Transplanting livers from deceased donors who tested positive for SARS-CoV-2 is safe and has no significant impact on short-term outcomes of allografts or recipients, based on a national study with the longest follow-up to date.

Using livers from deceased patients with COVID-19 could be an opportunity expand organ availability, reported principal investigator Nadim Mahmud, MD, of the University of Pennsylvania, Philadelphia, and colleagues.

Findings were presented in November at the annual meeting of the American Association for the Study of Liver Diseases.

“During the COVID-19 pandemic, a few centers trialed transplanting solid organs from COVID-19 positive donors with promising initial results,” presenting author Roy X. Wang, MD, of the University of Pennsylvania, said in a written comment. “However, these were smaller experiences with short follow-up that were not exclusively focused on liver transplantation. We wanted to explore the safety of liver transplantation from COVID-19 positive donors using a large national dataset with the longest follow up time to date.”

The dataset included 13,096 COVID-negative donors and 299 COVID-positive donors who died between July 2020 and July 2022, with cases and controls matched via propensity scoring. COVID-positive donors were significantly more likely to be younger and have died of brain death. Beyond this difference in age, no significant demographic differences were detected.

After 1 year of follow-up, no statistically significant differences in patient survival (subhazard ratio, 1.11; log-rank P = .70) or allograft survival (hazard ratio, 1.44; log-rank P = .14) were detected when comparing livers transplanted from positive versus negative donors.

“Our findings support and expand upon the results from earlier studies,” Dr. Wang concluded. “Liver transplant from COVID-19-positive donors has acceptable short-term outcomes and may represent an opportunity to expand organ access.”

Still, more work is needed to assess other clinical metrics and long-term outcomes, he added.

“While we were able to show similar patient and graft survival post-transplant between COVID-19-positive and negative donors, rates of other complications were not investigated such as episodes of rejection, liver injury, and hospitalizations,” Dr. Wang said. “Due to data limitations, we are only able to report on outcomes up to 1 year post transplant. Additional investigation will be needed to continue monitoring future outcomes and identifying any differences between recipients of COVID-19-positive and negative donors.”

Timucin Taner, MD, PhD, division chair of transplant surgery at Mayo Clinic, Rochester, Minnesota, said the study is important because it reaffirms the majority opinion among transplant physicians: These livers are safe.

In an interview, Dr. Taner suggested that Dr. Wang’s call for longer term data is “mostly science speak,” since 1 year of follow-up should be sufficient to determine liver viability.

Mayo Clinic

“If a liver from a COVID-19 donor behaved well for a year, then chances are it’s not going to behave badly [later on] because of the virus at the time of donation,” Dr. Taner said.

He said the reported trends in usage of COVID-positive livers reflect early hesitancy that waned with rising vaccination rates, and recognition that the virus could not be spread via liver donation.

“To date, the only transmission [of SARS-CoV-2] from a transplant has been from a lung transplant,” Dr. Taner said, “and that was back in the days that we didn’t know about this. Other organs don’t transmit the disease, so they are easily usable.”

These new data should further increase confidence among both health care providers and patients, he added.

“[This study is] reassuring to the patients on the waitlist that these organs are very safe to use,” Dr. Taner said. “We as the transplant society are comfortable using them without any hesitation.”

The investigators and Dr. Taner disclosed no conflicts of interest.

Transplanting livers from deceased donors who tested positive for SARS-CoV-2 is safe and has no significant impact on short-term outcomes of allografts or recipients, based on a national study with the longest follow-up to date.

Using livers from deceased patients with COVID-19 could be an opportunity expand organ availability, reported principal investigator Nadim Mahmud, MD, of the University of Pennsylvania, Philadelphia, and colleagues.

Findings were presented in November at the annual meeting of the American Association for the Study of Liver Diseases.

“During the COVID-19 pandemic, a few centers trialed transplanting solid organs from COVID-19 positive donors with promising initial results,” presenting author Roy X. Wang, MD, of the University of Pennsylvania, said in a written comment. “However, these were smaller experiences with short follow-up that were not exclusively focused on liver transplantation. We wanted to explore the safety of liver transplantation from COVID-19 positive donors using a large national dataset with the longest follow up time to date.”

The dataset included 13,096 COVID-negative donors and 299 COVID-positive donors who died between July 2020 and July 2022, with cases and controls matched via propensity scoring. COVID-positive donors were significantly more likely to be younger and have died of brain death. Beyond this difference in age, no significant demographic differences were detected.

After 1 year of follow-up, no statistically significant differences in patient survival (subhazard ratio, 1.11; log-rank P = .70) or allograft survival (hazard ratio, 1.44; log-rank P = .14) were detected when comparing livers transplanted from positive versus negative donors.

“Our findings support and expand upon the results from earlier studies,” Dr. Wang concluded. “Liver transplant from COVID-19-positive donors has acceptable short-term outcomes and may represent an opportunity to expand organ access.”

Still, more work is needed to assess other clinical metrics and long-term outcomes, he added.

“While we were able to show similar patient and graft survival post-transplant between COVID-19-positive and negative donors, rates of other complications were not investigated such as episodes of rejection, liver injury, and hospitalizations,” Dr. Wang said. “Due to data limitations, we are only able to report on outcomes up to 1 year post transplant. Additional investigation will be needed to continue monitoring future outcomes and identifying any differences between recipients of COVID-19-positive and negative donors.”

Timucin Taner, MD, PhD, division chair of transplant surgery at Mayo Clinic, Rochester, Minnesota, said the study is important because it reaffirms the majority opinion among transplant physicians: These livers are safe.

In an interview, Dr. Taner suggested that Dr. Wang’s call for longer term data is “mostly science speak,” since 1 year of follow-up should be sufficient to determine liver viability.

Mayo Clinic

“If a liver from a COVID-19 donor behaved well for a year, then chances are it’s not going to behave badly [later on] because of the virus at the time of donation,” Dr. Taner said.

He said the reported trends in usage of COVID-positive livers reflect early hesitancy that waned with rising vaccination rates, and recognition that the virus could not be spread via liver donation.

“To date, the only transmission [of SARS-CoV-2] from a transplant has been from a lung transplant,” Dr. Taner said, “and that was back in the days that we didn’t know about this. Other organs don’t transmit the disease, so they are easily usable.”

These new data should further increase confidence among both health care providers and patients, he added.

“[This study is] reassuring to the patients on the waitlist that these organs are very safe to use,” Dr. Taner said. “We as the transplant society are comfortable using them without any hesitation.”

The investigators and Dr. Taner disclosed no conflicts of interest.

Transplanting livers from deceased donors who tested positive for SARS-CoV-2 is safe and has no significant impact on short-term outcomes of allografts or recipients, based on a national study with the longest follow-up to date.

Using livers from deceased patients with COVID-19 could be an opportunity expand organ availability, reported principal investigator Nadim Mahmud, MD, of the University of Pennsylvania, Philadelphia, and colleagues.

Findings were presented in November at the annual meeting of the American Association for the Study of Liver Diseases.

“During the COVID-19 pandemic, a few centers trialed transplanting solid organs from COVID-19 positive donors with promising initial results,” presenting author Roy X. Wang, MD, of the University of Pennsylvania, said in a written comment. “However, these were smaller experiences with short follow-up that were not exclusively focused on liver transplantation. We wanted to explore the safety of liver transplantation from COVID-19 positive donors using a large national dataset with the longest follow up time to date.”

The dataset included 13,096 COVID-negative donors and 299 COVID-positive donors who died between July 2020 and July 2022, with cases and controls matched via propensity scoring. COVID-positive donors were significantly more likely to be younger and have died of brain death. Beyond this difference in age, no significant demographic differences were detected.

After 1 year of follow-up, no statistically significant differences in patient survival (subhazard ratio, 1.11; log-rank P = .70) or allograft survival (hazard ratio, 1.44; log-rank P = .14) were detected when comparing livers transplanted from positive versus negative donors.

“Our findings support and expand upon the results from earlier studies,” Dr. Wang concluded. “Liver transplant from COVID-19-positive donors has acceptable short-term outcomes and may represent an opportunity to expand organ access.”

Still, more work is needed to assess other clinical metrics and long-term outcomes, he added.

“While we were able to show similar patient and graft survival post-transplant between COVID-19-positive and negative donors, rates of other complications were not investigated such as episodes of rejection, liver injury, and hospitalizations,” Dr. Wang said. “Due to data limitations, we are only able to report on outcomes up to 1 year post transplant. Additional investigation will be needed to continue monitoring future outcomes and identifying any differences between recipients of COVID-19-positive and negative donors.”

Timucin Taner, MD, PhD, division chair of transplant surgery at Mayo Clinic, Rochester, Minnesota, said the study is important because it reaffirms the majority opinion among transplant physicians: These livers are safe.

In an interview, Dr. Taner suggested that Dr. Wang’s call for longer term data is “mostly science speak,” since 1 year of follow-up should be sufficient to determine liver viability.

Mayo Clinic

“If a liver from a COVID-19 donor behaved well for a year, then chances are it’s not going to behave badly [later on] because of the virus at the time of donation,” Dr. Taner said.

He said the reported trends in usage of COVID-positive livers reflect early hesitancy that waned with rising vaccination rates, and recognition that the virus could not be spread via liver donation.

“To date, the only transmission [of SARS-CoV-2] from a transplant has been from a lung transplant,” Dr. Taner said, “and that was back in the days that we didn’t know about this. Other organs don’t transmit the disease, so they are easily usable.”

These new data should further increase confidence among both health care providers and patients, he added.

“[This study is] reassuring to the patients on the waitlist that these organs are very safe to use,” Dr. Taner said. “We as the transplant society are comfortable using them without any hesitation.”

The investigators and Dr. Taner disclosed no conflicts of interest.

More than one out of three adults in the United States could have nonalcoholic fatty liver disease (NAFLD) by 2050, substantially increasing the national clinical burden, according to investigators.

These findings suggest that health care systems should prepare for “large increases” in cases of hepatocellular carcinoma (HCC) and need for liver transplants, reported lead author Phuc Le, PhD, MPH, of the Cleveland Clinic, and colleagues.

Cleveland Clinic

“Following the alarming rise in prevalence of obesity and diabetes, NAFLD is projected to become the leading indication for liver transplant in the United States in the next decade,” Dr. Le and colleagues wrote in their abstract for the annual meeting of the American Association for the Study of Liver Diseases. “A better understanding of the clinical burden associated with NAFLD will enable health systems to prepare to meet this imminent demand from patients.”

To this end, Dr. Le and colleagues developed an agent-based state transition model to predict future prevalence of NAFLD and associated outcomes.

In the first part of the model, the investigators simulated population growth in the United States using Census Bureau data, including new births and immigration, from the year 2000 onward. The second part of the model simulated natural progression of NAFLD in adults via 14 associated conditions and events, including steatosis, nonalcoholic steatohepatitis (NASH), HCC, liver transplants, liver-related mortality, and others.

By first comparing simulated findings with actual findings between 2000 and 2018, the investigators confirmed that their model could reliably predict the intended epidemiological parameters.

Next, they turned their model toward the future.

It predicted that the prevalence of NAFLD among US adults will rise from 27.8% in 2020 to 34.3% in 2050. Over the same timeframe, prevalence of NASH is predicted to increase from 20.0% to 21.8%, proportion of NAFLD cases developing cirrhosis is expected to increase from 1.9% to 3.1%, and liver-related mortality is estimated to rise from 0.4% to 1% of all deaths.

The model also predicted that the burden of HCC will increase from 10,400 to 19,300 new cases per year, while liver transplant burden will more than double, from 1,700 to 4,200 transplants per year.

“Our model forecasts substantial clinical burden of NAFLD over the next three decades,” Dr. Le said in a virtual press conference. “And in the absence of effective treatments, health systems should plan for large increases in the number of liver cancer cases and the need for liver transplant.”

During the press conference, Norah Terrault, MD, president of the AASLD from the University of Southern California, Los Angeles, noted that all of the reported outcomes, including increasing rates of liver cancer, cirrhosis, and transplants are “potentially preventable.”

Keck School of Medicine

Dr. Terrault went on to suggest ways of combating this increasing burden of NAFLD, which she referred to as metabolic dysfunction–associated steatotic liver disease (MASLD), the name now recommended by the AASLD.

“There’s no way we’re going to be able to transplant our way out of this,” Dr. Terrault said. “We need to be bringing greater awareness both to patients, as well as to providers about how we seek out the diagnosis. And we need to bring greater awareness to the population around the things that contribute to MASLD.”

Rates of obesity and diabetes continue to rise, Dr. Terrault said, explaining why MASLD is more common than ever. To counteract these trends, she called for greater awareness of driving factors, such as dietary choices and sedentary lifestyle.

“These are all really important messages that we want to get out to the population, and are really the cornerstones for how we approach the management of patients who have MASLD,” Dr. Terrault said.

In discussion with Dr. Terrault, Dr. Le agreed that increased education may help stem the rising tide of disease, while treatment advances could also increase the odds of a brighter future.

“If we improve our management of NAFLD, or NAFLD-related comorbidities, and if we can develop an effective treatment for NAFLD, then obviously the future would not be so dark,” Dr. Le said, noting promising phase 3 data that would be presented at the meeting. “We are hopeful that the future of disease burden will not be as bad as our model predicts.”

The study was funded by the Agency for Healthcare Research and Quality. The investigators disclosed no conflicts of interest.

More than one out of three adults in the United States could have nonalcoholic fatty liver disease (NAFLD) by 2050, substantially increasing the national clinical burden, according to investigators.

These findings suggest that health care systems should prepare for “large increases” in cases of hepatocellular carcinoma (HCC) and need for liver transplants, reported lead author Phuc Le, PhD, MPH, of the Cleveland Clinic, and colleagues.

Cleveland Clinic

“Following the alarming rise in prevalence of obesity and diabetes, NAFLD is projected to become the leading indication for liver transplant in the United States in the next decade,” Dr. Le and colleagues wrote in their abstract for the annual meeting of the American Association for the Study of Liver Diseases. “A better understanding of the clinical burden associated with NAFLD will enable health systems to prepare to meet this imminent demand from patients.”

To this end, Dr. Le and colleagues developed an agent-based state transition model to predict future prevalence of NAFLD and associated outcomes.

In the first part of the model, the investigators simulated population growth in the United States using Census Bureau data, including new births and immigration, from the year 2000 onward. The second part of the model simulated natural progression of NAFLD in adults via 14 associated conditions and events, including steatosis, nonalcoholic steatohepatitis (NASH), HCC, liver transplants, liver-related mortality, and others.

By first comparing simulated findings with actual findings between 2000 and 2018, the investigators confirmed that their model could reliably predict the intended epidemiological parameters.

Next, they turned their model toward the future.

It predicted that the prevalence of NAFLD among US adults will rise from 27.8% in 2020 to 34.3% in 2050. Over the same timeframe, prevalence of NASH is predicted to increase from 20.0% to 21.8%, proportion of NAFLD cases developing cirrhosis is expected to increase from 1.9% to 3.1%, and liver-related mortality is estimated to rise from 0.4% to 1% of all deaths.

The model also predicted that the burden of HCC will increase from 10,400 to 19,300 new cases per year, while liver transplant burden will more than double, from 1,700 to 4,200 transplants per year.

“Our model forecasts substantial clinical burden of NAFLD over the next three decades,” Dr. Le said in a virtual press conference. “And in the absence of effective treatments, health systems should plan for large increases in the number of liver cancer cases and the need for liver transplant.”

During the press conference, Norah Terrault, MD, president of the AASLD from the University of Southern California, Los Angeles, noted that all of the reported outcomes, including increasing rates of liver cancer, cirrhosis, and transplants are “potentially preventable.”

Keck School of Medicine

Dr. Terrault went on to suggest ways of combating this increasing burden of NAFLD, which she referred to as metabolic dysfunction–associated steatotic liver disease (MASLD), the name now recommended by the AASLD.

“There’s no way we’re going to be able to transplant our way out of this,” Dr. Terrault said. “We need to be bringing greater awareness both to patients, as well as to providers about how we seek out the diagnosis. And we need to bring greater awareness to the population around the things that contribute to MASLD.”

Rates of obesity and diabetes continue to rise, Dr. Terrault said, explaining why MASLD is more common than ever. To counteract these trends, she called for greater awareness of driving factors, such as dietary choices and sedentary lifestyle.

“These are all really important messages that we want to get out to the population, and are really the cornerstones for how we approach the management of patients who have MASLD,” Dr. Terrault said.

In discussion with Dr. Terrault, Dr. Le agreed that increased education may help stem the rising tide of disease, while treatment advances could also increase the odds of a brighter future.

“If we improve our management of NAFLD, or NAFLD-related comorbidities, and if we can develop an effective treatment for NAFLD, then obviously the future would not be so dark,” Dr. Le said, noting promising phase 3 data that would be presented at the meeting. “We are hopeful that the future of disease burden will not be as bad as our model predicts.”

The study was funded by the Agency for Healthcare Research and Quality. The investigators disclosed no conflicts of interest.

More than one out of three adults in the United States could have nonalcoholic fatty liver disease (NAFLD) by 2050, substantially increasing the national clinical burden, according to investigators.

These findings suggest that health care systems should prepare for “large increases” in cases of hepatocellular carcinoma (HCC) and need for liver transplants, reported lead author Phuc Le, PhD, MPH, of the Cleveland Clinic, and colleagues.

Cleveland Clinic

“Following the alarming rise in prevalence of obesity and diabetes, NAFLD is projected to become the leading indication for liver transplant in the United States in the next decade,” Dr. Le and colleagues wrote in their abstract for the annual meeting of the American Association for the Study of Liver Diseases. “A better understanding of the clinical burden associated with NAFLD will enable health systems to prepare to meet this imminent demand from patients.”

To this end, Dr. Le and colleagues developed an agent-based state transition model to predict future prevalence of NAFLD and associated outcomes.

In the first part of the model, the investigators simulated population growth in the United States using Census Bureau data, including new births and immigration, from the year 2000 onward. The second part of the model simulated natural progression of NAFLD in adults via 14 associated conditions and events, including steatosis, nonalcoholic steatohepatitis (NASH), HCC, liver transplants, liver-related mortality, and others.

By first comparing simulated findings with actual findings between 2000 and 2018, the investigators confirmed that their model could reliably predict the intended epidemiological parameters.

Next, they turned their model toward the future.

It predicted that the prevalence of NAFLD among US adults will rise from 27.8% in 2020 to 34.3% in 2050. Over the same timeframe, prevalence of NASH is predicted to increase from 20.0% to 21.8%, proportion of NAFLD cases developing cirrhosis is expected to increase from 1.9% to 3.1%, and liver-related mortality is estimated to rise from 0.4% to 1% of all deaths.

The model also predicted that the burden of HCC will increase from 10,400 to 19,300 new cases per year, while liver transplant burden will more than double, from 1,700 to 4,200 transplants per year.

“Our model forecasts substantial clinical burden of NAFLD over the next three decades,” Dr. Le said in a virtual press conference. “And in the absence of effective treatments, health systems should plan for large increases in the number of liver cancer cases and the need for liver transplant.”

During the press conference, Norah Terrault, MD, president of the AASLD from the University of Southern California, Los Angeles, noted that all of the reported outcomes, including increasing rates of liver cancer, cirrhosis, and transplants are “potentially preventable.”

Keck School of Medicine

Dr. Terrault went on to suggest ways of combating this increasing burden of NAFLD, which she referred to as metabolic dysfunction–associated steatotic liver disease (MASLD), the name now recommended by the AASLD.

“There’s no way we’re going to be able to transplant our way out of this,” Dr. Terrault said. “We need to be bringing greater awareness both to patients, as well as to providers about how we seek out the diagnosis. And we need to bring greater awareness to the population around the things that contribute to MASLD.”

Rates of obesity and diabetes continue to rise, Dr. Terrault said, explaining why MASLD is more common than ever. To counteract these trends, she called for greater awareness of driving factors, such as dietary choices and sedentary lifestyle.

“These are all really important messages that we want to get out to the population, and are really the cornerstones for how we approach the management of patients who have MASLD,” Dr. Terrault said.

In discussion with Dr. Terrault, Dr. Le agreed that increased education may help stem the rising tide of disease, while treatment advances could also increase the odds of a brighter future.

“If we improve our management of NAFLD, or NAFLD-related comorbidities, and if we can develop an effective treatment for NAFLD, then obviously the future would not be so dark,” Dr. Le said, noting promising phase 3 data that would be presented at the meeting. “We are hopeful that the future of disease burden will not be as bad as our model predicts.”

The study was funded by the Agency for Healthcare Research and Quality. The investigators disclosed no conflicts of interest.

Adolescents facing food insecurity have a significantly increased risk of metabolic dysfunction-associated steatotic liver disease (MASLD), likely due to overconsumption of low-cost, ultra-processed, unbalanced diets, according to a recent study.

These findings suggest that more work is needed to ensure that eligible adolescents can access Supplemental Nutrition Assistance Program (SNAP) benefits and have opportunities to engage in physical activities through school-associated programs, reported principal investigator Zobair M. Younossi, MD, MPH, professor and chairman of the Beatty Liver and Obesity Research Program, Inova Health System, Falls Church, Virginia, and colleagues.

Dr. Younossi presented the findings in November during a press conference at the annual meeting of the American Association for the Study of Liver Diseases.

“Food insecurity among children is about 10.2% in the United States,” Dr. Younossi said. “[Food insecurity has] been shown to be a risk factor for MASLD among adults, but the data and children and adolescents are really lacking at the moment.”

To address this knowledge gap, Dr. Younossi and colleagues analyzed data from 771 adolescents aged 12-18 years in the National Health and Nutrition Examination Survey (2017-2018). Among these participants, 9.8% reported food insecurity and 10.8% had MASLD. Rates of obesity and central obesity were 22.5% and 45.4%, respectively, while 1.0% had diabetes and 20.9% had prediabetes.

Among adolescents facing food insecurity, more than half (51.5%) did not eat enough food, a vast majority (93.2%) could not access a balanced meal, and almost all (98.9%) relied upon low-cost food for daily sustenance.

The prevalence of MASLD in the food insecure group was almost twice as high as in the food secure group (18.7% vs 9.9%), and advanced fibrosis was about 9 times more common (2.8% vs. 0.3%). Food insecure participants were also more likely to come from a low-income household (70.4% vs. 25.7%) and participate in SNAP (62.4% vs. 25.1%).

Adjusting for SNAP participation, demographic factors, and metabolic disease showed that food insecurity independently increased risk of MASLD by more than twofold (odds ratio [OR], 2.62; 95% CI, 1.07–6.41). The negative effect of food insecurity was almost twice as strong in participants living in a low-income household (OR, 4.79; 95% CI, 1.44–15.86).

“The association between food insecurity and MASLD/NAFLD is most likely the result of not being able to eat a balanced meal and more likely having to purchase low-cost food,” Dr. Younossi said. “Together, these factors may lead to a cycle of overeating along with the overconsumption of ultra-processed foods and sugar-sweetened food and beverages.”

He went on to suggest that more work is needed to remove “systemic and structural barriers” that prevent eligible adolescents from participating in SNAP, while offering support so they can participate in “more physical activity in school and in after-school programs.”

Elliot Benjamin Tapper, MD, associate professor of medicine at the University of Michigan, Ann Arbor, recently published a similar study in the Journal of Clinical Gastroenterology linking food scarcity and MASLD in adults.

Michigan Medicine

In an interview, Dr. Tapper praised this new study by Dr. Younossi and colleagues because it “identifies a serious unmet need” among younger individuals, who may stand to benefit most from early intervention.

“The goal [of screening] is to prevent the development of progressive disease,” Dr. Tapper said. “Our current guidelines for screening for advanced liver disease and people with risk factors focus exclusively on adults. If you waited longer, then there’s a risk that these [younger] people [in the study] would have progressed to a later stage of disease.”

Dr. Tapper predicted increased enthusiasm for MAFLD screening among adolescents in response to these findings, but he cautioned that conventional educational intervention is unlikely to yield significant benefit.

“If you’re food insecure, you can’t go out and buy salmon and olive oil to follow the Mediterranean diet,” Dr. Tapper said. In this era, where the people who are at risk tomorrow are young and food insecure, we have to come up with a way of tailoring our interventions to the means that are available to these patients.”

To this end, health care providers need to collaborate with individuals who have personally dealt with food scarcity to implement practicable interventions.

“Referral to social work has to be paired with some kind of standard teaching,” Dr. Tapper said. “How would I use social and nutritional assistance programs to eat in a liver-healthy way? What can I avoid? [Educational materials] should be written by and edited by people with lived experience; i.e., people who have food insecurity or have walked a mile in those shoes.”

Dr. Younossi disclosed relationships with Merck, Abbott, AstraZeneca, and others. Dr. Tapper disclosed relationships with Takeda, Novo Nordisk, Madrigal, and others.

Adolescents facing food insecurity have a significantly increased risk of metabolic dysfunction-associated steatotic liver disease (MASLD), likely due to overconsumption of low-cost, ultra-processed, unbalanced diets, according to a recent study.

These findings suggest that more work is needed to ensure that eligible adolescents can access Supplemental Nutrition Assistance Program (SNAP) benefits and have opportunities to engage in physical activities through school-associated programs, reported principal investigator Zobair M. Younossi, MD, MPH, professor and chairman of the Beatty Liver and Obesity Research Program, Inova Health System, Falls Church, Virginia, and colleagues.

Dr. Younossi presented the findings in November during a press conference at the annual meeting of the American Association for the Study of Liver Diseases.

“Food insecurity among children is about 10.2% in the United States,” Dr. Younossi said. “[Food insecurity has] been shown to be a risk factor for MASLD among adults, but the data and children and adolescents are really lacking at the moment.”

To address this knowledge gap, Dr. Younossi and colleagues analyzed data from 771 adolescents aged 12-18 years in the National Health and Nutrition Examination Survey (2017-2018). Among these participants, 9.8% reported food insecurity and 10.8% had MASLD. Rates of obesity and central obesity were 22.5% and 45.4%, respectively, while 1.0% had diabetes and 20.9% had prediabetes.

Among adolescents facing food insecurity, more than half (51.5%) did not eat enough food, a vast majority (93.2%) could not access a balanced meal, and almost all (98.9%) relied upon low-cost food for daily sustenance.

The prevalence of MASLD in the food insecure group was almost twice as high as in the food secure group (18.7% vs 9.9%), and advanced fibrosis was about 9 times more common (2.8% vs. 0.3%). Food insecure participants were also more likely to come from a low-income household (70.4% vs. 25.7%) and participate in SNAP (62.4% vs. 25.1%).

Adjusting for SNAP participation, demographic factors, and metabolic disease showed that food insecurity independently increased risk of MASLD by more than twofold (odds ratio [OR], 2.62; 95% CI, 1.07–6.41). The negative effect of food insecurity was almost twice as strong in participants living in a low-income household (OR, 4.79; 95% CI, 1.44–15.86).

“The association between food insecurity and MASLD/NAFLD is most likely the result of not being able to eat a balanced meal and more likely having to purchase low-cost food,” Dr. Younossi said. “Together, these factors may lead to a cycle of overeating along with the overconsumption of ultra-processed foods and sugar-sweetened food and beverages.”

He went on to suggest that more work is needed to remove “systemic and structural barriers” that prevent eligible adolescents from participating in SNAP, while offering support so they can participate in “more physical activity in school and in after-school programs.”

Elliot Benjamin Tapper, MD, associate professor of medicine at the University of Michigan, Ann Arbor, recently published a similar study in the Journal of Clinical Gastroenterology linking food scarcity and MASLD in adults.

Michigan Medicine

In an interview, Dr. Tapper praised this new study by Dr. Younossi and colleagues because it “identifies a serious unmet need” among younger individuals, who may stand to benefit most from early intervention.

“The goal [of screening] is to prevent the development of progressive disease,” Dr. Tapper said. “Our current guidelines for screening for advanced liver disease and people with risk factors focus exclusively on adults. If you waited longer, then there’s a risk that these [younger] people [in the study] would have progressed to a later stage of disease.”

Dr. Tapper predicted increased enthusiasm for MAFLD screening among adolescents in response to these findings, but he cautioned that conventional educational intervention is unlikely to yield significant benefit.

“If you’re food insecure, you can’t go out and buy salmon and olive oil to follow the Mediterranean diet,” Dr. Tapper said. In this era, where the people who are at risk tomorrow are young and food insecure, we have to come up with a way of tailoring our interventions to the means that are available to these patients.”

To this end, health care providers need to collaborate with individuals who have personally dealt with food scarcity to implement practicable interventions.

“Referral to social work has to be paired with some kind of standard teaching,” Dr. Tapper said. “How would I use social and nutritional assistance programs to eat in a liver-healthy way? What can I avoid? [Educational materials] should be written by and edited by people with lived experience; i.e., people who have food insecurity or have walked a mile in those shoes.”

Dr. Younossi disclosed relationships with Merck, Abbott, AstraZeneca, and others. Dr. Tapper disclosed relationships with Takeda, Novo Nordisk, Madrigal, and others.

Adolescents facing food insecurity have a significantly increased risk of metabolic dysfunction-associated steatotic liver disease (MASLD), likely due to overconsumption of low-cost, ultra-processed, unbalanced diets, according to a recent study.

These findings suggest that more work is needed to ensure that eligible adolescents can access Supplemental Nutrition Assistance Program (SNAP) benefits and have opportunities to engage in physical activities through school-associated programs, reported principal investigator Zobair M. Younossi, MD, MPH, professor and chairman of the Beatty Liver and Obesity Research Program, Inova Health System, Falls Church, Virginia, and colleagues.

Dr. Younossi presented the findings in November during a press conference at the annual meeting of the American Association for the Study of Liver Diseases.

“Food insecurity among children is about 10.2% in the United States,” Dr. Younossi said. “[Food insecurity has] been shown to be a risk factor for MASLD among adults, but the data and children and adolescents are really lacking at the moment.”

To address this knowledge gap, Dr. Younossi and colleagues analyzed data from 771 adolescents aged 12-18 years in the National Health and Nutrition Examination Survey (2017-2018). Among these participants, 9.8% reported food insecurity and 10.8% had MASLD. Rates of obesity and central obesity were 22.5% and 45.4%, respectively, while 1.0% had diabetes and 20.9% had prediabetes.

Among adolescents facing food insecurity, more than half (51.5%) did not eat enough food, a vast majority (93.2%) could not access a balanced meal, and almost all (98.9%) relied upon low-cost food for daily sustenance.

The prevalence of MASLD in the food insecure group was almost twice as high as in the food secure group (18.7% vs 9.9%), and advanced fibrosis was about 9 times more common (2.8% vs. 0.3%). Food insecure participants were also more likely to come from a low-income household (70.4% vs. 25.7%) and participate in SNAP (62.4% vs. 25.1%).

Adjusting for SNAP participation, demographic factors, and metabolic disease showed that food insecurity independently increased risk of MASLD by more than twofold (odds ratio [OR], 2.62; 95% CI, 1.07–6.41). The negative effect of food insecurity was almost twice as strong in participants living in a low-income household (OR, 4.79; 95% CI, 1.44–15.86).

“The association between food insecurity and MASLD/NAFLD is most likely the result of not being able to eat a balanced meal and more likely having to purchase low-cost food,” Dr. Younossi said. “Together, these factors may lead to a cycle of overeating along with the overconsumption of ultra-processed foods and sugar-sweetened food and beverages.”

He went on to suggest that more work is needed to remove “systemic and structural barriers” that prevent eligible adolescents from participating in SNAP, while offering support so they can participate in “more physical activity in school and in after-school programs.”

Elliot Benjamin Tapper, MD, associate professor of medicine at the University of Michigan, Ann Arbor, recently published a similar study in the Journal of Clinical Gastroenterology linking food scarcity and MASLD in adults.

Michigan Medicine

In an interview, Dr. Tapper praised this new study by Dr. Younossi and colleagues because it “identifies a serious unmet need” among younger individuals, who may stand to benefit most from early intervention.

“The goal [of screening] is to prevent the development of progressive disease,” Dr. Tapper said. “Our current guidelines for screening for advanced liver disease and people with risk factors focus exclusively on adults. If you waited longer, then there’s a risk that these [younger] people [in the study] would have progressed to a later stage of disease.”

Dr. Tapper predicted increased enthusiasm for MAFLD screening among adolescents in response to these findings, but he cautioned that conventional educational intervention is unlikely to yield significant benefit.

“If you’re food insecure, you can’t go out and buy salmon and olive oil to follow the Mediterranean diet,” Dr. Tapper said. In this era, where the people who are at risk tomorrow are young and food insecure, we have to come up with a way of tailoring our interventions to the means that are available to these patients.”

To this end, health care providers need to collaborate with individuals who have personally dealt with food scarcity to implement practicable interventions.

“Referral to social work has to be paired with some kind of standard teaching,” Dr. Tapper said. “How would I use social and nutritional assistance programs to eat in a liver-healthy way? What can I avoid? [Educational materials] should be written by and edited by people with lived experience; i.e., people who have food insecurity or have walked a mile in those shoes.”

Dr. Younossi disclosed relationships with Merck, Abbott, AstraZeneca, and others. Dr. Tapper disclosed relationships with Takeda, Novo Nordisk, Madrigal, and others.

The Diagnosis: Giant Acrochordon

Based on the clinical and histologic findings, our patient was diagnosed with a giant acrochordon. Acrochordons (also known as fibroepithelial polyps or skin tags) are among the most commonly identified skin lesions and are believed to affect up to 46% of the general population.^1,2 These benign growths typically appear after middle age in men and women alike and are believed to be of ectodermal and mesenchymal origin.³ The most common locations include the axillae, neck, and inguinal folds. They generally are small, measuring only a few millimeters, and frequently present as multiple lesions that are called giant acrochordons when their size exceeds 5 cm in length.² Acrochordons are benign lesions with only rare reports of the presence of basal or squamous cell carcinoma within the lesion on pathology.⁴ In addition to being cosmetically unsightly, patients with acrochordons often report pruritus. These lesions are easily removed in an outpatient setting via snip excision, cryosurgery, or electrodesiccation. Once removed, recurrence is unlikely. Despite the prevalence of fibroepithelial polyps worldwide, reports of giant acrochordons are limited. The histopathology of giant acrochordons is similar to smaller acrochordons, with features including epidermal acanthosis and a central core of fibrovascular tissue without adnexal structures (Figure).⁴

The differential diagnosis of giant acrochordon includes neurofibroma, nodular melanoma, squamous cell carcinoma, and giant condylomata acuminata (Buschke-Löwenstein tumor).¹ It is important to consider the clinical presentation and histopathologic findings to differentiate giant acrochordons from these other entities.

Neurofibromas typically present as multiple flesh-colored to brown nodules that invaginate into the skin when minimal external pressure is applied.⁵ Histopathology demonstrates a discrete, nonencapsulated, dermal collection of small nerve fibers and loosely arranged spindle cells. In contrast, giant acrochordons typically present as large, fleshcolored, pedunculated, verrucous tumors with a central stalk. Histopathology reveals epidermal acanthosis and a central core of fibrovascular tissue without adnexal structures.

Nodular melanomas usually are blue to black and grow rapidly over the course of several months.⁶ They have signs of hemorrhagic crust, and histopathology reveals atypical melanocytes, frequent mitoses, pleomorphic tumor cells, and irregular clumping of chromatin within the nuclei. Giant acrochordons are flesh colored, benign, and do not have these malignant features.

Squamous cell carcinoma often presents as an erythematous scaly patch or red plaque on sun-exposed areas of the skin.¹ Histopathology of squamous cell carcinoma shows atypical keratinocytes with an invasive growth pattern; giant acrochordon does not show keratinocytic atypia or invasive epidermal growth.

Giant condylomata acuminata (Buschke-Löwenstein tumor) is a locally destructive verrucous plaque that typically appears on the penis but can occur elsewhere in the anogenital region.⁷ Histopathologic features include epidermal hyperplasia, papillomatosis, and koilocytes. In contrast, giant acrochordons typically are located on the buttocks and do not present with these epidermal changes.

Based on the clinical and histologic findings, our patient was diagnosed with a giant acrochordon, a rare variant of the common skin lesion. Excisional removal was critical for both diagnostic and treatment purposes. By considering the clinical presentation and histopathologic features of other conditions in the differential, giant acrochordons can be distinguished from other similar entities. Diagnosis and prompt surgical removal are important for management of these neoplasms and prevention of misdiagnosis.

The Diagnosis: Giant Acrochordon

Based on the clinical and histologic findings, our patient was diagnosed with a giant acrochordon. Acrochordons (also known as fibroepithelial polyps or skin tags) are among the most commonly identified skin lesions and are believed to affect up to 46% of the general population.^1,2 These benign growths typically appear after middle age in men and women alike and are believed to be of ectodermal and mesenchymal origin.³ The most common locations include the axillae, neck, and inguinal folds. They generally are small, measuring only a few millimeters, and frequently present as multiple lesions that are called giant acrochordons when their size exceeds 5 cm in length.² Acrochordons are benign lesions with only rare reports of the presence of basal or squamous cell carcinoma within the lesion on pathology.⁴ In addition to being cosmetically unsightly, patients with acrochordons often report pruritus. These lesions are easily removed in an outpatient setting via snip excision, cryosurgery, or electrodesiccation. Once removed, recurrence is unlikely. Despite the prevalence of fibroepithelial polyps worldwide, reports of giant acrochordons are limited. The histopathology of giant acrochordons is similar to smaller acrochordons, with features including epidermal acanthosis and a central core of fibrovascular tissue without adnexal structures (Figure).⁴

The differential diagnosis of giant acrochordon includes neurofibroma, nodular melanoma, squamous cell carcinoma, and giant condylomata acuminata (Buschke-Löwenstein tumor).¹ It is important to consider the clinical presentation and histopathologic findings to differentiate giant acrochordons from these other entities.

Neurofibromas typically present as multiple flesh-colored to brown nodules that invaginate into the skin when minimal external pressure is applied.⁵ Histopathology demonstrates a discrete, nonencapsulated, dermal collection of small nerve fibers and loosely arranged spindle cells. In contrast, giant acrochordons typically present as large, fleshcolored, pedunculated, verrucous tumors with a central stalk. Histopathology reveals epidermal acanthosis and a central core of fibrovascular tissue without adnexal structures.

Nodular melanomas usually are blue to black and grow rapidly over the course of several months.⁶ They have signs of hemorrhagic crust, and histopathology reveals atypical melanocytes, frequent mitoses, pleomorphic tumor cells, and irregular clumping of chromatin within the nuclei. Giant acrochordons are flesh colored, benign, and do not have these malignant features.

Squamous cell carcinoma often presents as an erythematous scaly patch or red plaque on sun-exposed areas of the skin.¹ Histopathology of squamous cell carcinoma shows atypical keratinocytes with an invasive growth pattern; giant acrochordon does not show keratinocytic atypia or invasive epidermal growth.

Giant condylomata acuminata (Buschke-Löwenstein tumor) is a locally destructive verrucous plaque that typically appears on the penis but can occur elsewhere in the anogenital region.⁷ Histopathologic features include epidermal hyperplasia, papillomatosis, and koilocytes. In contrast, giant acrochordons typically are located on the buttocks and do not present with these epidermal changes.

Based on the clinical and histologic findings, our patient was diagnosed with a giant acrochordon, a rare variant of the common skin lesion. Excisional removal was critical for both diagnostic and treatment purposes. By considering the clinical presentation and histopathologic features of other conditions in the differential, giant acrochordons can be distinguished from other similar entities. Diagnosis and prompt surgical removal are important for management of these neoplasms and prevention of misdiagnosis.

The Diagnosis: Giant Acrochordon

Based on the clinical and histologic findings, our patient was diagnosed with a giant acrochordon. Acrochordons (also known as fibroepithelial polyps or skin tags) are among the most commonly identified skin lesions and are believed to affect up to 46% of the general population.^1,2 These benign growths typically appear after middle age in men and women alike and are believed to be of ectodermal and mesenchymal origin.³ The most common locations include the axillae, neck, and inguinal folds. They generally are small, measuring only a few millimeters, and frequently present as multiple lesions that are called giant acrochordons when their size exceeds 5 cm in length.² Acrochordons are benign lesions with only rare reports of the presence of basal or squamous cell carcinoma within the lesion on pathology.⁴ In addition to being cosmetically unsightly, patients with acrochordons often report pruritus. These lesions are easily removed in an outpatient setting via snip excision, cryosurgery, or electrodesiccation. Once removed, recurrence is unlikely. Despite the prevalence of fibroepithelial polyps worldwide, reports of giant acrochordons are limited. The histopathology of giant acrochordons is similar to smaller acrochordons, with features including epidermal acanthosis and a central core of fibrovascular tissue without adnexal structures (Figure).⁴

The differential diagnosis of giant acrochordon includes neurofibroma, nodular melanoma, squamous cell carcinoma, and giant condylomata acuminata (Buschke-Löwenstein tumor).¹ It is important to consider the clinical presentation and histopathologic findings to differentiate giant acrochordons from these other entities.

Neurofibromas typically present as multiple flesh-colored to brown nodules that invaginate into the skin when minimal external pressure is applied.⁵ Histopathology demonstrates a discrete, nonencapsulated, dermal collection of small nerve fibers and loosely arranged spindle cells. In contrast, giant acrochordons typically present as large, fleshcolored, pedunculated, verrucous tumors with a central stalk. Histopathology reveals epidermal acanthosis and a central core of fibrovascular tissue without adnexal structures.

Nodular melanomas usually are blue to black and grow rapidly over the course of several months.⁶ They have signs of hemorrhagic crust, and histopathology reveals atypical melanocytes, frequent mitoses, pleomorphic tumor cells, and irregular clumping of chromatin within the nuclei. Giant acrochordons are flesh colored, benign, and do not have these malignant features.

Squamous cell carcinoma often presents as an erythematous scaly patch or red plaque on sun-exposed areas of the skin.¹ Histopathology of squamous cell carcinoma shows atypical keratinocytes with an invasive growth pattern; giant acrochordon does not show keratinocytic atypia or invasive epidermal growth.

Giant condylomata acuminata (Buschke-Löwenstein tumor) is a locally destructive verrucous plaque that typically appears on the penis but can occur elsewhere in the anogenital region.⁷ Histopathologic features include epidermal hyperplasia, papillomatosis, and koilocytes. In contrast, giant acrochordons typically are located on the buttocks and do not present with these epidermal changes.

Based on the clinical and histologic findings, our patient was diagnosed with a giant acrochordon, a rare variant of the common skin lesion. Excisional removal was critical for both diagnostic and treatment purposes. By considering the clinical presentation and histopathologic features of other conditions in the differential, giant acrochordons can be distinguished from other similar entities. Diagnosis and prompt surgical removal are important for management of these neoplasms and prevention of misdiagnosis.

The US Food and Drug Administration (FDA) has granted accelerated approval to pirtobrutinib (Jaypirca; Eli Lilly and Company) for third-line or later treatment in adults with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) who previously received a Bruton tyrosine kinase (BTK) inhibitor and a BCL-2 inhibitor.

The agent was initially approved in January 2023 for patients with mantle cell lymphoma who had previously received a BTK inhibitor.

Like the mantle cell approval, the CLL/SLL approval was based on findings from the open-label, single-arm, phase 1/2 BRUIN study that included adults with at least two prior lines of therapy, including a BTK inhibitor and a BCL-2 inhibitor.

The trial included 108 patients with either CLL or SLL. Overall, patients demonstrated an overall response rate of 72%, all of which were partial responses, and median duration of response of 12.2 months.

Before starting pirtobrutinib, 77% of patients with CLL or SLL had discontinued their last BTK inhibitor for refractory or progressive disease.

“Once patients with CLL or SLL have progressed on covalent BTK inhibitor and BCL-2 inhibitor therapies, treatments are limited and outcomes can be poor, making the approval of Jaypirca a meaningful advance and much-needed new treatment option for these patients,” William G. Wierda, MD, PhD, of the University of Texas MD Anderson Cancer Center, Houston, said in an Eli Lilly press release. 

Treatment during the study included the recommended dose of 200 mg given orally once daily until disease progression or unacceptable toxicity. Common adverse reactions that occurred in at least 20% of patients included fatigue, bruising, cough, musculoskeletal pain, COVID-19, diarrhea, pneumonia, abdominal pain, dyspnea, hemorrhage, edema, nausea, pyrexia, and headache. Grade 3 or 4 laboratory abnormalities occurring in more than 10% of patients included decreased neutrophil counts, anemia, and decreased platelet counts.

Serious infections occurred in 32% of patients, including fatal infections in 10% of patients. The prescribing information for pirtobrutinib includes warnings about infections, hemorrhage, cytopenias, cardiac arrhythmias, and secondary primary malignancies.

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

The US Food and Drug Administration (FDA) has granted accelerated approval to pirtobrutinib (Jaypirca; Eli Lilly and Company) for third-line or later treatment in adults with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) who previously received a Bruton tyrosine kinase (BTK) inhibitor and a BCL-2 inhibitor.

The agent was initially approved in January 2023 for patients with mantle cell lymphoma who had previously received a BTK inhibitor.

Like the mantle cell approval, the CLL/SLL approval was based on findings from the open-label, single-arm, phase 1/2 BRUIN study that included adults with at least two prior lines of therapy, including a BTK inhibitor and a BCL-2 inhibitor.

The trial included 108 patients with either CLL or SLL. Overall, patients demonstrated an overall response rate of 72%, all of which were partial responses, and median duration of response of 12.2 months.

Before starting pirtobrutinib, 77% of patients with CLL or SLL had discontinued their last BTK inhibitor for refractory or progressive disease.

“Once patients with CLL or SLL have progressed on covalent BTK inhibitor and BCL-2 inhibitor therapies, treatments are limited and outcomes can be poor, making the approval of Jaypirca a meaningful advance and much-needed new treatment option for these patients,” William G. Wierda, MD, PhD, of the University of Texas MD Anderson Cancer Center, Houston, said in an Eli Lilly press release. 

Treatment during the study included the recommended dose of 200 mg given orally once daily until disease progression or unacceptable toxicity. Common adverse reactions that occurred in at least 20% of patients included fatigue, bruising, cough, musculoskeletal pain, COVID-19, diarrhea, pneumonia, abdominal pain, dyspnea, hemorrhage, edema, nausea, pyrexia, and headache. Grade 3 or 4 laboratory abnormalities occurring in more than 10% of patients included decreased neutrophil counts, anemia, and decreased platelet counts.

Serious infections occurred in 32% of patients, including fatal infections in 10% of patients. The prescribing information for pirtobrutinib includes warnings about infections, hemorrhage, cytopenias, cardiac arrhythmias, and secondary primary malignancies.

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

The US Food and Drug Administration (FDA) has granted accelerated approval to pirtobrutinib (Jaypirca; Eli Lilly and Company) for third-line or later treatment in adults with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) who previously received a Bruton tyrosine kinase (BTK) inhibitor and a BCL-2 inhibitor.

The agent was initially approved in January 2023 for patients with mantle cell lymphoma who had previously received a BTK inhibitor.

Like the mantle cell approval, the CLL/SLL approval was based on findings from the open-label, single-arm, phase 1/2 BRUIN study that included adults with at least two prior lines of therapy, including a BTK inhibitor and a BCL-2 inhibitor.

The trial included 108 patients with either CLL or SLL. Overall, patients demonstrated an overall response rate of 72%, all of which were partial responses, and median duration of response of 12.2 months.

Before starting pirtobrutinib, 77% of patients with CLL or SLL had discontinued their last BTK inhibitor for refractory or progressive disease.

“Once patients with CLL or SLL have progressed on covalent BTK inhibitor and BCL-2 inhibitor therapies, treatments are limited and outcomes can be poor, making the approval of Jaypirca a meaningful advance and much-needed new treatment option for these patients,” William G. Wierda, MD, PhD, of the University of Texas MD Anderson Cancer Center, Houston, said in an Eli Lilly press release. 

Treatment during the study included the recommended dose of 200 mg given orally once daily until disease progression or unacceptable toxicity. Common adverse reactions that occurred in at least 20% of patients included fatigue, bruising, cough, musculoskeletal pain, COVID-19, diarrhea, pneumonia, abdominal pain, dyspnea, hemorrhage, edema, nausea, pyrexia, and headache. Grade 3 or 4 laboratory abnormalities occurring in more than 10% of patients included decreased neutrophil counts, anemia, and decreased platelet counts.

Serious infections occurred in 32% of patients, including fatal infections in 10% of patients. The prescribing information for pirtobrutinib includes warnings about infections, hemorrhage, cytopenias, cardiac arrhythmias, and secondary primary malignancies.

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

The average physician makes $352,000, and some earn well into the $500,000s. So, doctors don’t have to worry about money, right?

You know the answer to that.

One thing all physicians have in common about money, says James M. Dahle, MD, FACEP, founder of The White Coat Investor, is that they don’t receive any training in business, personal finance, or investing throughout their schooling or careers unless they seek it out. This leaves many unprepared to make the best investing and money-saving decisions, while others get too frustrated about their lack of knowledge to even dip their toe into the investing pool.

Exhibit A: Four out of 10 physicians have a net worth below $1 million, according to the Medscape Physician Wealth & Debt Report 2023. Elizabeth Chiang, MD, PhD, an oculoplastic surgeon and a physician money coach at Grow Your Wealthy Mindset, notes that many of those doctors are over age 65, “which means they essentially can’t retire.”

And that’s just one pain point.

Physicians have money concerns specific to their profession and background. Luckily, some fellow doctors also serve as financial and wealth advisors just for other doctors. We sought out a few to get their advice--and fixes--for common physician blind spots.

Blind Spot #1

The early lean years skew doctors’ money outlook. “We have an extended training period, which commonly consists of taking on a large amount of debt, followed by 3 to 8 years of being paid a modest salary, and then finally a large boost in income,” explains Dr. Chiang. This can lay a shaky foundation for the earning years to come, and as a result, a lot of doctors just don’t think about money in healthy ways. Once their incomes increase, physicians may be surprised, for example, that making a multiple six-figure salary means paying six figures in taxes.

The Fix

Treat financial health like physical health. That means money cannot be a taboo subject. “The misguided mindset is that we didn’t become physicians to make money, we did it to help people,” explains Jordan Frey, MD, creator of the blog, The Prudent Plastic Surgeon.

Dr. Frey acknowledges that the desire to help is certainly true. But the result is a false idea that “to think about our personal finances makes us a worse doctor.”

Blind Spot #2

Because doctors know a lot about one thing (medicine), they might assume they know a lot about everything (such as investing). “Totally different fields with a different language and different way to think about it,” Dahle explains. This overconfidence could lead to some negligent or risky financial decisions.

The Fix

Educate yourself. There are several books on personal finance and investing written by physicians for physicians. Dr. Chiang recommends The Physician Philosopher’s Guide to Personal Finance, by James Turner, MD; Financial Freedom Rx, by Chirag Shah, MD, and Jayanth Sridhar, MD; and The Physician’s Guide to Finance, by Nicholas Christian and Amanda Christian, MD. There are also podcasts, blogs, and courses to help educate doctors on finance, such as the Fire Your Financial Advisor course by The White Coat Investor.

Blind Spot #3

Undersaving. Retirement saving is one thing, but 24% of doctors say they don’t even put money away in a taxable savings account, according to the Wealth & Debt Report.

Cobin Soelberg, MD, JD, a board-certified anesthesiologist and founder and principal advisor with Greeley Wealth Management, is the treasurer of his anesthesiology group. “I get to see every month how much people are saving, and even on an anesthesiologist salary, where everyone’s making about $400,000 a year, a lot of people are not saving anything, which is crazy.”

Undersaving can be both a time issue and a mindset one.

Time: Doctors often start investing in their retirement accounts later than the average professional, says Dr. Chiang. “A lot of physicians will max out their 401k or 403b,” she explains. “But if you’re putting in $20,000 a year and only starting when you’re in your early 30s, that’s not enough to get you to retirement.”

Mindset: Doctors also see people of all ages who are sick, dying, and injured. “They all know someone who worked hard and saved and then dropped dead at 55,” explains Dr. Dahle. This, he says, can lead to a bit of a “you only live once” attitude that prioritizes spending over saving.

The Fix

Shoot for 20%. If you can’t save 20% of your gross now, strive to get to that point. Think of it as telling a patient they have to change their behavior or trouble will come - not if, but when. “Develop a written investing plan and then stick with it through thick and thin,” says Dr. Dahle. “Once you have a reasonable plan, all you have to do is fund it adequately by saving 20% of your gross income, and a doctor will easily retire as a multimillionaire.”

Blind Spot #4

Bad investment strategies. Thirty-six percent of doctors experience their largest financial losses from lousy investments, according to the Wealth & Debt Report. Meanwhile, 17% of PCPs and 12% of specialists say they haven’t made any investments at all. That’s a terrible mix of doing the wrong thing and doing a worse thing.

The Fix

Don’t overthink investing, but don’t underthink it either. “As high-income earners, doctors just don’t need to take this high level of risk to reach their financial goals,” Dr. Frey says. A good investment plan doesn’t require you to time the stock market or predict individual stock winners. Consider what Vanguard founder Jack Bogle once said about investing: “Be bored by the process but elated by the outcome.”

Dr. Frey suggests going super-simple: index funds. Ignore investing strategies with actively managed mutual funds or individual stocks, as well as risky alternative investments such as cryptocurrency and angel investments. Everyone assumes doctors have money to burn, and they will push sketchy investment ideas at them. Avoid.

Blind Spot #5

Not taking debt seriously enough. The average medical student debt is $250,000 and can exceed $500,000, says Dr. Soelberg. Many doctors spend the first 10 to 20 years of their careers paying this off. Today’s graduates are paying more than 7% on their loans.

And it’s not just student debt: 39% of physicians carry five or more credit cards, and 34% have mortgages larger than $300,000 (with half of those are more than than $500K), per the Wealth & Debt Report.

The Fix

Treat debt like cancer. It’s a lethal enemy you can’t get rid of right away, but a steady, aggressive, long-term attack will have the best results. Dr. Soelberg suggests allocating the most you can afford per month, whether that’s $1000 or $5000, toward debt. Raise the amount as your income grows. Do the same with your 401k or retirement plan. Whatever is left, you can spend. Five to 10 years later, you will realize, “Wow. I’m debt free.”

Blind Spot #6

Not putting in the work to improve your situation. Seventy-one percent of doctors admit they haven’t done anything to reduce major expenses, according to the Wealth & Debt Report. Are you leaving major money on the table?

The Fix

Audit yourself in major areas like housing and taxes. While the average professional may need to put 10% to 20% down on a home, physicians can qualify for physician mortgage loans and can often put down 3% or less, says Dr. Chiang. If you can afford the higher mortgage payment, excess savings earmarked for a larger down payment can be put toward debt or invested.

Another trick, if you’re able, is to seek an area that is less in demand at a higher salary. “Physicians in places like New York City or San Francisco tend to make less than physicians in the Midwest or the South,” Dr. Chiang explains. A colleague of hers moved to rural Pennsylvania, where he made a high salary and had a low cost of living for 3½ years, paid off his student debt, and then relocated to an area where he wanted to live long term.

As for taxes, become familiar with tax law. Research things like, “What is considered a business expense for doctors?” says Brett Mollard, MD, a diagnostic radiologist who provides financial advice to younger physicians. “What will your estimated total tax burden be at the end of the year? Will you need to make extra payments to prevent owing a large sum of money from underpaying or to avoid tax penalties?”

Blind Spot #7

Living like a rock star on a doctor’s income. Getting caught up in trying to live the same lifestyle as your colleagues is a classic bear trap. “Sitting in the doctor’s lounge, it’s so crazy,” Dr. Soelberg says. He describes conversations like, “‘Where did you go on your trip?’ ‘What new toys are you buying?’” There’s pressure to live up to an image of what a doctor’s life is supposed to look like before you’ve sorted the basic things like paying off debt.

The Fix

Live like a resident even if you haven’t been one for years, at least until you’re in a better financial position. “You’re already used to living a life of lower means, and you’re an expert when it comes to delaying gratification,” says Dr. Mollard. “Do it a little longer.” Live frugally and spend only on things that bring you joy. “A lot of physicians are trying to be really rich in all areas of their life instead of the ones that actually matter to them,” Dr. Soelberg says. Identify what’s important to you and only splurge on that.

Blind Spot #8

Never asking for help. The right financial planner can provide expert help. Emphasis on right. “Doctors can be very trusting of other professionals, even when they should not be,” says Dr. Dahle. He notes that in financial services, many people masquerade as knowledgeable advisors who are really just salespeople. While legitimate financial advisors strive to make their clients money, they are also ultimately out to line their pockets and love to work with physician salaries. Thus, doctors can end up working with financial planners that don’t specifically understand their situations or end up taking too much from their clients.

The Fix

Find a planner who specializes in, or at least understands, physicians. Ask them how they make money, says Dr. Chiang. If someone hesitates to tell you about their fee structure or if it sounds like a lot, shop around and ask colleagues for recommendations.

“Ultimately, the path to wealth is to create and grow the margin between what you make and what you spend,” says Dr. Frey. Throw some investing into the mix and physicians can set themselves up on a path for a stress-free financial life.


A version of this article appeared on Medscape.com.

The average physician makes $352,000, and some earn well into the $500,000s. So, doctors don’t have to worry about money, right?

You know the answer to that.

One thing all physicians have in common about money, says James M. Dahle, MD, FACEP, founder of The White Coat Investor, is that they don’t receive any training in business, personal finance, or investing throughout their schooling or careers unless they seek it out. This leaves many unprepared to make the best investing and money-saving decisions, while others get too frustrated about their lack of knowledge to even dip their toe into the investing pool.

Exhibit A: Four out of 10 physicians have a net worth below $1 million, according to the Medscape Physician Wealth & Debt Report 2023. Elizabeth Chiang, MD, PhD, an oculoplastic surgeon and a physician money coach at Grow Your Wealthy Mindset, notes that many of those doctors are over age 65, “which means they essentially can’t retire.”

And that’s just one pain point.

Physicians have money concerns specific to their profession and background. Luckily, some fellow doctors also serve as financial and wealth advisors just for other doctors. We sought out a few to get their advice--and fixes--for common physician blind spots.

Blind Spot #1

The early lean years skew doctors’ money outlook. “We have an extended training period, which commonly consists of taking on a large amount of debt, followed by 3 to 8 years of being paid a modest salary, and then finally a large boost in income,” explains Dr. Chiang. This can lay a shaky foundation for the earning years to come, and as a result, a lot of doctors just don’t think about money in healthy ways. Once their incomes increase, physicians may be surprised, for example, that making a multiple six-figure salary means paying six figures in taxes.

The Fix

Treat financial health like physical health. That means money cannot be a taboo subject. “The misguided mindset is that we didn’t become physicians to make money, we did it to help people,” explains Jordan Frey, MD, creator of the blog, The Prudent Plastic Surgeon.

Dr. Frey acknowledges that the desire to help is certainly true. But the result is a false idea that “to think about our personal finances makes us a worse doctor.”

Blind Spot #2

Because doctors know a lot about one thing (medicine), they might assume they know a lot about everything (such as investing). “Totally different fields with a different language and different way to think about it,” Dahle explains. This overconfidence could lead to some negligent or risky financial decisions.

The Fix

Educate yourself. There are several books on personal finance and investing written by physicians for physicians. Dr. Chiang recommends The Physician Philosopher’s Guide to Personal Finance, by James Turner, MD; Financial Freedom Rx, by Chirag Shah, MD, and Jayanth Sridhar, MD; and The Physician’s Guide to Finance, by Nicholas Christian and Amanda Christian, MD. There are also podcasts, blogs, and courses to help educate doctors on finance, such as the Fire Your Financial Advisor course by The White Coat Investor.

Blind Spot #3

Undersaving. Retirement saving is one thing, but 24% of doctors say they don’t even put money away in a taxable savings account, according to the Wealth & Debt Report.

Cobin Soelberg, MD, JD, a board-certified anesthesiologist and founder and principal advisor with Greeley Wealth Management, is the treasurer of his anesthesiology group. “I get to see every month how much people are saving, and even on an anesthesiologist salary, where everyone’s making about $400,000 a year, a lot of people are not saving anything, which is crazy.”

Undersaving can be both a time issue and a mindset one.

Time: Doctors often start investing in their retirement accounts later than the average professional, says Dr. Chiang. “A lot of physicians will max out their 401k or 403b,” she explains. “But if you’re putting in $20,000 a year and only starting when you’re in your early 30s, that’s not enough to get you to retirement.”

Mindset: Doctors also see people of all ages who are sick, dying, and injured. “They all know someone who worked hard and saved and then dropped dead at 55,” explains Dr. Dahle. This, he says, can lead to a bit of a “you only live once” attitude that prioritizes spending over saving.

The Fix

Shoot for 20%. If you can’t save 20% of your gross now, strive to get to that point. Think of it as telling a patient they have to change their behavior or trouble will come - not if, but when. “Develop a written investing plan and then stick with it through thick and thin,” says Dr. Dahle. “Once you have a reasonable plan, all you have to do is fund it adequately by saving 20% of your gross income, and a doctor will easily retire as a multimillionaire.”

Blind Spot #4

Bad investment strategies. Thirty-six percent of doctors experience their largest financial losses from lousy investments, according to the Wealth & Debt Report. Meanwhile, 17% of PCPs and 12% of specialists say they haven’t made any investments at all. That’s a terrible mix of doing the wrong thing and doing a worse thing.

The Fix

Don’t overthink investing, but don’t underthink it either. “As high-income earners, doctors just don’t need to take this high level of risk to reach their financial goals,” Dr. Frey says. A good investment plan doesn’t require you to time the stock market or predict individual stock winners. Consider what Vanguard founder Jack Bogle once said about investing: “Be bored by the process but elated by the outcome.”

Dr. Frey suggests going super-simple: index funds. Ignore investing strategies with actively managed mutual funds or individual stocks, as well as risky alternative investments such as cryptocurrency and angel investments. Everyone assumes doctors have money to burn, and they will push sketchy investment ideas at them. Avoid.

Blind Spot #5

Not taking debt seriously enough. The average medical student debt is $250,000 and can exceed $500,000, says Dr. Soelberg. Many doctors spend the first 10 to 20 years of their careers paying this off. Today’s graduates are paying more than 7% on their loans.

And it’s not just student debt: 39% of physicians carry five or more credit cards, and 34% have mortgages larger than $300,000 (with half of those are more than than $500K), per the Wealth & Debt Report.

The Fix

Treat debt like cancer. It’s a lethal enemy you can’t get rid of right away, but a steady, aggressive, long-term attack will have the best results. Dr. Soelberg suggests allocating the most you can afford per month, whether that’s $1000 or $5000, toward debt. Raise the amount as your income grows. Do the same with your 401k or retirement plan. Whatever is left, you can spend. Five to 10 years later, you will realize, “Wow. I’m debt free.”

Blind Spot #6

Not putting in the work to improve your situation. Seventy-one percent of doctors admit they haven’t done anything to reduce major expenses, according to the Wealth & Debt Report. Are you leaving major money on the table?

The Fix

Audit yourself in major areas like housing and taxes. While the average professional may need to put 10% to 20% down on a home, physicians can qualify for physician mortgage loans and can often put down 3% or less, says Dr. Chiang. If you can afford the higher mortgage payment, excess savings earmarked for a larger down payment can be put toward debt or invested.

Another trick, if you’re able, is to seek an area that is less in demand at a higher salary. “Physicians in places like New York City or San Francisco tend to make less than physicians in the Midwest or the South,” Dr. Chiang explains. A colleague of hers moved to rural Pennsylvania, where he made a high salary and had a low cost of living for 3½ years, paid off his student debt, and then relocated to an area where he wanted to live long term.

As for taxes, become familiar with tax law. Research things like, “What is considered a business expense for doctors?” says Brett Mollard, MD, a diagnostic radiologist who provides financial advice to younger physicians. “What will your estimated total tax burden be at the end of the year? Will you need to make extra payments to prevent owing a large sum of money from underpaying or to avoid tax penalties?”

Blind Spot #7

Living like a rock star on a doctor’s income. Getting caught up in trying to live the same lifestyle as your colleagues is a classic bear trap. “Sitting in the doctor’s lounge, it’s so crazy,” Dr. Soelberg says. He describes conversations like, “‘Where did you go on your trip?’ ‘What new toys are you buying?’” There’s pressure to live up to an image of what a doctor’s life is supposed to look like before you’ve sorted the basic things like paying off debt.

The Fix

Live like a resident even if you haven’t been one for years, at least until you’re in a better financial position. “You’re already used to living a life of lower means, and you’re an expert when it comes to delaying gratification,” says Dr. Mollard. “Do it a little longer.” Live frugally and spend only on things that bring you joy. “A lot of physicians are trying to be really rich in all areas of their life instead of the ones that actually matter to them,” Dr. Soelberg says. Identify what’s important to you and only splurge on that.

Blind Spot #8

Never asking for help. The right financial planner can provide expert help. Emphasis on right. “Doctors can be very trusting of other professionals, even when they should not be,” says Dr. Dahle. He notes that in financial services, many people masquerade as knowledgeable advisors who are really just salespeople. While legitimate financial advisors strive to make their clients money, they are also ultimately out to line their pockets and love to work with physician salaries. Thus, doctors can end up working with financial planners that don’t specifically understand their situations or end up taking too much from their clients.

The Fix

Find a planner who specializes in, or at least understands, physicians. Ask them how they make money, says Dr. Chiang. If someone hesitates to tell you about their fee structure or if it sounds like a lot, shop around and ask colleagues for recommendations.

“Ultimately, the path to wealth is to create and grow the margin between what you make and what you spend,” says Dr. Frey. Throw some investing into the mix and physicians can set themselves up on a path for a stress-free financial life.


A version of this article appeared on Medscape.com.

The average physician makes $352,000, and some earn well into the $500,000s. So, doctors don’t have to worry about money, right?

You know the answer to that.

One thing all physicians have in common about money, says James M. Dahle, MD, FACEP, founder of The White Coat Investor, is that they don’t receive any training in business, personal finance, or investing throughout their schooling or careers unless they seek it out. This leaves many unprepared to make the best investing and money-saving decisions, while others get too frustrated about their lack of knowledge to even dip their toe into the investing pool.

Exhibit A: Four out of 10 physicians have a net worth below $1 million, according to the Medscape Physician Wealth & Debt Report 2023. Elizabeth Chiang, MD, PhD, an oculoplastic surgeon and a physician money coach at Grow Your Wealthy Mindset, notes that many of those doctors are over age 65, “which means they essentially can’t retire.”

And that’s just one pain point.

Physicians have money concerns specific to their profession and background. Luckily, some fellow doctors also serve as financial and wealth advisors just for other doctors. We sought out a few to get their advice--and fixes--for common physician blind spots.

Blind Spot #1

The early lean years skew doctors’ money outlook. “We have an extended training period, which commonly consists of taking on a large amount of debt, followed by 3 to 8 years of being paid a modest salary, and then finally a large boost in income,” explains Dr. Chiang. This can lay a shaky foundation for the earning years to come, and as a result, a lot of doctors just don’t think about money in healthy ways. Once their incomes increase, physicians may be surprised, for example, that making a multiple six-figure salary means paying six figures in taxes.

The Fix

Treat financial health like physical health. That means money cannot be a taboo subject. “The misguided mindset is that we didn’t become physicians to make money, we did it to help people,” explains Jordan Frey, MD, creator of the blog, The Prudent Plastic Surgeon.

Dr. Frey acknowledges that the desire to help is certainly true. But the result is a false idea that “to think about our personal finances makes us a worse doctor.”

Blind Spot #2

Because doctors know a lot about one thing (medicine), they might assume they know a lot about everything (such as investing). “Totally different fields with a different language and different way to think about it,” Dahle explains. This overconfidence could lead to some negligent or risky financial decisions.

The Fix

Educate yourself. There are several books on personal finance and investing written by physicians for physicians. Dr. Chiang recommends The Physician Philosopher’s Guide to Personal Finance, by James Turner, MD; Financial Freedom Rx, by Chirag Shah, MD, and Jayanth Sridhar, MD; and The Physician’s Guide to Finance, by Nicholas Christian and Amanda Christian, MD. There are also podcasts, blogs, and courses to help educate doctors on finance, such as the Fire Your Financial Advisor course by The White Coat Investor.

Blind Spot #3

Undersaving. Retirement saving is one thing, but 24% of doctors say they don’t even put money away in a taxable savings account, according to the Wealth & Debt Report.

Cobin Soelberg, MD, JD, a board-certified anesthesiologist and founder and principal advisor with Greeley Wealth Management, is the treasurer of his anesthesiology group. “I get to see every month how much people are saving, and even on an anesthesiologist salary, where everyone’s making about $400,000 a year, a lot of people are not saving anything, which is crazy.”

Undersaving can be both a time issue and a mindset one.

Time: Doctors often start investing in their retirement accounts later than the average professional, says Dr. Chiang. “A lot of physicians will max out their 401k or 403b,” she explains. “But if you’re putting in $20,000 a year and only starting when you’re in your early 30s, that’s not enough to get you to retirement.”

Mindset: Doctors also see people of all ages who are sick, dying, and injured. “They all know someone who worked hard and saved and then dropped dead at 55,” explains Dr. Dahle. This, he says, can lead to a bit of a “you only live once” attitude that prioritizes spending over saving.

The Fix

Shoot for 20%. If you can’t save 20% of your gross now, strive to get to that point. Think of it as telling a patient they have to change their behavior or trouble will come - not if, but when. “Develop a written investing plan and then stick with it through thick and thin,” says Dr. Dahle. “Once you have a reasonable plan, all you have to do is fund it adequately by saving 20% of your gross income, and a doctor will easily retire as a multimillionaire.”

Blind Spot #4

Bad investment strategies. Thirty-six percent of doctors experience their largest financial losses from lousy investments, according to the Wealth & Debt Report. Meanwhile, 17% of PCPs and 12% of specialists say they haven’t made any investments at all. That’s a terrible mix of doing the wrong thing and doing a worse thing.

The Fix

Don’t overthink investing, but don’t underthink it either. “As high-income earners, doctors just don’t need to take this high level of risk to reach their financial goals,” Dr. Frey says. A good investment plan doesn’t require you to time the stock market or predict individual stock winners. Consider what Vanguard founder Jack Bogle once said about investing: “Be bored by the process but elated by the outcome.”

Dr. Frey suggests going super-simple: index funds. Ignore investing strategies with actively managed mutual funds or individual stocks, as well as risky alternative investments such as cryptocurrency and angel investments. Everyone assumes doctors have money to burn, and they will push sketchy investment ideas at them. Avoid.

Blind Spot #5

Not taking debt seriously enough. The average medical student debt is $250,000 and can exceed $500,000, says Dr. Soelberg. Many doctors spend the first 10 to 20 years of their careers paying this off. Today’s graduates are paying more than 7% on their loans.

And it’s not just student debt: 39% of physicians carry five or more credit cards, and 34% have mortgages larger than $300,000 (with half of those are more than than $500K), per the Wealth & Debt Report.

The Fix

Treat debt like cancer. It’s a lethal enemy you can’t get rid of right away, but a steady, aggressive, long-term attack will have the best results. Dr. Soelberg suggests allocating the most you can afford per month, whether that’s $1000 or $5000, toward debt. Raise the amount as your income grows. Do the same with your 401k or retirement plan. Whatever is left, you can spend. Five to 10 years later, you will realize, “Wow. I’m debt free.”

Blind Spot #6

Not putting in the work to improve your situation. Seventy-one percent of doctors admit they haven’t done anything to reduce major expenses, according to the Wealth & Debt Report. Are you leaving major money on the table?

The Fix

Audit yourself in major areas like housing and taxes. While the average professional may need to put 10% to 20% down on a home, physicians can qualify for physician mortgage loans and can often put down 3% or less, says Dr. Chiang. If you can afford the higher mortgage payment, excess savings earmarked for a larger down payment can be put toward debt or invested.

Another trick, if you’re able, is to seek an area that is less in demand at a higher salary. “Physicians in places like New York City or San Francisco tend to make less than physicians in the Midwest or the South,” Dr. Chiang explains. A colleague of hers moved to rural Pennsylvania, where he made a high salary and had a low cost of living for 3½ years, paid off his student debt, and then relocated to an area where he wanted to live long term.

As for taxes, become familiar with tax law. Research things like, “What is considered a business expense for doctors?” says Brett Mollard, MD, a diagnostic radiologist who provides financial advice to younger physicians. “What will your estimated total tax burden be at the end of the year? Will you need to make extra payments to prevent owing a large sum of money from underpaying or to avoid tax penalties?”

Blind Spot #7

Living like a rock star on a doctor’s income. Getting caught up in trying to live the same lifestyle as your colleagues is a classic bear trap. “Sitting in the doctor’s lounge, it’s so crazy,” Dr. Soelberg says. He describes conversations like, “‘Where did you go on your trip?’ ‘What new toys are you buying?’” There’s pressure to live up to an image of what a doctor’s life is supposed to look like before you’ve sorted the basic things like paying off debt.

The Fix

Live like a resident even if you haven’t been one for years, at least until you’re in a better financial position. “You’re already used to living a life of lower means, and you’re an expert when it comes to delaying gratification,” says Dr. Mollard. “Do it a little longer.” Live frugally and spend only on things that bring you joy. “A lot of physicians are trying to be really rich in all areas of their life instead of the ones that actually matter to them,” Dr. Soelberg says. Identify what’s important to you and only splurge on that.

Blind Spot #8

Never asking for help. The right financial planner can provide expert help. Emphasis on right. “Doctors can be very trusting of other professionals, even when they should not be,” says Dr. Dahle. He notes that in financial services, many people masquerade as knowledgeable advisors who are really just salespeople. While legitimate financial advisors strive to make their clients money, they are also ultimately out to line their pockets and love to work with physician salaries. Thus, doctors can end up working with financial planners that don’t specifically understand their situations or end up taking too much from their clients.

The Fix

Find a planner who specializes in, or at least understands, physicians. Ask them how they make money, says Dr. Chiang. If someone hesitates to tell you about their fee structure or if it sounds like a lot, shop around and ask colleagues for recommendations.

“Ultimately, the path to wealth is to create and grow the margin between what you make and what you spend,” says Dr. Frey. Throw some investing into the mix and physicians can set themselves up on a path for a stress-free financial life.


A version of this article appeared on Medscape.com.

Repairing patent foramen ovale (PFO) and other right-to-left shunt disorders for the prevention of migraine has generated mixed results, but the potential for these repairs also includes reducing the risk of stroke, according to a discussion at the 2023 Scottsdale Headache Symposium.

In two clinical trials evaluating whether PFO closure reduces migraine risk, the primary endpoints were not met, but a signal of benefit on secondary endpoints and the association between PFO, migraine, and stroke are among the reasons that PFO closure should be reevaluated, according to Andrew Charles MD, Director of the Goldberg Migraine Program, University of California, Los Angeles.

UCLA

One Intervention, Two Potential Benefits

Fixing these defects is therefore at least theoretically attractive for preventing both migraine and stroke, but Dr. Charles said the opportunity for preventing both migraine and stroke is most attractive in migraine patients who have additional stroke risk factors.

Use of oral contraceptives, which produce a hypercoagulable state, is an example.

“Are these the people we should really be thinking about if they have PFO and migraine, particularly migraine with aura?” Dr. Charles asked.

The association between right-to-left shunts and migraine is strong. Although PFO is common, presenting in 20%-25% of the adult population, it has been found in up to 50% of individuals who have migraine with aura. In patients with migraine but no aura, the prevalence of PFO has been estimated to be approximately 35% or still somewhat elevated relative to the general population.
 

Primary Endpoint Missed in Clinical Trials

The question of whether risk of migraine can be reduced with repair of PFO or other right-to-left shunts remains unresolved. In two high-quality randomized trials undertaken in PFO repair, neither met its primary endpoint. In one of these, called PRIMA, which was terminated early for slow enrollment, the reduction in mean headache attacks was not significant relative to medical therapy.

In the second, called PREMIUM, device closure of PFO also failed to significantly reduce migraine attacks over sham procedure although it was associated with complete migraine remission (10% vs 1%).

A pooled analysis of these two studies that was conducted subsequently concluded that PFO closure reduces mean monthly migraine days (-3.1 vs. -1.9 days; P = -.02) and increases the likelihood of complete migraine cessation (9% vs. 0.7%; P < .001), but Dr. Charles pointed out the primary endpoint was migraine attacks not migraine days, so other analyses can only be considered hypothesis-generating.

There are several reasons to relook at the relationship between migraine and PFO but the potential to prevent both migraine and stroke with PFO closure could be one of the most important.

Several years ago, Dr. Charles and his coinvestigators from UCLA evaluated more than 700 ischemic strokes. Of these, 127 strokes were characterized as cryptogenic because of lack of another identifiable etiology. While 59% of these patients had PFO, which is several times higher than the general population, the prevalence of PFO in patients with a cryptogenic stroke and a history of migraine was 79% in this published study.

“So, in this group of patients who did not have any other clear cause for a stroke, a diagnosis of PFO was very much overrepresented,” Dr. Charles said.
 

Migraine Days Might Be a Better Endpoint

For patients with migraine who have risk factors for stroke, this makes PFO closure an attractive intervention, but a positive randomized trial is needed. Several are underway. Importantly, the trials now enrolling are using migraine days, which was significantly reduced in both PREMIUM and PRIMA, rather than migraine attacks as the primary endpoint.

“Migraine days is now accepted by the Food and Drug Administration as a criterion of benefit,” reported Jonathan Tobis, MD, Research Director, Interventional Cardiology, UCLA David Geffen School of Medicine, Los Angeles.

He explained that the FDA insisted on migraine attacks as the endpoint for the PREMIUM trial, but this was a far more challenging endpoint on which to show a statistical benefit. He emphasized that a new set of trials will now test efficacy on the basis of migraine days.

One of these trials, called RELIEF, which is randomizing patients to device closure of PFO or a sham procedure. Both groups are receiving clopidogrel or prasugrel based on a previous observation that patients who respond to these drugs are also more likely to respond to PFO closure.

Another trial, called COMPETE-2, is comparing PFO closure with a device to aspirin plus a sham closure. This trial is ongoing in China.

Stroke is not being evaluated as an endpoint in either trial, but Dr. Charles suggested that this does warrant attention.

“I would also just put it out there that, apart from simply migraine, this is a therapeutic approach that we might actually think about in terms of helping to prevent stroke in our migraine patients,” he said.

Senior author of a recent meta-analysis of trials evaluating PFO closure and control of migraine, Ling Liu, MD, Department of Neurology, University of Sichuan, Chengdu, China, agreed that PFO closure for the treatment of migraine deserves “a reevaluation.”

In his meta-analysis of three randomized trials, one pooled study, and eight retrospective case series with 1,165 patients, PFO closure was associated with a nearly 75% reduction (odds ratio [OR], 0.259; P = .0048) reduction in migraine days and 50% increase in resolution of migraine in patients with a history of migraine with aura (OR, 1.586; P = .227).

The incidence of stroke was not evaluated in this meta-analysis, but Dr. Liu believes that the evidence of reducing the burden of migraine with PFO closure is compelling. Given the evidence from this meta-analysis that PFO closure is safe, Dr. Liu maintained that a definitive trial is needed “especially for migraine with frequent aura.”

As an interventional cardiologist, Dr. Tobis said that when PFO closures is performed for prevention of stroke in patients with migraine, it often leads to reduced migraine activity and, in some cases, elimination of migraine. Like others, he believes new analyses should be conducted.

“Everyone involved in this field believes there is something there,” Dr. Tobis said. The missing link is a clinical trial to confirm it.

Dr. Charles and Dr. Liu report no potential conflicts of interest. Dr. Tobis reports a financial relationship with Holistick Medical.

Repairing patent foramen ovale (PFO) and other right-to-left shunt disorders for the prevention of migraine has generated mixed results, but the potential for these repairs also includes reducing the risk of stroke, according to a discussion at the 2023 Scottsdale Headache Symposium.

In two clinical trials evaluating whether PFO closure reduces migraine risk, the primary endpoints were not met, but a signal of benefit on secondary endpoints and the association between PFO, migraine, and stroke are among the reasons that PFO closure should be reevaluated, according to Andrew Charles MD, Director of the Goldberg Migraine Program, University of California, Los Angeles.

UCLA

One Intervention, Two Potential Benefits

Fixing these defects is therefore at least theoretically attractive for preventing both migraine and stroke, but Dr. Charles said the opportunity for preventing both migraine and stroke is most attractive in migraine patients who have additional stroke risk factors.

Use of oral contraceptives, which produce a hypercoagulable state, is an example.

“Are these the people we should really be thinking about if they have PFO and migraine, particularly migraine with aura?” Dr. Charles asked.

The association between right-to-left shunts and migraine is strong. Although PFO is common, presenting in 20%-25% of the adult population, it has been found in up to 50% of individuals who have migraine with aura. In patients with migraine but no aura, the prevalence of PFO has been estimated to be approximately 35% or still somewhat elevated relative to the general population.
 

Primary Endpoint Missed in Clinical Trials

The question of whether risk of migraine can be reduced with repair of PFO or other right-to-left shunts remains unresolved. In two high-quality randomized trials undertaken in PFO repair, neither met its primary endpoint. In one of these, called PRIMA, which was terminated early for slow enrollment, the reduction in mean headache attacks was not significant relative to medical therapy.

In the second, called PREMIUM, device closure of PFO also failed to significantly reduce migraine attacks over sham procedure although it was associated with complete migraine remission (10% vs 1%).

A pooled analysis of these two studies that was conducted subsequently concluded that PFO closure reduces mean monthly migraine days (-3.1 vs. -1.9 days; P = -.02) and increases the likelihood of complete migraine cessation (9% vs. 0.7%; P < .001), but Dr. Charles pointed out the primary endpoint was migraine attacks not migraine days, so other analyses can only be considered hypothesis-generating.

There are several reasons to relook at the relationship between migraine and PFO but the potential to prevent both migraine and stroke with PFO closure could be one of the most important.

Several years ago, Dr. Charles and his coinvestigators from UCLA evaluated more than 700 ischemic strokes. Of these, 127 strokes were characterized as cryptogenic because of lack of another identifiable etiology. While 59% of these patients had PFO, which is several times higher than the general population, the prevalence of PFO in patients with a cryptogenic stroke and a history of migraine was 79% in this published study.

“So, in this group of patients who did not have any other clear cause for a stroke, a diagnosis of PFO was very much overrepresented,” Dr. Charles said.
 

Migraine Days Might Be a Better Endpoint

For patients with migraine who have risk factors for stroke, this makes PFO closure an attractive intervention, but a positive randomized trial is needed. Several are underway. Importantly, the trials now enrolling are using migraine days, which was significantly reduced in both PREMIUM and PRIMA, rather than migraine attacks as the primary endpoint.

“Migraine days is now accepted by the Food and Drug Administration as a criterion of benefit,” reported Jonathan Tobis, MD, Research Director, Interventional Cardiology, UCLA David Geffen School of Medicine, Los Angeles.

He explained that the FDA insisted on migraine attacks as the endpoint for the PREMIUM trial, but this was a far more challenging endpoint on which to show a statistical benefit. He emphasized that a new set of trials will now test efficacy on the basis of migraine days.

One of these trials, called RELIEF, which is randomizing patients to device closure of PFO or a sham procedure. Both groups are receiving clopidogrel or prasugrel based on a previous observation that patients who respond to these drugs are also more likely to respond to PFO closure.

Another trial, called COMPETE-2, is comparing PFO closure with a device to aspirin plus a sham closure. This trial is ongoing in China.

Stroke is not being evaluated as an endpoint in either trial, but Dr. Charles suggested that this does warrant attention.

“I would also just put it out there that, apart from simply migraine, this is a therapeutic approach that we might actually think about in terms of helping to prevent stroke in our migraine patients,” he said.

Senior author of a recent meta-analysis of trials evaluating PFO closure and control of migraine, Ling Liu, MD, Department of Neurology, University of Sichuan, Chengdu, China, agreed that PFO closure for the treatment of migraine deserves “a reevaluation.”

In his meta-analysis of three randomized trials, one pooled study, and eight retrospective case series with 1,165 patients, PFO closure was associated with a nearly 75% reduction (odds ratio [OR], 0.259; P = .0048) reduction in migraine days and 50% increase in resolution of migraine in patients with a history of migraine with aura (OR, 1.586; P = .227).

The incidence of stroke was not evaluated in this meta-analysis, but Dr. Liu believes that the evidence of reducing the burden of migraine with PFO closure is compelling. Given the evidence from this meta-analysis that PFO closure is safe, Dr. Liu maintained that a definitive trial is needed “especially for migraine with frequent aura.”

As an interventional cardiologist, Dr. Tobis said that when PFO closures is performed for prevention of stroke in patients with migraine, it often leads to reduced migraine activity and, in some cases, elimination of migraine. Like others, he believes new analyses should be conducted.

“Everyone involved in this field believes there is something there,” Dr. Tobis said. The missing link is a clinical trial to confirm it.

Dr. Charles and Dr. Liu report no potential conflicts of interest. Dr. Tobis reports a financial relationship with Holistick Medical.

Repairing patent foramen ovale (PFO) and other right-to-left shunt disorders for the prevention of migraine has generated mixed results, but the potential for these repairs also includes reducing the risk of stroke, according to a discussion at the 2023 Scottsdale Headache Symposium.

In two clinical trials evaluating whether PFO closure reduces migraine risk, the primary endpoints were not met, but a signal of benefit on secondary endpoints and the association between PFO, migraine, and stroke are among the reasons that PFO closure should be reevaluated, according to Andrew Charles MD, Director of the Goldberg Migraine Program, University of California, Los Angeles.

UCLA

One Intervention, Two Potential Benefits

Fixing these defects is therefore at least theoretically attractive for preventing both migraine and stroke, but Dr. Charles said the opportunity for preventing both migraine and stroke is most attractive in migraine patients who have additional stroke risk factors.

Use of oral contraceptives, which produce a hypercoagulable state, is an example.

“Are these the people we should really be thinking about if they have PFO and migraine, particularly migraine with aura?” Dr. Charles asked.

The association between right-to-left shunts and migraine is strong. Although PFO is common, presenting in 20%-25% of the adult population, it has been found in up to 50% of individuals who have migraine with aura. In patients with migraine but no aura, the prevalence of PFO has been estimated to be approximately 35% or still somewhat elevated relative to the general population.
 

Primary Endpoint Missed in Clinical Trials

The question of whether risk of migraine can be reduced with repair of PFO or other right-to-left shunts remains unresolved. In two high-quality randomized trials undertaken in PFO repair, neither met its primary endpoint. In one of these, called PRIMA, which was terminated early for slow enrollment, the reduction in mean headache attacks was not significant relative to medical therapy.

In the second, called PREMIUM, device closure of PFO also failed to significantly reduce migraine attacks over sham procedure although it was associated with complete migraine remission (10% vs 1%).

A pooled analysis of these two studies that was conducted subsequently concluded that PFO closure reduces mean monthly migraine days (-3.1 vs. -1.9 days; P = -.02) and increases the likelihood of complete migraine cessation (9% vs. 0.7%; P < .001), but Dr. Charles pointed out the primary endpoint was migraine attacks not migraine days, so other analyses can only be considered hypothesis-generating.

There are several reasons to relook at the relationship between migraine and PFO but the potential to prevent both migraine and stroke with PFO closure could be one of the most important.

Several years ago, Dr. Charles and his coinvestigators from UCLA evaluated more than 700 ischemic strokes. Of these, 127 strokes were characterized as cryptogenic because of lack of another identifiable etiology. While 59% of these patients had PFO, which is several times higher than the general population, the prevalence of PFO in patients with a cryptogenic stroke and a history of migraine was 79% in this published study.

“So, in this group of patients who did not have any other clear cause for a stroke, a diagnosis of PFO was very much overrepresented,” Dr. Charles said.
 

Migraine Days Might Be a Better Endpoint

For patients with migraine who have risk factors for stroke, this makes PFO closure an attractive intervention, but a positive randomized trial is needed. Several are underway. Importantly, the trials now enrolling are using migraine days, which was significantly reduced in both PREMIUM and PRIMA, rather than migraine attacks as the primary endpoint.

“Migraine days is now accepted by the Food and Drug Administration as a criterion of benefit,” reported Jonathan Tobis, MD, Research Director, Interventional Cardiology, UCLA David Geffen School of Medicine, Los Angeles.

He explained that the FDA insisted on migraine attacks as the endpoint for the PREMIUM trial, but this was a far more challenging endpoint on which to show a statistical benefit. He emphasized that a new set of trials will now test efficacy on the basis of migraine days.

One of these trials, called RELIEF, which is randomizing patients to device closure of PFO or a sham procedure. Both groups are receiving clopidogrel or prasugrel based on a previous observation that patients who respond to these drugs are also more likely to respond to PFO closure.

Another trial, called COMPETE-2, is comparing PFO closure with a device to aspirin plus a sham closure. This trial is ongoing in China.

Stroke is not being evaluated as an endpoint in either trial, but Dr. Charles suggested that this does warrant attention.

“I would also just put it out there that, apart from simply migraine, this is a therapeutic approach that we might actually think about in terms of helping to prevent stroke in our migraine patients,” he said.

Senior author of a recent meta-analysis of trials evaluating PFO closure and control of migraine, Ling Liu, MD, Department of Neurology, University of Sichuan, Chengdu, China, agreed that PFO closure for the treatment of migraine deserves “a reevaluation.”

In his meta-analysis of three randomized trials, one pooled study, and eight retrospective case series with 1,165 patients, PFO closure was associated with a nearly 75% reduction (odds ratio [OR], 0.259; P = .0048) reduction in migraine days and 50% increase in resolution of migraine in patients with a history of migraine with aura (OR, 1.586; P = .227).

The incidence of stroke was not evaluated in this meta-analysis, but Dr. Liu believes that the evidence of reducing the burden of migraine with PFO closure is compelling. Given the evidence from this meta-analysis that PFO closure is safe, Dr. Liu maintained that a definitive trial is needed “especially for migraine with frequent aura.”

As an interventional cardiologist, Dr. Tobis said that when PFO closures is performed for prevention of stroke in patients with migraine, it often leads to reduced migraine activity and, in some cases, elimination of migraine. Like others, he believes new analyses should be conducted.

“Everyone involved in this field believes there is something there,” Dr. Tobis said. The missing link is a clinical trial to confirm it.

Dr. Charles and Dr. Liu report no potential conflicts of interest. Dr. Tobis reports a financial relationship with Holistick Medical.

With the growing number of treatment options for psoriatic arthritis (PsA), therapeutic decision-making has shifted to an increasingly tailored and patient-centered approach. A number of factors contribute to the treatment decision-making process, including age, insurance restrictions, route of administration, side effect profile, comorbidities, and extra-articular manifestations of the disease. In this article, we discuss an extra-articular comorbidity, uveitis, which is frequently seen in patients with PsA. We discuss clinical characteristics of uveitis associated with PsA and describe how the presence of uveitis influences our treatment approach to PsA, based on existing data.

Uveitis refers broadly to inflammation of the uvea, the vascularized and pigmented layer of the eye composed of the iris, the ciliary body, and the choroid. While infection is a common cause of uveitis, many cases are noninfectious and are often associated with an underlying autoimmune or systemic inflammatory disorder. Uveitis is frequently reported in diseases in the spondyloarthritis (SpA) family, including axial spondyloarthritis (AxSpA) and reactive arthritis, as well as PsA. Exact estimates of the prevalence of uveitis in PsA vary widely from 7%-25%, depending on the particular cohort studied.^1,2 In all forms of SpA, the anterior chamber of the uvea is the most likely to be affected.³ However, compared to patients with AxSpA, patients with PsA appear to have a higher rate of posterior involvement. In addition, patients with PsA appear to have higher frequencies of insidious, bilateral uveitis, as compared to the acute, unilateral, anterior uveitis that is most characteristic of AxSpA.⁴ Women with PsA may be more likely than men to experience uveitis, although this has not been a consistent finding.⁵ 

Patients with PsA who are human leukocyte antigen B27 (HLA-B27) positive may be at risk for more severe and refractory anterior uveitis compared to those who do not express the allele.⁵ Those who are HLA-B27 positive are also known to have higher rates of axial involvement. It has therefore been postulated that 2 phenotypes of uveitis may exist in PsA: patients who are HLA-B27 positive who have axial disease and severe, unilateral anterior uveitis reminiscent of other forms of SpA, and patients who are HLA-B27 negative, often women, with peripheral-predominant arthritis who are prone to the classic anterior uveitis but may also develop atypical bilateral, insidious, and/or posterior involvement.⁴ Specific characteristics of PsA may also provide information about the risk for developing uveitis. For example, dactylitis has been linked to a higher risk of developing uveitis in some, but not all, cohorts of patients with PsA, and the risk of uveitis in PsA has been found in many studies to correlate with longer duration of disease.^6-8

The presence of uveitis signals a disruption in the blood-retina barrier and the subsequent entrance of inflammatory cells into the eye. An entire explanation of pathogenesis is beyond the scope of this article; however, it is worth noting that many of the inflammatory mediators of active uveitis mirror those of PsA. For instance, both the mesenchymal cells in enthesitis and the cells of the ciliary body express receptors for interleukin (IL)-23, suggesting a potential role of the signaling pathways involving this cytokine in both diseases.⁹ Another study found increased serum levels of IL-17, a known mediator of PsA disease, in patients with active uveitis.¹⁰ Despite these common pathogenesis links, there are limited data on the utility of certain existing PsA treatments on uveitis manifestations.

Our approach is always to manage uveitis associated with PsA in collaboration with a specialized and experienced ophthalmologist. Uncontrolled uveitis can be vision threatening and contribute to long-term morbidity associated with PsA, so timely recognition, evaluation, and appropriate treatment are important. Ocular glucocorticoid (GC) drops may be used as first-line therapy, particularly for anterior uveitis, to quickly quell inflammation. Escalation to systemic GCs for more severe or posteriorly localized disease may be considered carefully, given the known risk of worsening skin psoriasis (PsO) with GC withdrawal after a course of therapy. Use of GC-sparing therapy should be determined on a case-by-case basis. While generalized, noninfectious uveitis often resolves with GC treatment, the risk of uveitis recurrence in patients with PsA and the challenges of systemic GCs with PsO lead us to frequently consider GC-sparing therapy that addresses ocular, musculoskeletal, and cutaneous manifestations. Tumor necrosis factor inhibitors (TNF-I) are our typical first-line considerations for GC-sparing therapy in patients with PsA with inflammatory joint symptoms and uveitis, although nonbiologic therapy can be considered first-line therapy in select populations.

Data establishing the efficacy of TNF-I come largely from randomized controlled trials (RCTs) of adalimumab (ADA) compared to placebo in noninfectious uveitis.¹¹ While these trials focused on idiopathic posterior or pan-uveitis, these data have been extrapolated to SpA-associated anterior uveitis, and large registry analyses have supported use of TNF-I in this population.¹² When selecting a particular TNF-I in a patient with current or past uveitis, we frequently start with ADA, based on supportive, albeit uncontrolled, data suggesting a reduction in the risk of recurrence with this agent in patients with SpA and uveitis.¹² For patients who are unable to tolerate subcutaneous injections, who fail ADA, or who we suspect will require higher, titratable dosing, we favor infliximab infusions. Other data suggest that golimumab and certolizumab are also reasonable alternatives.^13,14 We do not generally use etanercept, as the limited data that are available suggest that it is less effective at reducing risk of uveitis recurrence.¹² Methotrexate or leflunomide may be an appropriate first line choice for patients with peripheral-predominant PsA and uveitis, but it is important to note that these agents are not effective for axial disease.

Despite the mechanistic data implicating the role of IL-17 in uveitis associated with PsA, the IL-17A inhibitor, secukinumab, failed to show a reduction in uveitis recurrence, compared to placebo, in pooled analysis of RCTs of noninfectious uveitis.¹⁵ However, a phase 2 trial of intravenous secukinumab in noninfectious uveitis showed promise, possibly because this dosing regimen can achieve higher effective concentrations.¹⁶ It is not our current practice to use secukinumab or ixekizumab as a first-line therapy in patients with PsA and concurrent uveitis, owing to a lack of data supporting efficacy. A novel IL-17A/F inhibitor, bimekizumab (BKZ), has recently been used in several successful phase 3 trials in patients with both TNF-naïve and TNF-nonresponder SpA, including AxSpA and PsA.¹⁷ Interestingly, data from the phase 2 and 3 trials of BKZ found low incidence rates of uveitis in patients with SpA treated with BKZ compared to placebo, suggesting that BKZ might be more effective in uveitis than other IL-17 inhibitors, but these data need to be confirmed.

Successful use of Janus kinase (JAK) inhibitors in noninfectious uveitis, including cases associated with inflammatory arthritis, has been described in case reports as well as in current phase 2 trials.¹⁸ The dual IL-12/IL-23 inhibitor, ustekinumab, also showed initial promise in a small, nonrandomized, uncontrolled phase 1/2 study of the treatment of posterior uveitis, as well as success in few case reports of PsA-associated uveitis.¹⁹ However, a post-hoc analysis of extra-intestinal manifestations, including uveitis and iritis, in patients with inflammatory bowel disease treated with ustekinumab found no benefit in preventing or treating ocular disease compared to placebo.²⁰ Given the paucity of available data, JAK inhibitors and the IL-12/IL-23 inhibitor, ustekinumab, are not part of our typical treatment algorithm for patients with PsA-associated uveitis.

In conclusion, uveitis is a frequent extra-articular comorbidity of PsA, and it may present differently than the typical acute onset, unilateral anterior uveitis seen in SpA. While uveitis may share many different immunologic threads with PsA, the most convincing data support the use of TNF-I as a GC-sparing agent in this setting, particularly ADA, infliximab, golimumab, or certolizumab. Our approach is generally to start with these agents or methotrexate when directed therapy is needed for uveitis in PsA. Further investigation into the use of the IL-17A/F inhibitor BKZ and JAK inhibitors, as well as tyrosine kinase 2 inhibitors, in PsA associated uveitis may yield additional options for our patients.²¹

With the growing number of treatment options for psoriatic arthritis (PsA), therapeutic decision-making has shifted to an increasingly tailored and patient-centered approach. A number of factors contribute to the treatment decision-making process, including age, insurance restrictions, route of administration, side effect profile, comorbidities, and extra-articular manifestations of the disease. In this article, we discuss an extra-articular comorbidity, uveitis, which is frequently seen in patients with PsA. We discuss clinical characteristics of uveitis associated with PsA and describe how the presence of uveitis influences our treatment approach to PsA, based on existing data.

Uveitis refers broadly to inflammation of the uvea, the vascularized and pigmented layer of the eye composed of the iris, the ciliary body, and the choroid. While infection is a common cause of uveitis, many cases are noninfectious and are often associated with an underlying autoimmune or systemic inflammatory disorder. Uveitis is frequently reported in diseases in the spondyloarthritis (SpA) family, including axial spondyloarthritis (AxSpA) and reactive arthritis, as well as PsA. Exact estimates of the prevalence of uveitis in PsA vary widely from 7%-25%, depending on the particular cohort studied.^1,2 In all forms of SpA, the anterior chamber of the uvea is the most likely to be affected.³ However, compared to patients with AxSpA, patients with PsA appear to have a higher rate of posterior involvement. In addition, patients with PsA appear to have higher frequencies of insidious, bilateral uveitis, as compared to the acute, unilateral, anterior uveitis that is most characteristic of AxSpA.⁴ Women with PsA may be more likely than men to experience uveitis, although this has not been a consistent finding.⁵ 

Patients with PsA who are human leukocyte antigen B27 (HLA-B27) positive may be at risk for more severe and refractory anterior uveitis compared to those who do not express the allele.⁵ Those who are HLA-B27 positive are also known to have higher rates of axial involvement. It has therefore been postulated that 2 phenotypes of uveitis may exist in PsA: patients who are HLA-B27 positive who have axial disease and severe, unilateral anterior uveitis reminiscent of other forms of SpA, and patients who are HLA-B27 negative, often women, with peripheral-predominant arthritis who are prone to the classic anterior uveitis but may also develop atypical bilateral, insidious, and/or posterior involvement.⁴ Specific characteristics of PsA may also provide information about the risk for developing uveitis. For example, dactylitis has been linked to a higher risk of developing uveitis in some, but not all, cohorts of patients with PsA, and the risk of uveitis in PsA has been found in many studies to correlate with longer duration of disease.^6-8

The presence of uveitis signals a disruption in the blood-retina barrier and the subsequent entrance of inflammatory cells into the eye. An entire explanation of pathogenesis is beyond the scope of this article; however, it is worth noting that many of the inflammatory mediators of active uveitis mirror those of PsA. For instance, both the mesenchymal cells in enthesitis and the cells of the ciliary body express receptors for interleukin (IL)-23, suggesting a potential role of the signaling pathways involving this cytokine in both diseases.⁹ Another study found increased serum levels of IL-17, a known mediator of PsA disease, in patients with active uveitis.¹⁰ Despite these common pathogenesis links, there are limited data on the utility of certain existing PsA treatments on uveitis manifestations.

Our approach is always to manage uveitis associated with PsA in collaboration with a specialized and experienced ophthalmologist. Uncontrolled uveitis can be vision threatening and contribute to long-term morbidity associated with PsA, so timely recognition, evaluation, and appropriate treatment are important. Ocular glucocorticoid (GC) drops may be used as first-line therapy, particularly for anterior uveitis, to quickly quell inflammation. Escalation to systemic GCs for more severe or posteriorly localized disease may be considered carefully, given the known risk of worsening skin psoriasis (PsO) with GC withdrawal after a course of therapy. Use of GC-sparing therapy should be determined on a case-by-case basis. While generalized, noninfectious uveitis often resolves with GC treatment, the risk of uveitis recurrence in patients with PsA and the challenges of systemic GCs with PsO lead us to frequently consider GC-sparing therapy that addresses ocular, musculoskeletal, and cutaneous manifestations. Tumor necrosis factor inhibitors (TNF-I) are our typical first-line considerations for GC-sparing therapy in patients with PsA with inflammatory joint symptoms and uveitis, although nonbiologic therapy can be considered first-line therapy in select populations.

Data establishing the efficacy of TNF-I come largely from randomized controlled trials (RCTs) of adalimumab (ADA) compared to placebo in noninfectious uveitis.¹¹ While these trials focused on idiopathic posterior or pan-uveitis, these data have been extrapolated to SpA-associated anterior uveitis, and large registry analyses have supported use of TNF-I in this population.¹² When selecting a particular TNF-I in a patient with current or past uveitis, we frequently start with ADA, based on supportive, albeit uncontrolled, data suggesting a reduction in the risk of recurrence with this agent in patients with SpA and uveitis.¹² For patients who are unable to tolerate subcutaneous injections, who fail ADA, or who we suspect will require higher, titratable dosing, we favor infliximab infusions. Other data suggest that golimumab and certolizumab are also reasonable alternatives.^13,14 We do not generally use etanercept, as the limited data that are available suggest that it is less effective at reducing risk of uveitis recurrence.¹² Methotrexate or leflunomide may be an appropriate first line choice for patients with peripheral-predominant PsA and uveitis, but it is important to note that these agents are not effective for axial disease.

Despite the mechanistic data implicating the role of IL-17 in uveitis associated with PsA, the IL-17A inhibitor, secukinumab, failed to show a reduction in uveitis recurrence, compared to placebo, in pooled analysis of RCTs of noninfectious uveitis.¹⁵ However, a phase 2 trial of intravenous secukinumab in noninfectious uveitis showed promise, possibly because this dosing regimen can achieve higher effective concentrations.¹⁶ It is not our current practice to use secukinumab or ixekizumab as a first-line therapy in patients with PsA and concurrent uveitis, owing to a lack of data supporting efficacy. A novel IL-17A/F inhibitor, bimekizumab (BKZ), has recently been used in several successful phase 3 trials in patients with both TNF-naïve and TNF-nonresponder SpA, including AxSpA and PsA.¹⁷ Interestingly, data from the phase 2 and 3 trials of BKZ found low incidence rates of uveitis in patients with SpA treated with BKZ compared to placebo, suggesting that BKZ might be more effective in uveitis than other IL-17 inhibitors, but these data need to be confirmed.

Successful use of Janus kinase (JAK) inhibitors in noninfectious uveitis, including cases associated with inflammatory arthritis, has been described in case reports as well as in current phase 2 trials.¹⁸ The dual IL-12/IL-23 inhibitor, ustekinumab, also showed initial promise in a small, nonrandomized, uncontrolled phase 1/2 study of the treatment of posterior uveitis, as well as success in few case reports of PsA-associated uveitis.¹⁹ However, a post-hoc analysis of extra-intestinal manifestations, including uveitis and iritis, in patients with inflammatory bowel disease treated with ustekinumab found no benefit in preventing or treating ocular disease compared to placebo.²⁰ Given the paucity of available data, JAK inhibitors and the IL-12/IL-23 inhibitor, ustekinumab, are not part of our typical treatment algorithm for patients with PsA-associated uveitis.

In conclusion, uveitis is a frequent extra-articular comorbidity of PsA, and it may present differently than the typical acute onset, unilateral anterior uveitis seen in SpA. While uveitis may share many different immunologic threads with PsA, the most convincing data support the use of TNF-I as a GC-sparing agent in this setting, particularly ADA, infliximab, golimumab, or certolizumab. Our approach is generally to start with these agents or methotrexate when directed therapy is needed for uveitis in PsA. Further investigation into the use of the IL-17A/F inhibitor BKZ and JAK inhibitors, as well as tyrosine kinase 2 inhibitors, in PsA associated uveitis may yield additional options for our patients.²¹

With the growing number of treatment options for psoriatic arthritis (PsA), therapeutic decision-making has shifted to an increasingly tailored and patient-centered approach. A number of factors contribute to the treatment decision-making process, including age, insurance restrictions, route of administration, side effect profile, comorbidities, and extra-articular manifestations of the disease. In this article, we discuss an extra-articular comorbidity, uveitis, which is frequently seen in patients with PsA. We discuss clinical characteristics of uveitis associated with PsA and describe how the presence of uveitis influences our treatment approach to PsA, based on existing data.

Uveitis refers broadly to inflammation of the uvea, the vascularized and pigmented layer of the eye composed of the iris, the ciliary body, and the choroid. While infection is a common cause of uveitis, many cases are noninfectious and are often associated with an underlying autoimmune or systemic inflammatory disorder. Uveitis is frequently reported in diseases in the spondyloarthritis (SpA) family, including axial spondyloarthritis (AxSpA) and reactive arthritis, as well as PsA. Exact estimates of the prevalence of uveitis in PsA vary widely from 7%-25%, depending on the particular cohort studied.^1,2 In all forms of SpA, the anterior chamber of the uvea is the most likely to be affected.³ However, compared to patients with AxSpA, patients with PsA appear to have a higher rate of posterior involvement. In addition, patients with PsA appear to have higher frequencies of insidious, bilateral uveitis, as compared to the acute, unilateral, anterior uveitis that is most characteristic of AxSpA.⁴ Women with PsA may be more likely than men to experience uveitis, although this has not been a consistent finding.⁵ 

Patients with PsA who are human leukocyte antigen B27 (HLA-B27) positive may be at risk for more severe and refractory anterior uveitis compared to those who do not express the allele.⁵ Those who are HLA-B27 positive are also known to have higher rates of axial involvement. It has therefore been postulated that 2 phenotypes of uveitis may exist in PsA: patients who are HLA-B27 positive who have axial disease and severe, unilateral anterior uveitis reminiscent of other forms of SpA, and patients who are HLA-B27 negative, often women, with peripheral-predominant arthritis who are prone to the classic anterior uveitis but may also develop atypical bilateral, insidious, and/or posterior involvement.⁴ Specific characteristics of PsA may also provide information about the risk for developing uveitis. For example, dactylitis has been linked to a higher risk of developing uveitis in some, but not all, cohorts of patients with PsA, and the risk of uveitis in PsA has been found in many studies to correlate with longer duration of disease.^6-8

The presence of uveitis signals a disruption in the blood-retina barrier and the subsequent entrance of inflammatory cells into the eye. An entire explanation of pathogenesis is beyond the scope of this article; however, it is worth noting that many of the inflammatory mediators of active uveitis mirror those of PsA. For instance, both the mesenchymal cells in enthesitis and the cells of the ciliary body express receptors for interleukin (IL)-23, suggesting a potential role of the signaling pathways involving this cytokine in both diseases.⁹ Another study found increased serum levels of IL-17, a known mediator of PsA disease, in patients with active uveitis.¹⁰ Despite these common pathogenesis links, there are limited data on the utility of certain existing PsA treatments on uveitis manifestations.

Our approach is always to manage uveitis associated with PsA in collaboration with a specialized and experienced ophthalmologist. Uncontrolled uveitis can be vision threatening and contribute to long-term morbidity associated with PsA, so timely recognition, evaluation, and appropriate treatment are important. Ocular glucocorticoid (GC) drops may be used as first-line therapy, particularly for anterior uveitis, to quickly quell inflammation. Escalation to systemic GCs for more severe or posteriorly localized disease may be considered carefully, given the known risk of worsening skin psoriasis (PsO) with GC withdrawal after a course of therapy. Use of GC-sparing therapy should be determined on a case-by-case basis. While generalized, noninfectious uveitis often resolves with GC treatment, the risk of uveitis recurrence in patients with PsA and the challenges of systemic GCs with PsO lead us to frequently consider GC-sparing therapy that addresses ocular, musculoskeletal, and cutaneous manifestations. Tumor necrosis factor inhibitors (TNF-I) are our typical first-line considerations for GC-sparing therapy in patients with PsA with inflammatory joint symptoms and uveitis, although nonbiologic therapy can be considered first-line therapy in select populations.

Data establishing the efficacy of TNF-I come largely from randomized controlled trials (RCTs) of adalimumab (ADA) compared to placebo in noninfectious uveitis.¹¹ While these trials focused on idiopathic posterior or pan-uveitis, these data have been extrapolated to SpA-associated anterior uveitis, and large registry analyses have supported use of TNF-I in this population.¹² When selecting a particular TNF-I in a patient with current or past uveitis, we frequently start with ADA, based on supportive, albeit uncontrolled, data suggesting a reduction in the risk of recurrence with this agent in patients with SpA and uveitis.¹² For patients who are unable to tolerate subcutaneous injections, who fail ADA, or who we suspect will require higher, titratable dosing, we favor infliximab infusions. Other data suggest that golimumab and certolizumab are also reasonable alternatives.^13,14 We do not generally use etanercept, as the limited data that are available suggest that it is less effective at reducing risk of uveitis recurrence.¹² Methotrexate or leflunomide may be an appropriate first line choice for patients with peripheral-predominant PsA and uveitis, but it is important to note that these agents are not effective for axial disease.

Despite the mechanistic data implicating the role of IL-17 in uveitis associated with PsA, the IL-17A inhibitor, secukinumab, failed to show a reduction in uveitis recurrence, compared to placebo, in pooled analysis of RCTs of noninfectious uveitis.¹⁵ However, a phase 2 trial of intravenous secukinumab in noninfectious uveitis showed promise, possibly because this dosing regimen can achieve higher effective concentrations.¹⁶ It is not our current practice to use secukinumab or ixekizumab as a first-line therapy in patients with PsA and concurrent uveitis, owing to a lack of data supporting efficacy. A novel IL-17A/F inhibitor, bimekizumab (BKZ), has recently been used in several successful phase 3 trials in patients with both TNF-naïve and TNF-nonresponder SpA, including AxSpA and PsA.¹⁷ Interestingly, data from the phase 2 and 3 trials of BKZ found low incidence rates of uveitis in patients with SpA treated with BKZ compared to placebo, suggesting that BKZ might be more effective in uveitis than other IL-17 inhibitors, but these data need to be confirmed.

Successful use of Janus kinase (JAK) inhibitors in noninfectious uveitis, including cases associated with inflammatory arthritis, has been described in case reports as well as in current phase 2 trials.¹⁸ The dual IL-12/IL-23 inhibitor, ustekinumab, also showed initial promise in a small, nonrandomized, uncontrolled phase 1/2 study of the treatment of posterior uveitis, as well as success in few case reports of PsA-associated uveitis.¹⁹ However, a post-hoc analysis of extra-intestinal manifestations, including uveitis and iritis, in patients with inflammatory bowel disease treated with ustekinumab found no benefit in preventing or treating ocular disease compared to placebo.²⁰ Given the paucity of available data, JAK inhibitors and the IL-12/IL-23 inhibitor, ustekinumab, are not part of our typical treatment algorithm for patients with PsA-associated uveitis.

In conclusion, uveitis is a frequent extra-articular comorbidity of PsA, and it may present differently than the typical acute onset, unilateral anterior uveitis seen in SpA. While uveitis may share many different immunologic threads with PsA, the most convincing data support the use of TNF-I as a GC-sparing agent in this setting, particularly ADA, infliximab, golimumab, or certolizumab. Our approach is generally to start with these agents or methotrexate when directed therapy is needed for uveitis in PsA. Further investigation into the use of the IL-17A/F inhibitor BKZ and JAK inhibitors, as well as tyrosine kinase 2 inhibitors, in PsA associated uveitis may yield additional options for our patients.²¹

TOPLINE:

Two doses of an mRNA COVID-19 vaccine slashes COVID-19-related hospitalizations and emergency department (ED) visits in children aged 6 months to 4 years by 40%, according to a new study by the Centers for Disease Control and Prevention (CDC).

METHODOLOGY:

• SARS-CoV-2 infection can severely affect children who have certain chronic conditions.
• Researchers assessed the effectiveness of COVID-19 vaccines in preventing emergency ED visits and hospitalizations associated with the illness from July 2022 to September 2023.
• They drew data from the New Vaccine Surveillance Network, which conducts population-based, prospective surveillance for acute respiratory illness in children at seven pediatric medical centers.
• The period assessed was the first year vaccines were authorized for children aged 6 months to 4 years; during that period, several Omicron subvariants arose.
• Researchers used data from 7,434 infants and children; data included patients’ vaccine status and their test results for SARS-CoV-2.

TAKEAWAY:

• Of the 7,434 infants and children who had an acute respiratory illness and were hospitalized or visited the ED, 387 had COVID-19.
• Children who received two doses of a COVID-19 vaccine were 40% less likely to have a COVID-19-associated hospitalization or ED visit compared with unvaccinated youth.
• One dose of a COVID-19 vaccine reduced ED visits and hospitalizations by 31%.

IN PRACTICE:

“The findings in this report support the recommendation for COVID-19 vaccination for all children aged ≥6 months and highlight the importance of completion of a primary series for young children,” the researchers reported.

SOURCE:

The study was led by Heidi L. Moline, MD, of the CDC.

LIMITATIONS:

Because the number of children with antibodies and immunity against SARS-CoV-2 has grown, vaccine effectiveness rates in the study may no longer be as relevant. Children with preexisting chronic conditions may be more likely to be vaccinated and receive medical attention. The low rates of vaccination may have prevented researchers from conducting a more detailed analysis. The Pfizer-BioNTech vaccine requires three doses, whereas Moderna’s requires two doses; this may have skewed the estimated efficacy of the Pfizer-BioNTech vaccine.

DISCLOSURES:

The authors report a variety of potential conflicts of interest, which are detailed in the article.

A version of this article appeared on Medscape.com.

TOPLINE:

Two doses of an mRNA COVID-19 vaccine slashes COVID-19-related hospitalizations and emergency department (ED) visits in children aged 6 months to 4 years by 40%, according to a new study by the Centers for Disease Control and Prevention (CDC).

METHODOLOGY:

• SARS-CoV-2 infection can severely affect children who have certain chronic conditions.
• Researchers assessed the effectiveness of COVID-19 vaccines in preventing emergency ED visits and hospitalizations associated with the illness from July 2022 to September 2023.
• They drew data from the New Vaccine Surveillance Network, which conducts population-based, prospective surveillance for acute respiratory illness in children at seven pediatric medical centers.
• The period assessed was the first year vaccines were authorized for children aged 6 months to 4 years; during that period, several Omicron subvariants arose.
• Researchers used data from 7,434 infants and children; data included patients’ vaccine status and their test results for SARS-CoV-2.

TAKEAWAY:

• Of the 7,434 infants and children who had an acute respiratory illness and were hospitalized or visited the ED, 387 had COVID-19.
• Children who received two doses of a COVID-19 vaccine were 40% less likely to have a COVID-19-associated hospitalization or ED visit compared with unvaccinated youth.
• One dose of a COVID-19 vaccine reduced ED visits and hospitalizations by 31%.

IN PRACTICE:

“The findings in this report support the recommendation for COVID-19 vaccination for all children aged ≥6 months and highlight the importance of completion of a primary series for young children,” the researchers reported.

SOURCE:

The study was led by Heidi L. Moline, MD, of the CDC.

LIMITATIONS:

Because the number of children with antibodies and immunity against SARS-CoV-2 has grown, vaccine effectiveness rates in the study may no longer be as relevant. Children with preexisting chronic conditions may be more likely to be vaccinated and receive medical attention. The low rates of vaccination may have prevented researchers from conducting a more detailed analysis. The Pfizer-BioNTech vaccine requires three doses, whereas Moderna’s requires two doses; this may have skewed the estimated efficacy of the Pfizer-BioNTech vaccine.

DISCLOSURES:

The authors report a variety of potential conflicts of interest, which are detailed in the article.

A version of this article appeared on Medscape.com.

TOPLINE:

Two doses of an mRNA COVID-19 vaccine slashes COVID-19-related hospitalizations and emergency department (ED) visits in children aged 6 months to 4 years by 40%, according to a new study by the Centers for Disease Control and Prevention (CDC).

METHODOLOGY:

• SARS-CoV-2 infection can severely affect children who have certain chronic conditions.
• Researchers assessed the effectiveness of COVID-19 vaccines in preventing emergency ED visits and hospitalizations associated with the illness from July 2022 to September 2023.
• They drew data from the New Vaccine Surveillance Network, which conducts population-based, prospective surveillance for acute respiratory illness in children at seven pediatric medical centers.
• The period assessed was the first year vaccines were authorized for children aged 6 months to 4 years; during that period, several Omicron subvariants arose.
• Researchers used data from 7,434 infants and children; data included patients’ vaccine status and their test results for SARS-CoV-2.

TAKEAWAY:

• Of the 7,434 infants and children who had an acute respiratory illness and were hospitalized or visited the ED, 387 had COVID-19.
• Children who received two doses of a COVID-19 vaccine were 40% less likely to have a COVID-19-associated hospitalization or ED visit compared with unvaccinated youth.
• One dose of a COVID-19 vaccine reduced ED visits and hospitalizations by 31%.

IN PRACTICE:

“The findings in this report support the recommendation for COVID-19 vaccination for all children aged ≥6 months and highlight the importance of completion of a primary series for young children,” the researchers reported.

SOURCE:

The study was led by Heidi L. Moline, MD, of the CDC.

LIMITATIONS:

Because the number of children with antibodies and immunity against SARS-CoV-2 has grown, vaccine effectiveness rates in the study may no longer be as relevant. Children with preexisting chronic conditions may be more likely to be vaccinated and receive medical attention. The low rates of vaccination may have prevented researchers from conducting a more detailed analysis. The Pfizer-BioNTech vaccine requires three doses, whereas Moderna’s requires two doses; this may have skewed the estimated efficacy of the Pfizer-BioNTech vaccine.

DISCLOSURES:

The authors report a variety of potential conflicts of interest, which are detailed in the article.

A version of this article appeared on Medscape.com.

TOPLINE:

Heavy secondhand smoke (SHS) exposure is associated with severe headache or migraine in adults who have never smoked, with effects of exposure varying depending on body mass index (BMI) and level of physical activity, new research shows.

METHODOLOGY:

Investigators analyzed data on 4,560 participants (median age, 43 years; 60% female; 71.5% White) from the 1999-2004 National Health and Nutrition Examination Survey.

Participants were aged 20 years or older and had never smoked.

Migraine headache status was determined by asking whether participants experienced severe headaches or migraines during the previous 3 months.

SHS exposure was categorized as unexposed (serum cotinine levels <0.05 ng/mL and no smoker in the home), low (0.05 ng/mL ≤ serum cotinine level <1 ng/mL), or heavy (1 ng/mL ≤ serum cotinine level ≤ 10 ng/mL).

TAKEAWAY:

In all, 919 (20%) participants had severe headaches or migraines.

After adjustment for demographic and lifestyle factors (including medication use), heavy SHS exposure was positively associated with severe headache or migraine (adjusted odds ratio [aOR], 2.02; 95% CI, 1.19-3.43).

No significant association was found between low SHS exposure and severe headaches or migraine (aOR, 1.15; 95% CI, 0.91-1.47).

In participants who were sedentary (P=.016) and those with a BMI <25 (P=.001), significant associations between SHS and severe headache or migraine were observed.

IN PRACTICE:

Noting a linear dose-response relationship between cotinine and severe headaches or migraine, the investigators write, “These findings underscore the need for stronger regulation of tobacco exposure, particularly in homes and public places.”

SOURCE:

Junpeng Wu, MMc, and Haitang Wang, MD, of Southern Medical University in Guangzhou, China, and their colleagues conducted the study. It was published online in Headache.

LIMITATIONS:

The study could not establish causal relationships between SHS and migraine or severe headache. In addition, the half-life of serum cotinine is 15-40 hours and thus this measure can reflect only recent SHS exposure.

DISCLOSURES:

The study was not funded. The investigators reported no disclosures.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Heavy secondhand smoke (SHS) exposure is associated with severe headache or migraine in adults who have never smoked, with effects of exposure varying depending on body mass index (BMI) and level of physical activity, new research shows.

METHODOLOGY:

Investigators analyzed data on 4,560 participants (median age, 43 years; 60% female; 71.5% White) from the 1999-2004 National Health and Nutrition Examination Survey.

Participants were aged 20 years or older and had never smoked.

Migraine headache status was determined by asking whether participants experienced severe headaches or migraines during the previous 3 months.

SHS exposure was categorized as unexposed (serum cotinine levels <0.05 ng/mL and no smoker in the home), low (0.05 ng/mL ≤ serum cotinine level <1 ng/mL), or heavy (1 ng/mL ≤ serum cotinine level ≤ 10 ng/mL).

TAKEAWAY:

In all, 919 (20%) participants had severe headaches or migraines.

After adjustment for demographic and lifestyle factors (including medication use), heavy SHS exposure was positively associated with severe headache or migraine (adjusted odds ratio [aOR], 2.02; 95% CI, 1.19-3.43).

No significant association was found between low SHS exposure and severe headaches or migraine (aOR, 1.15; 95% CI, 0.91-1.47).

In participants who were sedentary (P=.016) and those with a BMI <25 (P=.001), significant associations between SHS and severe headache or migraine were observed.

IN PRACTICE:

Noting a linear dose-response relationship between cotinine and severe headaches or migraine, the investigators write, “These findings underscore the need for stronger regulation of tobacco exposure, particularly in homes and public places.”

SOURCE:

Junpeng Wu, MMc, and Haitang Wang, MD, of Southern Medical University in Guangzhou, China, and their colleagues conducted the study. It was published online in Headache.

LIMITATIONS:

The study could not establish causal relationships between SHS and migraine or severe headache. In addition, the half-life of serum cotinine is 15-40 hours and thus this measure can reflect only recent SHS exposure.

DISCLOSURES:

The study was not funded. The investigators reported no disclosures.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Heavy secondhand smoke (SHS) exposure is associated with severe headache or migraine in adults who have never smoked, with effects of exposure varying depending on body mass index (BMI) and level of physical activity, new research shows.

METHODOLOGY:

Investigators analyzed data on 4,560 participants (median age, 43 years; 60% female; 71.5% White) from the 1999-2004 National Health and Nutrition Examination Survey.

Participants were aged 20 years or older and had never smoked.

Migraine headache status was determined by asking whether participants experienced severe headaches or migraines during the previous 3 months.

SHS exposure was categorized as unexposed (serum cotinine levels <0.05 ng/mL and no smoker in the home), low (0.05 ng/mL ≤ serum cotinine level <1 ng/mL), or heavy (1 ng/mL ≤ serum cotinine level ≤ 10 ng/mL).

TAKEAWAY:

In all, 919 (20%) participants had severe headaches or migraines.

After adjustment for demographic and lifestyle factors (including medication use), heavy SHS exposure was positively associated with severe headache or migraine (adjusted odds ratio [aOR], 2.02; 95% CI, 1.19-3.43).

No significant association was found between low SHS exposure and severe headaches or migraine (aOR, 1.15; 95% CI, 0.91-1.47).

In participants who were sedentary (P=.016) and those with a BMI <25 (P=.001), significant associations between SHS and severe headache or migraine were observed.

IN PRACTICE:

Noting a linear dose-response relationship between cotinine and severe headaches or migraine, the investigators write, “These findings underscore the need for stronger regulation of tobacco exposure, particularly in homes and public places.”

SOURCE:

Junpeng Wu, MMc, and Haitang Wang, MD, of Southern Medical University in Guangzhou, China, and their colleagues conducted the study. It was published online in Headache.

LIMITATIONS:

The study could not establish causal relationships between SHS and migraine or severe headache. In addition, the half-life of serum cotinine is 15-40 hours and thus this measure can reflect only recent SHS exposure.

DISCLOSURES:

The study was not funded. The investigators reported no disclosures.
 

A version of this article appeared on Medscape.com.