexia nervosa, bulimia nervosa, body dysmorphic disorder, binge eating disorder, and eating disorder, unspecified. Obsessive-compulsive disorder (OCD) was also included because of its association with bulimia. They used statistical models to compare cohorts and comorbidities. “What makes this work unique is its focus on the link between HS and eating disorders, a relationship previously underexplored,” he said.

The mean age of the overall study cohort was 46.8 years, and 78.6% were female. Univariate analysis revealed that, compared with controls, individuals in the HS cohort showed significantly increased diagnoses of bulimia, binge eating disorder, OCD, and eating disorder, unspecified, by 2.6, 5.48, 2.50, and 2.43 times, respectively (P < .05 for all associations). After adjusting for age, race, sex, and ethnicity, the researchers observed that patients with HS were 4.46 times as likely to have a diagnosis of binge eating disorder and 3.51 times as likely to have a diagnosis of bulimia as those who did not have HS (P < .05 for both associations).

Guirguis said that the absence of body dysmorphic disorder diagnoses in the HS cohort was unexpected. “Given HS’s known association with body image issues, we anticipated a higher prevalence of BDD,” he said. “This discrepancy may reflect underreporting or diagnostic overshadowing, where the physical symptoms of HS dominate clinical attention, potentially masking or complicating the identification of psychological conditions like BDD.”

He acknowledged certain limitations of the study, including the potential for variations in documentation practices in the database. “Additionally, there may be bias due to underrepresentation of certain demographic groups or underreporting of psychological comorbidities, which could influence the findings.”

Patricia M. Richey, MD, assistant professor of dermatology, at Boston University School of Medicine in Massachusetts, who was asked to comment on the study, said the results “should affect how physicians discuss lifestyle recommendations in those already at increased risk of psychiatric disease and disrupted body image.” The findings should also “prompt physicians to screen this patient population more thoroughly for eating disorders as we know they are an underrecognized and often undertreated entity,” she added.

Neither the study authors nor Richey reported having relevant disclosures.

A version of this article appeared on Medscape.com.

A growing body of research explores the link between stroke risk and regular consumption of coffee, tea, soda, and alcohol. This research roundup reviews the latest findings, highlighting both promising insights and remaining uncertainties to help guide discussions with your patients.

Coffee and Tea: Good or Bad? 

In the INTERSTROKE study, high coffee consumption (> 4 cups daily) was associated with an significantly increased risk for all strokes (odds ratio [OR], 1.37) or ischemic stroke (OR, 1.31), while low to moderate coffee had no link to increased stroke risk. In contrast, tea consumption was associated with lower odds of all stroke (OR, 0.81 for highest intake) or ischemic stroke (OR, 0.81). 

In a recent UK Biobank study, consumption of coffee or tea was associated with reduced risk for stroke and dementia, with the biggest benefit associated with consuming both beverages. 

Specifically, the investigators found that individuals who drank two to three cups of coffee and two to three cups of tea per day had a 30% decrease in incidence of stroke and a 28% lower risk for dementia versus those who did not.

A recent systematic review and dose-response meta-analysis showed that each daily cup increase in tea was associated with an average 4% reduced risk for stroke and a 2% reduced risk for cardiovascular disease (CVD) events. 

The protective effect of coffee and tea on stroke risk may be driven, in part, by flavonoids, which have antioxidant and anti-inflammatory properties, as well as positive effects on vascular function.

“The advice to patients should be that coffee and tea may protect against stroke, but that sweetening either beverage with sugar probably should be minimized,” said Cheryl Bushnell, MD, MHS, of Wake Forest University School of Medicine in Winston-Salem, North Carolina, and chair of the American Stroke Association (ASA) 2024 Guideline for the Primary Prevention of Stroke. 

Taylor Wallace, PhD, a certified food scientist, said, “most people should consume a cup or two of unsweetened tea per day in moderation for cardiometabolic health. It is an easy step in the right direction for good health but not a cure-all.”

When it comes to coffee, adults who like it should drink it “in moderation — just lay off the cream and sugar,” said Wallace, adjunct associate professor at George Washington University, Washington, DC, and Tufts University, Boston, Massachusetts.

“A cup or two of black coffee with low-fat or nonfat milk with breakfast is a healthy way to start the day, especially when you’re like me and have an 8-year-old that is full of energy!” Wallace said. 
 

The Skinny on Soda

When it comes to sugar-sweetened and diet beverages, data from the Nurses’ Health Study and Health Professionals Follow-Up Study, showed a 16% increased risk for stroke with one or more daily servings of sugar-sweetened or low-calorie soda per day (vs none), independent of established dietary and nondietary cardiovascular risk factors. 

In the Women’s Health Initiative Observational Study of postmenopausal women, a higher intake of artificially sweetened beverages was associated with increased risk for all stroke (adjusted hazard ratio [aHR], 1.23), ischemic stroke (aHR, 1.31), coronary heart disease (aHR, 1.29) and all-cause mortality (aHR, 1.16).

In the Framingham Heart Study Offspring cohort, consumption of one can of diet soda or more each day (vs none) was associated with a nearly threefold increased risk for stroke and dementia over a 10-year follow-up period. 

A separate French study showed that total artificial sweetener intake from all sources was associated with increased overall risk for cardiovascular and cerebrovascular disease.

However, given the limitations of these studies, it’s hard to draw any firm conclusions, Wallace cautioned. 

“We know that sugar-sweetened beverages are correlated with weight gain and cardiometabolic dysfunction promotion in children and adults,” he said. 

Yet, “there really isn’t any convincing evidence that diet soda has much impact on human health at all. Most observational studies are mixed and likely very confounded by other diet and lifestyle factors. That doesn’t mean go overboard; a daily diet soda is probably fine, but that doesn’t mean go drink 10 of them every day,” he added. 
 

Alcohol: Moderation or Abstinence?

Evidence on alcohol use and stroke risk have been mixed over the years. For decades, the evidence was suggestive that a moderate amount of alcohol daily (one to two drinks in men and one drink in women) may be beneficial at reducing major vascular outcomes.

Yet, over the past few years, some research has found no evidence of benefit with moderate alcohol intake. And the detrimental effects of excessive alcohol use are clear. 

A large meta-analysis showed that light to moderate alcohol consumption (up to one drink per day) was associated with a reduced risk for ischemic stroke. However, heavy drinking (more than two drinks per day) significantly increased the risk for both ischemic and hemorrhagic stroke.

A separate study showed young adults who are moderate to heavy drinkers are at increased risk for stroke — and the risk increases with more years of imbibing.

In the INTERSTROKE study, high to moderate alcohol consumption was associated with increased stroke risk, whereas low alcohol consumption conferred no increased risk. 

However, Bushnell pointed out that the study data was derived from based on self-report, and that other healthy behaviors may counteract the risk for alcohol consumption.

“For alcohol, regardless of stroke risk, the most important data shows that any alcohol consumption is associated with worse cognitive function, so generally, the lower the alcohol consumption the better,” Bushnell said. 

She noted that, currently, the American Heart Association (AHA)/ASA recommend a maximum of two drinks per day for men and one drink per day for women to reduce stroke risk.

“However, the data for the risk for cognitive impairment with any alcohol is convincing and should be kept in mind in addition to the maximum alcohol recommended by the AHA/ASA,” Bushnell advised. 

“We know excessive intake puts you at major risk for CVD, cancer, cognitive decline, and a whole host of other health ailments — no question there,” said Wallace.

The impact of moderate intake, on the other hand, is less clear. “Alcohol is a highly biased and political issue and the evidence (or lack thereof) on both sides is shoddy at best,” Wallace added.

A key challenge is that accurate self-reporting of alcohol intake is difficult, even for scientists, and most studies rely on self-reported data from observational cohorts. These often include limited dietary assessments, which provide only a partial picture of long-term consumption patterns, Wallace noted. 

“The short answer is we don’t know if moderation is beneficial, detrimental, or null with respect to health,” he said.

Bushnell reports no relevant disclosures. Wallace (www.drtaylorwallace.com) is CEO of Think Healthy Group; editor of The Journal of Dietary Supplements, deputy editor of The Journal of the American Nutrition Association (www.nutrition.org), nutrition section editor of Annals of Medicine, and an advisory board member with Forbes Health.

A version of this article appeared on Medscape.com.

A growing body of research explores the link between stroke risk and regular consumption of coffee, tea, soda, and alcohol. This research roundup reviews the latest findings, highlighting both promising insights and remaining uncertainties to help guide discussions with your patients.

Coffee and Tea: Good or Bad? 

In the INTERSTROKE study, high coffee consumption (> 4 cups daily) was associated with an significantly increased risk for all strokes (odds ratio [OR], 1.37) or ischemic stroke (OR, 1.31), while low to moderate coffee had no link to increased stroke risk. In contrast, tea consumption was associated with lower odds of all stroke (OR, 0.81 for highest intake) or ischemic stroke (OR, 0.81). 

In a recent UK Biobank study, consumption of coffee or tea was associated with reduced risk for stroke and dementia, with the biggest benefit associated with consuming both beverages. 

Specifically, the investigators found that individuals who drank two to three cups of coffee and two to three cups of tea per day had a 30% decrease in incidence of stroke and a 28% lower risk for dementia versus those who did not.

A recent systematic review and dose-response meta-analysis showed that each daily cup increase in tea was associated with an average 4% reduced risk for stroke and a 2% reduced risk for cardiovascular disease (CVD) events. 

The protective effect of coffee and tea on stroke risk may be driven, in part, by flavonoids, which have antioxidant and anti-inflammatory properties, as well as positive effects on vascular function.

“The advice to patients should be that coffee and tea may protect against stroke, but that sweetening either beverage with sugar probably should be minimized,” said Cheryl Bushnell, MD, MHS, of Wake Forest University School of Medicine in Winston-Salem, North Carolina, and chair of the American Stroke Association (ASA) 2024 Guideline for the Primary Prevention of Stroke. 

Taylor Wallace, PhD, a certified food scientist, said, “most people should consume a cup or two of unsweetened tea per day in moderation for cardiometabolic health. It is an easy step in the right direction for good health but not a cure-all.”

When it comes to coffee, adults who like it should drink it “in moderation — just lay off the cream and sugar,” said Wallace, adjunct associate professor at George Washington University, Washington, DC, and Tufts University, Boston, Massachusetts.

“A cup or two of black coffee with low-fat or nonfat milk with breakfast is a healthy way to start the day, especially when you’re like me and have an 8-year-old that is full of energy!” Wallace said. 
 

The Skinny on Soda

When it comes to sugar-sweetened and diet beverages, data from the Nurses’ Health Study and Health Professionals Follow-Up Study, showed a 16% increased risk for stroke with one or more daily servings of sugar-sweetened or low-calorie soda per day (vs none), independent of established dietary and nondietary cardiovascular risk factors. 

In the Women’s Health Initiative Observational Study of postmenopausal women, a higher intake of artificially sweetened beverages was associated with increased risk for all stroke (adjusted hazard ratio [aHR], 1.23), ischemic stroke (aHR, 1.31), coronary heart disease (aHR, 1.29) and all-cause mortality (aHR, 1.16).

In the Framingham Heart Study Offspring cohort, consumption of one can of diet soda or more each day (vs none) was associated with a nearly threefold increased risk for stroke and dementia over a 10-year follow-up period. 

A separate French study showed that total artificial sweetener intake from all sources was associated with increased overall risk for cardiovascular and cerebrovascular disease.

However, given the limitations of these studies, it’s hard to draw any firm conclusions, Wallace cautioned. 

“We know that sugar-sweetened beverages are correlated with weight gain and cardiometabolic dysfunction promotion in children and adults,” he said. 

Yet, “there really isn’t any convincing evidence that diet soda has much impact on human health at all. Most observational studies are mixed and likely very confounded by other diet and lifestyle factors. That doesn’t mean go overboard; a daily diet soda is probably fine, but that doesn’t mean go drink 10 of them every day,” he added. 
 

Alcohol: Moderation or Abstinence?

Evidence on alcohol use and stroke risk have been mixed over the years. For decades, the evidence was suggestive that a moderate amount of alcohol daily (one to two drinks in men and one drink in women) may be beneficial at reducing major vascular outcomes.

Yet, over the past few years, some research has found no evidence of benefit with moderate alcohol intake. And the detrimental effects of excessive alcohol use are clear. 

A large meta-analysis showed that light to moderate alcohol consumption (up to one drink per day) was associated with a reduced risk for ischemic stroke. However, heavy drinking (more than two drinks per day) significantly increased the risk for both ischemic and hemorrhagic stroke.

A separate study showed young adults who are moderate to heavy drinkers are at increased risk for stroke — and the risk increases with more years of imbibing.

In the INTERSTROKE study, high to moderate alcohol consumption was associated with increased stroke risk, whereas low alcohol consumption conferred no increased risk. 

However, Bushnell pointed out that the study data was derived from based on self-report, and that other healthy behaviors may counteract the risk for alcohol consumption.

“For alcohol, regardless of stroke risk, the most important data shows that any alcohol consumption is associated with worse cognitive function, so generally, the lower the alcohol consumption the better,” Bushnell said. 

She noted that, currently, the American Heart Association (AHA)/ASA recommend a maximum of two drinks per day for men and one drink per day for women to reduce stroke risk.

“However, the data for the risk for cognitive impairment with any alcohol is convincing and should be kept in mind in addition to the maximum alcohol recommended by the AHA/ASA,” Bushnell advised. 

“We know excessive intake puts you at major risk for CVD, cancer, cognitive decline, and a whole host of other health ailments — no question there,” said Wallace.

The impact of moderate intake, on the other hand, is less clear. “Alcohol is a highly biased and political issue and the evidence (or lack thereof) on both sides is shoddy at best,” Wallace added.

A key challenge is that accurate self-reporting of alcohol intake is difficult, even for scientists, and most studies rely on self-reported data from observational cohorts. These often include limited dietary assessments, which provide only a partial picture of long-term consumption patterns, Wallace noted. 

“The short answer is we don’t know if moderation is beneficial, detrimental, or null with respect to health,” he said.

Bushnell reports no relevant disclosures. Wallace (www.drtaylorwallace.com) is CEO of Think Healthy Group; editor of The Journal of Dietary Supplements, deputy editor of The Journal of the American Nutrition Association (www.nutrition.org), nutrition section editor of Annals of Medicine, and an advisory board member with Forbes Health.

A version of this article appeared on Medscape.com.

A growing body of research explores the link between stroke risk and regular consumption of coffee, tea, soda, and alcohol. This research roundup reviews the latest findings, highlighting both promising insights and remaining uncertainties to help guide discussions with your patients.

Coffee and Tea: Good or Bad? 

In the INTERSTROKE study, high coffee consumption (> 4 cups daily) was associated with an significantly increased risk for all strokes (odds ratio [OR], 1.37) or ischemic stroke (OR, 1.31), while low to moderate coffee had no link to increased stroke risk. In contrast, tea consumption was associated with lower odds of all stroke (OR, 0.81 for highest intake) or ischemic stroke (OR, 0.81). 

In a recent UK Biobank study, consumption of coffee or tea was associated with reduced risk for stroke and dementia, with the biggest benefit associated with consuming both beverages. 

Specifically, the investigators found that individuals who drank two to three cups of coffee and two to three cups of tea per day had a 30% decrease in incidence of stroke and a 28% lower risk for dementia versus those who did not.

A recent systematic review and dose-response meta-analysis showed that each daily cup increase in tea was associated with an average 4% reduced risk for stroke and a 2% reduced risk for cardiovascular disease (CVD) events. 

The protective effect of coffee and tea on stroke risk may be driven, in part, by flavonoids, which have antioxidant and anti-inflammatory properties, as well as positive effects on vascular function.

“The advice to patients should be that coffee and tea may protect against stroke, but that sweetening either beverage with sugar probably should be minimized,” said Cheryl Bushnell, MD, MHS, of Wake Forest University School of Medicine in Winston-Salem, North Carolina, and chair of the American Stroke Association (ASA) 2024 Guideline for the Primary Prevention of Stroke. 

Taylor Wallace, PhD, a certified food scientist, said, “most people should consume a cup or two of unsweetened tea per day in moderation for cardiometabolic health. It is an easy step in the right direction for good health but not a cure-all.”

When it comes to coffee, adults who like it should drink it “in moderation — just lay off the cream and sugar,” said Wallace, adjunct associate professor at George Washington University, Washington, DC, and Tufts University, Boston, Massachusetts.

“A cup or two of black coffee with low-fat or nonfat milk with breakfast is a healthy way to start the day, especially when you’re like me and have an 8-year-old that is full of energy!” Wallace said. 
 

The Skinny on Soda

When it comes to sugar-sweetened and diet beverages, data from the Nurses’ Health Study and Health Professionals Follow-Up Study, showed a 16% increased risk for stroke with one or more daily servings of sugar-sweetened or low-calorie soda per day (vs none), independent of established dietary and nondietary cardiovascular risk factors. 

In the Women’s Health Initiative Observational Study of postmenopausal women, a higher intake of artificially sweetened beverages was associated with increased risk for all stroke (adjusted hazard ratio [aHR], 1.23), ischemic stroke (aHR, 1.31), coronary heart disease (aHR, 1.29) and all-cause mortality (aHR, 1.16).

In the Framingham Heart Study Offspring cohort, consumption of one can of diet soda or more each day (vs none) was associated with a nearly threefold increased risk for stroke and dementia over a 10-year follow-up period. 

A separate French study showed that total artificial sweetener intake from all sources was associated with increased overall risk for cardiovascular and cerebrovascular disease.

However, given the limitations of these studies, it’s hard to draw any firm conclusions, Wallace cautioned. 

“We know that sugar-sweetened beverages are correlated with weight gain and cardiometabolic dysfunction promotion in children and adults,” he said. 

Yet, “there really isn’t any convincing evidence that diet soda has much impact on human health at all. Most observational studies are mixed and likely very confounded by other diet and lifestyle factors. That doesn’t mean go overboard; a daily diet soda is probably fine, but that doesn’t mean go drink 10 of them every day,” he added. 
 

Alcohol: Moderation or Abstinence?

Evidence on alcohol use and stroke risk have been mixed over the years. For decades, the evidence was suggestive that a moderate amount of alcohol daily (one to two drinks in men and one drink in women) may be beneficial at reducing major vascular outcomes.

Yet, over the past few years, some research has found no evidence of benefit with moderate alcohol intake. And the detrimental effects of excessive alcohol use are clear. 

A large meta-analysis showed that light to moderate alcohol consumption (up to one drink per day) was associated with a reduced risk for ischemic stroke. However, heavy drinking (more than two drinks per day) significantly increased the risk for both ischemic and hemorrhagic stroke.

A separate study showed young adults who are moderate to heavy drinkers are at increased risk for stroke — and the risk increases with more years of imbibing.

In the INTERSTROKE study, high to moderate alcohol consumption was associated with increased stroke risk, whereas low alcohol consumption conferred no increased risk. 

However, Bushnell pointed out that the study data was derived from based on self-report, and that other healthy behaviors may counteract the risk for alcohol consumption.

“For alcohol, regardless of stroke risk, the most important data shows that any alcohol consumption is associated with worse cognitive function, so generally, the lower the alcohol consumption the better,” Bushnell said. 

She noted that, currently, the American Heart Association (AHA)/ASA recommend a maximum of two drinks per day for men and one drink per day for women to reduce stroke risk.

“However, the data for the risk for cognitive impairment with any alcohol is convincing and should be kept in mind in addition to the maximum alcohol recommended by the AHA/ASA,” Bushnell advised. 

“We know excessive intake puts you at major risk for CVD, cancer, cognitive decline, and a whole host of other health ailments — no question there,” said Wallace.

The impact of moderate intake, on the other hand, is less clear. “Alcohol is a highly biased and political issue and the evidence (or lack thereof) on both sides is shoddy at best,” Wallace added.

A key challenge is that accurate self-reporting of alcohol intake is difficult, even for scientists, and most studies rely on self-reported data from observational cohorts. These often include limited dietary assessments, which provide only a partial picture of long-term consumption patterns, Wallace noted. 

“The short answer is we don’t know if moderation is beneficial, detrimental, or null with respect to health,” he said.

Bushnell reports no relevant disclosures. Wallace (www.drtaylorwallace.com) is CEO of Think Healthy Group; editor of The Journal of Dietary Supplements, deputy editor of The Journal of the American Nutrition Association (www.nutrition.org), nutrition section editor of Annals of Medicine, and an advisory board member with Forbes Health.

A version of this article appeared on Medscape.com.

VIENNA — Guselkumab has been shown to be efficacious vs placebo in patients with moderately to severely active Crohn’s disease (CD), regardless of prior biologic therapy exposure, according to a pooled analysis of the two phase 3 double-blind GALAXI 2 and 3 studies.

“We found that guselkumab was effective in both biologic-naive and biologic-inadequate subpopulations,” said coinvestigator Bruce E. Sands, MD, AGAF, gastroenterologist from Icahn School of Medicine at Mount Sinai, New York City.

These latest results add to the primary results of these studies reported earlier in 2024 that guselkumab was shown to be superior to both placebo and ustekinumab in the same patient population with moderately to severely active CD.

Sands reported the new data in a presentation at the United European Gastroenterology (UEG) Week 2024.

Guselkumab potently blocks interleukin (IL)–23 and binds to CD64, a receptor on cells that produce IL-23. The dual-acting IL-23p19 subunit inhibitor agent is currently under review by the Food and Drug Administration (FDA) for moderately to severely active CD. In September, guselkumab (Tremfya, Johnson & Johnson) was approved for use in moderately to severely active ulcerative colitis.
 

GALAXI 2 and 3 Pooled Dataset

In the two independent, identically designed GALAXI 2 and 3 studies, patients were randomized to guselkumab treatment at either 200 mg intravenous (IV) induction at weeks 0, 4, and 8, followed by 200 mg subcutaneous maintenance every 4 weeks, starting at week 12, or 200 mg IV induction at weeks 0, 4, and 8, followed by 100 mg subcutaneous maintenance every 8 weeks, starting at week 16; or to ustekinumab; or to placebo.

Participants were required to remain on their treatment of initial randomization for a long-term extension study (up to 5 years) looking at clinical, endoscopic, and safety outcomes, except for participants on placebo who were allowed to switch to ustekinumab if clinical response was not met at week 12.

Inclusion criteria for the studies comprised a Crohn’s Disease Activity Index score between 220 and 450, a mean daily stool frequency count > 3 or an abdominal pain score > 1, and a simple endoscopic score for CD score ≥ 6. Participants were also required to have shown an inadequate response or intolerance to oral corticosteroids, 6-mercaptopurine/azathioprine/methotrexate, or biologic therapies.

The pooled dataset included patients on either dose of guselkumab and patients on placebo (total n = 730). Of these, 52% of participants had shown a prior inadequate response to a biologic, 42% were biologic naive, and 6% had prior exposure to biologics but no documented failure. Patients on ustekinumab were not included in this analysis.

Almost all patients (97%) in the biologic-inadequate response group had previously received at least one anti–tumor necrosis factor agent, and around 15% had received vedolizumab. As expected, the biologic-inadequate responders were a lot sicker than the biologic-naive patients, Sands reported.

The composite co–primary endpoints for each guselkumab regimen vs placebo were clinical response at week 12 plus clinical remission at week 48, and clinical response at week 12 plus endoscopic response at week 48.

The major secondary endpoints comprised clinical remission at week 12 and endoscopic response also at week 12.
 

Short- and Long-Term Endpoints in Both Subgroups

In the biologic-naive subgroup, 54.7% of patients receiving the 200-mg dose regimen of guselkumab and 51.7% of those receiving the 100-mg dose regimen showed a clinical response at week 12 plus clinical remission at week 48, compared with 11.5% in the placebo group (P < .001 for both compared with placebo).

In the biologic-inadequate response group, 49.7% of those receiving the 200-mg dose regimen of guselkumab and 45.8% on the 100-mg dose regimen reached the composite endpoint, compared with the placebo response of 12.8% (P < .001 for both compared with placebo).

“You can see a slight decrease in response in the biologic-inadequate responders, but on the whole, the confidence intervals are highly overlapping,” said Sands.

Turning to major secondary endpoints at week 12, clinical remission was reached by 49.6% of the biologic-naive group on the 200-mg guselkumab regimen vs 16.4% on placebo, and by 46.0% of the biologic-inadequate group on the 200-mg regimen vs 19.2% on placebo (P < .001 for both subgroups). Endoscopic response was achieved by 46.3% of patients in the biologic-naive group and 29.0% in the biologic-inadequate group on the 200-mg regimen vs 18.0% and 6.4%, respectively, on placebo (P < .001 for both subgroups).

Sands noted that the drug has an excellent safety profile.

“These data show the drug works for naive patients who have failed conventional therapies, as well as for those who have failed biologic therapies,” so it could be used as a first- or second-line biologic, he added.

Sands reported potential conflicts of interest with AbbVie, Abivax, Adiso Therapeutics, Agomab, Alimentiv, Amgen, AnaptysBio, Arena Pharmaceuticals, Artugen Therapeutics, AstraZeneca, Biora Therapeutics, Boehringer Ingelheim, Boston Pharmaceuticals, Bristol-Myers Squibb, Calibr, Celgene, Celltrion, ClostraBio, Equillium, Enthera, Evommune, Ferring, Fresenius Kabi, Galapagos, Genentech (Roche), Gilead Sciences, GlaxoSmithKline, Gossamer Bio, Index Pharmaceuticals, Innovation Pharmaceuticals, Inotrem, Janssen, Kaleido, Kallyope, Lilly, Merck, Microbiotica, Mobius Care, Morphic Therapeutic, MRM Health, Pfizer, Nexus Therapeutics, Nimbus Discovery, Odyssey Therapeutics, Progenity, Prometheus Biosciences, Prometheus Laboratories, Protagonist Therapeutics, Q32 Bio, Rasayana Therapeutics, Recludix Pharma, Reistone Biopharma, Sun Pharma, Surrozen, Target RWE, Takeda, Teva, Theravance Biopharma, TLL Pharmaceutical, Tr1X, UNION Therapeutics, and Ventyx Biosciences.

A version of this article appeared on Medscape.com.

VIENNA — Guselkumab has been shown to be efficacious vs placebo in patients with moderately to severely active Crohn’s disease (CD), regardless of prior biologic therapy exposure, according to a pooled analysis of the two phase 3 double-blind GALAXI 2 and 3 studies.

“We found that guselkumab was effective in both biologic-naive and biologic-inadequate subpopulations,” said coinvestigator Bruce E. Sands, MD, AGAF, gastroenterologist from Icahn School of Medicine at Mount Sinai, New York City.

These latest results add to the primary results of these studies reported earlier in 2024 that guselkumab was shown to be superior to both placebo and ustekinumab in the same patient population with moderately to severely active CD.

Sands reported the new data in a presentation at the United European Gastroenterology (UEG) Week 2024.

Guselkumab potently blocks interleukin (IL)–23 and binds to CD64, a receptor on cells that produce IL-23. The dual-acting IL-23p19 subunit inhibitor agent is currently under review by the Food and Drug Administration (FDA) for moderately to severely active CD. In September, guselkumab (Tremfya, Johnson & Johnson) was approved for use in moderately to severely active ulcerative colitis.
 

GALAXI 2 and 3 Pooled Dataset

In the two independent, identically designed GALAXI 2 and 3 studies, patients were randomized to guselkumab treatment at either 200 mg intravenous (IV) induction at weeks 0, 4, and 8, followed by 200 mg subcutaneous maintenance every 4 weeks, starting at week 12, or 200 mg IV induction at weeks 0, 4, and 8, followed by 100 mg subcutaneous maintenance every 8 weeks, starting at week 16; or to ustekinumab; or to placebo.

Participants were required to remain on their treatment of initial randomization for a long-term extension study (up to 5 years) looking at clinical, endoscopic, and safety outcomes, except for participants on placebo who were allowed to switch to ustekinumab if clinical response was not met at week 12.

Inclusion criteria for the studies comprised a Crohn’s Disease Activity Index score between 220 and 450, a mean daily stool frequency count > 3 or an abdominal pain score > 1, and a simple endoscopic score for CD score ≥ 6. Participants were also required to have shown an inadequate response or intolerance to oral corticosteroids, 6-mercaptopurine/azathioprine/methotrexate, or biologic therapies.

The pooled dataset included patients on either dose of guselkumab and patients on placebo (total n = 730). Of these, 52% of participants had shown a prior inadequate response to a biologic, 42% were biologic naive, and 6% had prior exposure to biologics but no documented failure. Patients on ustekinumab were not included in this analysis.

Almost all patients (97%) in the biologic-inadequate response group had previously received at least one anti–tumor necrosis factor agent, and around 15% had received vedolizumab. As expected, the biologic-inadequate responders were a lot sicker than the biologic-naive patients, Sands reported.

The composite co–primary endpoints for each guselkumab regimen vs placebo were clinical response at week 12 plus clinical remission at week 48, and clinical response at week 12 plus endoscopic response at week 48.

The major secondary endpoints comprised clinical remission at week 12 and endoscopic response also at week 12.
 

Short- and Long-Term Endpoints in Both Subgroups

In the biologic-naive subgroup, 54.7% of patients receiving the 200-mg dose regimen of guselkumab and 51.7% of those receiving the 100-mg dose regimen showed a clinical response at week 12 plus clinical remission at week 48, compared with 11.5% in the placebo group (P < .001 for both compared with placebo).

In the biologic-inadequate response group, 49.7% of those receiving the 200-mg dose regimen of guselkumab and 45.8% on the 100-mg dose regimen reached the composite endpoint, compared with the placebo response of 12.8% (P < .001 for both compared with placebo).

“You can see a slight decrease in response in the biologic-inadequate responders, but on the whole, the confidence intervals are highly overlapping,” said Sands.

Turning to major secondary endpoints at week 12, clinical remission was reached by 49.6% of the biologic-naive group on the 200-mg guselkumab regimen vs 16.4% on placebo, and by 46.0% of the biologic-inadequate group on the 200-mg regimen vs 19.2% on placebo (P < .001 for both subgroups). Endoscopic response was achieved by 46.3% of patients in the biologic-naive group and 29.0% in the biologic-inadequate group on the 200-mg regimen vs 18.0% and 6.4%, respectively, on placebo (P < .001 for both subgroups).

Sands noted that the drug has an excellent safety profile.

“These data show the drug works for naive patients who have failed conventional therapies, as well as for those who have failed biologic therapies,” so it could be used as a first- or second-line biologic, he added.

Sands reported potential conflicts of interest with AbbVie, Abivax, Adiso Therapeutics, Agomab, Alimentiv, Amgen, AnaptysBio, Arena Pharmaceuticals, Artugen Therapeutics, AstraZeneca, Biora Therapeutics, Boehringer Ingelheim, Boston Pharmaceuticals, Bristol-Myers Squibb, Calibr, Celgene, Celltrion, ClostraBio, Equillium, Enthera, Evommune, Ferring, Fresenius Kabi, Galapagos, Genentech (Roche), Gilead Sciences, GlaxoSmithKline, Gossamer Bio, Index Pharmaceuticals, Innovation Pharmaceuticals, Inotrem, Janssen, Kaleido, Kallyope, Lilly, Merck, Microbiotica, Mobius Care, Morphic Therapeutic, MRM Health, Pfizer, Nexus Therapeutics, Nimbus Discovery, Odyssey Therapeutics, Progenity, Prometheus Biosciences, Prometheus Laboratories, Protagonist Therapeutics, Q32 Bio, Rasayana Therapeutics, Recludix Pharma, Reistone Biopharma, Sun Pharma, Surrozen, Target RWE, Takeda, Teva, Theravance Biopharma, TLL Pharmaceutical, Tr1X, UNION Therapeutics, and Ventyx Biosciences.

A version of this article appeared on Medscape.com.

VIENNA — Guselkumab has been shown to be efficacious vs placebo in patients with moderately to severely active Crohn’s disease (CD), regardless of prior biologic therapy exposure, according to a pooled analysis of the two phase 3 double-blind GALAXI 2 and 3 studies.

“We found that guselkumab was effective in both biologic-naive and biologic-inadequate subpopulations,” said coinvestigator Bruce E. Sands, MD, AGAF, gastroenterologist from Icahn School of Medicine at Mount Sinai, New York City.

These latest results add to the primary results of these studies reported earlier in 2024 that guselkumab was shown to be superior to both placebo and ustekinumab in the same patient population with moderately to severely active CD.

Sands reported the new data in a presentation at the United European Gastroenterology (UEG) Week 2024.

Guselkumab potently blocks interleukin (IL)–23 and binds to CD64, a receptor on cells that produce IL-23. The dual-acting IL-23p19 subunit inhibitor agent is currently under review by the Food and Drug Administration (FDA) for moderately to severely active CD. In September, guselkumab (Tremfya, Johnson & Johnson) was approved for use in moderately to severely active ulcerative colitis.
 

GALAXI 2 and 3 Pooled Dataset

In the two independent, identically designed GALAXI 2 and 3 studies, patients were randomized to guselkumab treatment at either 200 mg intravenous (IV) induction at weeks 0, 4, and 8, followed by 200 mg subcutaneous maintenance every 4 weeks, starting at week 12, or 200 mg IV induction at weeks 0, 4, and 8, followed by 100 mg subcutaneous maintenance every 8 weeks, starting at week 16; or to ustekinumab; or to placebo.

Participants were required to remain on their treatment of initial randomization for a long-term extension study (up to 5 years) looking at clinical, endoscopic, and safety outcomes, except for participants on placebo who were allowed to switch to ustekinumab if clinical response was not met at week 12.

Inclusion criteria for the studies comprised a Crohn’s Disease Activity Index score between 220 and 450, a mean daily stool frequency count > 3 or an abdominal pain score > 1, and a simple endoscopic score for CD score ≥ 6. Participants were also required to have shown an inadequate response or intolerance to oral corticosteroids, 6-mercaptopurine/azathioprine/methotrexate, or biologic therapies.

The pooled dataset included patients on either dose of guselkumab and patients on placebo (total n = 730). Of these, 52% of participants had shown a prior inadequate response to a biologic, 42% were biologic naive, and 6% had prior exposure to biologics but no documented failure. Patients on ustekinumab were not included in this analysis.

Almost all patients (97%) in the biologic-inadequate response group had previously received at least one anti–tumor necrosis factor agent, and around 15% had received vedolizumab. As expected, the biologic-inadequate responders were a lot sicker than the biologic-naive patients, Sands reported.

The composite co–primary endpoints for each guselkumab regimen vs placebo were clinical response at week 12 plus clinical remission at week 48, and clinical response at week 12 plus endoscopic response at week 48.

The major secondary endpoints comprised clinical remission at week 12 and endoscopic response also at week 12.
 

Short- and Long-Term Endpoints in Both Subgroups

In the biologic-naive subgroup, 54.7% of patients receiving the 200-mg dose regimen of guselkumab and 51.7% of those receiving the 100-mg dose regimen showed a clinical response at week 12 plus clinical remission at week 48, compared with 11.5% in the placebo group (P < .001 for both compared with placebo).

In the biologic-inadequate response group, 49.7% of those receiving the 200-mg dose regimen of guselkumab and 45.8% on the 100-mg dose regimen reached the composite endpoint, compared with the placebo response of 12.8% (P < .001 for both compared with placebo).

“You can see a slight decrease in response in the biologic-inadequate responders, but on the whole, the confidence intervals are highly overlapping,” said Sands.

Turning to major secondary endpoints at week 12, clinical remission was reached by 49.6% of the biologic-naive group on the 200-mg guselkumab regimen vs 16.4% on placebo, and by 46.0% of the biologic-inadequate group on the 200-mg regimen vs 19.2% on placebo (P < .001 for both subgroups). Endoscopic response was achieved by 46.3% of patients in the biologic-naive group and 29.0% in the biologic-inadequate group on the 200-mg regimen vs 18.0% and 6.4%, respectively, on placebo (P < .001 for both subgroups).

Sands noted that the drug has an excellent safety profile.

“These data show the drug works for naive patients who have failed conventional therapies, as well as for those who have failed biologic therapies,” so it could be used as a first- or second-line biologic, he added.

Sands reported potential conflicts of interest with AbbVie, Abivax, Adiso Therapeutics, Agomab, Alimentiv, Amgen, AnaptysBio, Arena Pharmaceuticals, Artugen Therapeutics, AstraZeneca, Biora Therapeutics, Boehringer Ingelheim, Boston Pharmaceuticals, Bristol-Myers Squibb, Calibr, Celgene, Celltrion, ClostraBio, Equillium, Enthera, Evommune, Ferring, Fresenius Kabi, Galapagos, Genentech (Roche), Gilead Sciences, GlaxoSmithKline, Gossamer Bio, Index Pharmaceuticals, Innovation Pharmaceuticals, Inotrem, Janssen, Kaleido, Kallyope, Lilly, Merck, Microbiotica, Mobius Care, Morphic Therapeutic, MRM Health, Pfizer, Nexus Therapeutics, Nimbus Discovery, Odyssey Therapeutics, Progenity, Prometheus Biosciences, Prometheus Laboratories, Protagonist Therapeutics, Q32 Bio, Rasayana Therapeutics, Recludix Pharma, Reistone Biopharma, Sun Pharma, Surrozen, Target RWE, Takeda, Teva, Theravance Biopharma, TLL Pharmaceutical, Tr1X, UNION Therapeutics, and Ventyx Biosciences.

A version of this article appeared on Medscape.com.

VIENNA — Researchers have determined a bidirectional relationship between inflammatory bowel disease (IBD) and type 1 diabetes (T1D), using both a cohort and case-control approach to analysis.

Their findings showed that patients with IBD had a moderately increased risk for T1D and higher odds of having prior T1D than the general population. These bidirectional associations were partially independent of shared familial factors.

Although the absolute risk for T1D is low in patients with IBD, these findings suggest that if there are nonspecific symptoms, such as weight loss and fatigue, which are typical of T1D but not of IBD, then it might be reasonable to test for diabetes, lead researcher Jiangwei Sun, PhD, postdoctoral researcher at the Karolinska Institutet, Stockholm, Sweden, told this news organization.

“Patients with IBD and T1D also tend to have worse disease outcomes for both diseases, but these two diseases are not recognized as comorbidities in the clinical guidelines,” he said.

Anecdotally, “many clinicians believe there is a higher risk of autoimmune disease in patients with IBD but not much attention is paid to type 1 diabetes,” he added.

Sun presented the study at United European Gastroenterology (UEG) Week 2024. It was also published recently in The Lancet.
 

Exploring the Bidirectional Relationship 

Prior research in the form of a systematic review found no association between IBD and T1D, which was surprising, Sun said. Further studies found an association between IBD and incident T1D; however, these studies did not explore bidirectionality between the two diseases.

These studies also did not take shared genetic and environmental factors into consideration, though “there is known to be familial co-aggregation of IBD and T1D based on previous findings,” he said.

In this current study, Sun and colleagues compared patients with IBD with the general population, as well as with siblings without IBD to consider the potential influence of shared genetics and earlier environmental factors. 

The research used two approaches to look for a bidirectional association: A nationwide matched cohort study (IBD and incident T1D) and a case-control study (IBD and prior T1D).

The cohort study included 20,314 patients with IBD aged ≤ 28 years, who were identified between 1987 and 2017. Of these, 7277 had Crohn’s disease, 10,112 had ulcerative colitis, and 2925 had unclassified IBD. There were 99,200 individually matched reference individuals.

The case-control study included 87,001 patients with IBD (without age restriction) and 431,054 matched control individuals.

Risk ratios were calculated using an adjusted hazard ratio (aHR) of incident T1D in the cohort study and an adjusted odds ratio (aOR) of prior T1D in the case-control study.

In the cohort study, the median follow-up was 14 years. Over that time, 116 patients with IBD and 353 reference individuals developed T1D. The aHR for a patient with IBD developing T1D was 1.58 (95% CI, 1.27-1.95). For patients with ulcerative colitis, the aHR of developing T1D increased to 2.02 (95% CI, 1.51-2.70); however, the association was not found for Crohn’s disease or unclassified IBD possibly because of the sample size of these latter categories, noted Sun.

In the case-control study, Sun and colleagues identified 1018 (1.2%) patients with IBD and 3496 (0.8%) control individuals who had been previously diagnosed with T1D. Patients with IBD had higher odds of having prior T1D than those without IBD (aOR, 1.36; 95% CI, 1.26-1.46). This positive association was observed in all IBD subtypes, said Sun, who added that the sample size was larger in this analysis than in the cohort analysis.

Upon comparing patients with IBD with their siblings without IBD, analyses showed similar associations between IBD and T1D; the aHR was 1.44 (95% CI, 0.97-2.15) for developing T1D, and the aOR was 1.32 (95% CI, 1.18-1.49) for prior T1D.

That these positive associations between IBD and T1D exist even when comparing patients with IBD with their siblings without IBD suggests genetics and shared environmental factors do not fully explain the association, and that later environmental factors might play a role, said Sun.

“I’m not surprised with these results,” he added. “They make sense because we know that both IBD and T1D are immunity-related diseases and have some shared pathways.”

Commenting on the study, Tine Jess, MD, director, Center for Molecular Prediction of Inflammatory Bowel Disease, PREDICT, Aalborg University in Copenhagen, Denmark, said: “The really interesting finding here is that type 1 diabetes may precede IBD, which points toward common etiologies rather than one disease leading to the other.”

“This is in line with mounting evidence that IBD is measurable at the molecular level years prior to diagnosis,” she added.

Awareness of the bidirectional association may facilitate early detection of both conditions, Sun and his colleagues noted.

Sun reported no relevant financial relationships. Jess reported receiving consultancy fees from Ferring and Pfizer.

A version of this article appeared on Medscape.com.

VIENNA — Researchers have determined a bidirectional relationship between inflammatory bowel disease (IBD) and type 1 diabetes (T1D), using both a cohort and case-control approach to analysis.

Their findings showed that patients with IBD had a moderately increased risk for T1D and higher odds of having prior T1D than the general population. These bidirectional associations were partially independent of shared familial factors.

Although the absolute risk for T1D is low in patients with IBD, these findings suggest that if there are nonspecific symptoms, such as weight loss and fatigue, which are typical of T1D but not of IBD, then it might be reasonable to test for diabetes, lead researcher Jiangwei Sun, PhD, postdoctoral researcher at the Karolinska Institutet, Stockholm, Sweden, told this news organization.

“Patients with IBD and T1D also tend to have worse disease outcomes for both diseases, but these two diseases are not recognized as comorbidities in the clinical guidelines,” he said.

Anecdotally, “many clinicians believe there is a higher risk of autoimmune disease in patients with IBD but not much attention is paid to type 1 diabetes,” he added.

Sun presented the study at United European Gastroenterology (UEG) Week 2024. It was also published recently in The Lancet.
 

Exploring the Bidirectional Relationship 

Prior research in the form of a systematic review found no association between IBD and T1D, which was surprising, Sun said. Further studies found an association between IBD and incident T1D; however, these studies did not explore bidirectionality between the two diseases.

These studies also did not take shared genetic and environmental factors into consideration, though “there is known to be familial co-aggregation of IBD and T1D based on previous findings,” he said.

In this current study, Sun and colleagues compared patients with IBD with the general population, as well as with siblings without IBD to consider the potential influence of shared genetics and earlier environmental factors. 

The research used two approaches to look for a bidirectional association: A nationwide matched cohort study (IBD and incident T1D) and a case-control study (IBD and prior T1D).

The cohort study included 20,314 patients with IBD aged ≤ 28 years, who were identified between 1987 and 2017. Of these, 7277 had Crohn’s disease, 10,112 had ulcerative colitis, and 2925 had unclassified IBD. There were 99,200 individually matched reference individuals.

The case-control study included 87,001 patients with IBD (without age restriction) and 431,054 matched control individuals.

Risk ratios were calculated using an adjusted hazard ratio (aHR) of incident T1D in the cohort study and an adjusted odds ratio (aOR) of prior T1D in the case-control study.

In the cohort study, the median follow-up was 14 years. Over that time, 116 patients with IBD and 353 reference individuals developed T1D. The aHR for a patient with IBD developing T1D was 1.58 (95% CI, 1.27-1.95). For patients with ulcerative colitis, the aHR of developing T1D increased to 2.02 (95% CI, 1.51-2.70); however, the association was not found for Crohn’s disease or unclassified IBD possibly because of the sample size of these latter categories, noted Sun.

In the case-control study, Sun and colleagues identified 1018 (1.2%) patients with IBD and 3496 (0.8%) control individuals who had been previously diagnosed with T1D. Patients with IBD had higher odds of having prior T1D than those without IBD (aOR, 1.36; 95% CI, 1.26-1.46). This positive association was observed in all IBD subtypes, said Sun, who added that the sample size was larger in this analysis than in the cohort analysis.

Upon comparing patients with IBD with their siblings without IBD, analyses showed similar associations between IBD and T1D; the aHR was 1.44 (95% CI, 0.97-2.15) for developing T1D, and the aOR was 1.32 (95% CI, 1.18-1.49) for prior T1D.

That these positive associations between IBD and T1D exist even when comparing patients with IBD with their siblings without IBD suggests genetics and shared environmental factors do not fully explain the association, and that later environmental factors might play a role, said Sun.

“I’m not surprised with these results,” he added. “They make sense because we know that both IBD and T1D are immunity-related diseases and have some shared pathways.”

Commenting on the study, Tine Jess, MD, director, Center for Molecular Prediction of Inflammatory Bowel Disease, PREDICT, Aalborg University in Copenhagen, Denmark, said: “The really interesting finding here is that type 1 diabetes may precede IBD, which points toward common etiologies rather than one disease leading to the other.”

“This is in line with mounting evidence that IBD is measurable at the molecular level years prior to diagnosis,” she added.

Awareness of the bidirectional association may facilitate early detection of both conditions, Sun and his colleagues noted.

Sun reported no relevant financial relationships. Jess reported receiving consultancy fees from Ferring and Pfizer.