Rheumatology News

Men prescribed drugs to treat newly diagnosed erectile dysfunction (ED) are 18% less likely to develop Alzheimer’s disease (AD) during a 5-year follow-up period, new research shows. 

The study is the second in recent years to suggest an association between the use of phosphodiesterase type 5 inhibitors (PDE5Is) such as sildenafil (Viagra) or tadalafil (Cialis) and AD risk. The findings contradict those in a third study, reported by this news organization, that showed no link between the two. 

Although the research is interesting, outside experts noted that there is no evidence that the drugs can treat AD and urge caution when interpreting the findings. 

Investigators agree but believe that the results offer a direction for future studies and underscore the importance of investigating whether existing approved therapies can be repurposed to treat AD. 

“The positive findings from our large study in over 250,000 men is promising and can be used to enhance research capacity and knowledge, with a potential future impact on clinical use and public health policy,” senior author Ruth Brauer, PhD, of the University College London, told this news organization.

“However, before recommending PDE5I are used to reduce the risk of AD, more work is required to validate the findings of our work, particularly in a more generalizable population that includes women and men without erectile dysfunction,” she continued.

The findings were published online February 7 in Neurology.

Strong Association

The study drew on primary healthcare data from the United Kingdom and included 269,725 men (average age, 59 years) with newly diagnosed ED, 55% of whom had received prescriptions for PDE5Is. 

Participants were free from memory or cognitive issues when the study began and were followed for a median of 5.1 years. Investigators accounted for a range of potential AD risk factors, including smoking status, alcohol use, body mass index, hypertension, diabetes, depression, anxiety, and concomitant medication use.

During the study period, 749 in the PDE5I group were diagnosed with AD, corresponding to a rate of 8.1 cases per 10,000 person-years. Among those who did not take the drugs, 370 developed AD, corresponding to a rate of 9.7 cases per 10,000 person-years.

Overall, initiation of a PDE5I was associated with an 18% lower risk for AD (adjusted hazard ration [aHR], 0.82; 95% CI, 0.72-0.93) compared with those with no prescriptions. 

The association was stronger in people aged 70 years or older and those with a history of hypertension or diabetes. The greatest risk reduction was found in people with the most prescriptions during the study period. Those with 21-50 prescriptions had a 44% lower risk for AD (aHR, 0.56; 95% CI, 0.43-0.73) and those with more than 50 were 35% less likely to be diagnosed with AD (aHR, 0.65; 95% CI, 0.49-0.87).

There was no association with AD risk in individuals who received fewer than 20 prescriptions. 

Investigators also analyzed associations after introducing a 1- and 3-year lag period after cohort entry to address the latent period between AD onset and diagnosis. The primary findings held with a 1-year lag period but lost significance with the inclusion of a 3-year lag period.

In subgroup analyses, investigators found evidence of reduced AD risk in those who received prescriptions for sildenafil (aHR, 0.81; 95% CI, 0.71-0.93), but there was no evidence for reduced risk compared with nonusers in those who received tadalafil and vardenafil.

Lower AD risk was found in patients with hypertension, diabetes, and in men aged 70 years or older, but there was no association in younger men or those with no history of hypertension or diabetes. 

Although investigators controlled for a wide range of potential risk factors, Dr. Brauer noted that unmeasured confounders such as physical and sexual activity, which were not tracked and may predict PDE5I exposure, may have affected the results. 

Interpret With Caution

Commenting on the findings, Ozama Ismail, PhD, Alzheimer’s Association director of scientific programs, noted that in addition to the limitations cited by the study authors, AD diagnoses were not made with the “gold standard” testing that typically includes imaging biomarkers and postmortem assessments. 

“While this study is interesting and adds to a potential association, there is no evidence that these drugs are able to treat Alzheimer’s disease,” said Dr. Brauer, who was not part of the current study. 

“People should not use over-the-counter phosphodiesterase type 5 inhibitors for prevention of Alzheimer’s or other dementias based on this very preliminary finding. Always consult with your physician before starting or changing your medications,” he cautioned.

However, Dr. Ismael added that the study does highlight a potential new avenue for drug repurposing. 

“Repurposing of existing, already-approved treatments can be a valuable part of drug development because, through already-completed testing, we know much about their safety and side effects,” which can decrease cost and time needed for studies, he said. 

“When considering repurposing an existing drug to an Alzheimer’s treatment, however, it is often important to conduct new studies over longer periods of time and in older people that reflect the diversity of individuals living with Alzheimer’s disease,” Dr. Ismael said.

Randomized Trials Needed

Dr. Brauer agreed, offering that such a trial should also include people with mild cognitive impairment and measure the effects of PDE5Is given in predefined doses plus an acetylcholinesterase inhibitor or placebo plus an acetylcholinesterase inhibitor. 

“The primary outcome would be the change in baseline cognitive function,” she said. “This approach would provide a comprehensive understanding of the potential therapeutic benefits of PDE5I and AD.”

Studies are also needed to better understand the mechanisms by which these drugs might influence AD risk, Sevil Yasar, MD, PhD, and Lolita Nidadavolu, MD, PhD, from the Division of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, noted in an accompanying editorial.

The strong association between PDE5I use and AD risk in people with a history of hypertension or diabetes suggests “a potential neuroprotective effect through a vascular pathway,” they wrote.

In vitro studies on the role of inflammation and clearance of beta-amyloid could strengthen findings from studies like this one, and in vivo studies could help explain the mechanisms behind PDE5I use and lower AD risk, Dr. Yasar and Dr. Nidadavolu noted. 

“In the end, however, further observational studies exploring mechanisms will not prove a causal association,” they wrote. “A well-designed randomized controlled trial is needed before PDE5I drugs can be prescribed for AD prevention.”

The study was unfunded. The study and editorial authors and Dr. Ismail report no relevant financial conflicts. 
 

A version of this article appeared on Medscape.com.

Men prescribed drugs to treat newly diagnosed erectile dysfunction (ED) are 18% less likely to develop Alzheimer’s disease (AD) during a 5-year follow-up period, new research shows. 

The study is the second in recent years to suggest an association between the use of phosphodiesterase type 5 inhibitors (PDE5Is) such as sildenafil (Viagra) or tadalafil (Cialis) and AD risk. The findings contradict those in a third study, reported by this news organization, that showed no link between the two. 

Although the research is interesting, outside experts noted that there is no evidence that the drugs can treat AD and urge caution when interpreting the findings. 

Investigators agree but believe that the results offer a direction for future studies and underscore the importance of investigating whether existing approved therapies can be repurposed to treat AD. 

“The positive findings from our large study in over 250,000 men is promising and can be used to enhance research capacity and knowledge, with a potential future impact on clinical use and public health policy,” senior author Ruth Brauer, PhD, of the University College London, told this news organization.

“However, before recommending PDE5I are used to reduce the risk of AD, more work is required to validate the findings of our work, particularly in a more generalizable population that includes women and men without erectile dysfunction,” she continued.

The findings were published online February 7 in Neurology.

Strong Association

The study drew on primary healthcare data from the United Kingdom and included 269,725 men (average age, 59 years) with newly diagnosed ED, 55% of whom had received prescriptions for PDE5Is. 

Participants were free from memory or cognitive issues when the study began and were followed for a median of 5.1 years. Investigators accounted for a range of potential AD risk factors, including smoking status, alcohol use, body mass index, hypertension, diabetes, depression, anxiety, and concomitant medication use.

During the study period, 749 in the PDE5I group were diagnosed with AD, corresponding to a rate of 8.1 cases per 10,000 person-years. Among those who did not take the drugs, 370 developed AD, corresponding to a rate of 9.7 cases per 10,000 person-years.

Overall, initiation of a PDE5I was associated with an 18% lower risk for AD (adjusted hazard ration [aHR], 0.82; 95% CI, 0.72-0.93) compared with those with no prescriptions. 

The association was stronger in people aged 70 years or older and those with a history of hypertension or diabetes. The greatest risk reduction was found in people with the most prescriptions during the study period. Those with 21-50 prescriptions had a 44% lower risk for AD (aHR, 0.56; 95% CI, 0.43-0.73) and those with more than 50 were 35% less likely to be diagnosed with AD (aHR, 0.65; 95% CI, 0.49-0.87).

There was no association with AD risk in individuals who received fewer than 20 prescriptions. 

Investigators also analyzed associations after introducing a 1- and 3-year lag period after cohort entry to address the latent period between AD onset and diagnosis. The primary findings held with a 1-year lag period but lost significance with the inclusion of a 3-year lag period.

In subgroup analyses, investigators found evidence of reduced AD risk in those who received prescriptions for sildenafil (aHR, 0.81; 95% CI, 0.71-0.93), but there was no evidence for reduced risk compared with nonusers in those who received tadalafil and vardenafil.

Lower AD risk was found in patients with hypertension, diabetes, and in men aged 70 years or older, but there was no association in younger men or those with no history of hypertension or diabetes. 

Although investigators controlled for a wide range of potential risk factors, Dr. Brauer noted that unmeasured confounders such as physical and sexual activity, which were not tracked and may predict PDE5I exposure, may have affected the results. 

Interpret With Caution

Commenting on the findings, Ozama Ismail, PhD, Alzheimer’s Association director of scientific programs, noted that in addition to the limitations cited by the study authors, AD diagnoses were not made with the “gold standard” testing that typically includes imaging biomarkers and postmortem assessments. 

“While this study is interesting and adds to a potential association, there is no evidence that these drugs are able to treat Alzheimer’s disease,” said Dr. Brauer, who was not part of the current study. 

“People should not use over-the-counter phosphodiesterase type 5 inhibitors for prevention of Alzheimer’s or other dementias based on this very preliminary finding. Always consult with your physician before starting or changing your medications,” he cautioned.

However, Dr. Ismael added that the study does highlight a potential new avenue for drug repurposing. 

“Repurposing of existing, already-approved treatments can be a valuable part of drug development because, through already-completed testing, we know much about their safety and side effects,” which can decrease cost and time needed for studies, he said. 

“When considering repurposing an existing drug to an Alzheimer’s treatment, however, it is often important to conduct new studies over longer periods of time and in older people that reflect the diversity of individuals living with Alzheimer’s disease,” Dr. Ismael said.

Randomized Trials Needed

Dr. Brauer agreed, offering that such a trial should also include people with mild cognitive impairment and measure the effects of PDE5Is given in predefined doses plus an acetylcholinesterase inhibitor or placebo plus an acetylcholinesterase inhibitor. 

“The primary outcome would be the change in baseline cognitive function,” she said. “This approach would provide a comprehensive understanding of the potential therapeutic benefits of PDE5I and AD.”

Studies are also needed to better understand the mechanisms by which these drugs might influence AD risk, Sevil Yasar, MD, PhD, and Lolita Nidadavolu, MD, PhD, from the Division of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, noted in an accompanying editorial.

The strong association between PDE5I use and AD risk in people with a history of hypertension or diabetes suggests “a potential neuroprotective effect through a vascular pathway,” they wrote.

In vitro studies on the role of inflammation and clearance of beta-amyloid could strengthen findings from studies like this one, and in vivo studies could help explain the mechanisms behind PDE5I use and lower AD risk, Dr. Yasar and Dr. Nidadavolu noted. 

“In the end, however, further observational studies exploring mechanisms will not prove a causal association,” they wrote. “A well-designed randomized controlled trial is needed before PDE5I drugs can be prescribed for AD prevention.”

The study was unfunded. The study and editorial authors and Dr. Ismail report no relevant financial conflicts. 
 

A version of this article appeared on Medscape.com.

Men prescribed drugs to treat newly diagnosed erectile dysfunction (ED) are 18% less likely to develop Alzheimer’s disease (AD) during a 5-year follow-up period, new research shows. 

The study is the second in recent years to suggest an association between the use of phosphodiesterase type 5 inhibitors (PDE5Is) such as sildenafil (Viagra) or tadalafil (Cialis) and AD risk. The findings contradict those in a third study, reported by this news organization, that showed no link between the two. 

Although the research is interesting, outside experts noted that there is no evidence that the drugs can treat AD and urge caution when interpreting the findings. 

Investigators agree but believe that the results offer a direction for future studies and underscore the importance of investigating whether existing approved therapies can be repurposed to treat AD. 

“The positive findings from our large study in over 250,000 men is promising and can be used to enhance research capacity and knowledge, with a potential future impact on clinical use and public health policy,” senior author Ruth Brauer, PhD, of the University College London, told this news organization.

“However, before recommending PDE5I are used to reduce the risk of AD, more work is required to validate the findings of our work, particularly in a more generalizable population that includes women and men without erectile dysfunction,” she continued.

The findings were published online February 7 in Neurology.

Strong Association

The study drew on primary healthcare data from the United Kingdom and included 269,725 men (average age, 59 years) with newly diagnosed ED, 55% of whom had received prescriptions for PDE5Is. 

Participants were free from memory or cognitive issues when the study began and were followed for a median of 5.1 years. Investigators accounted for a range of potential AD risk factors, including smoking status, alcohol use, body mass index, hypertension, diabetes, depression, anxiety, and concomitant medication use.

During the study period, 749 in the PDE5I group were diagnosed with AD, corresponding to a rate of 8.1 cases per 10,000 person-years. Among those who did not take the drugs, 370 developed AD, corresponding to a rate of 9.7 cases per 10,000 person-years.

Overall, initiation of a PDE5I was associated with an 18% lower risk for AD (adjusted hazard ration [aHR], 0.82; 95% CI, 0.72-0.93) compared with those with no prescriptions. 

The association was stronger in people aged 70 years or older and those with a history of hypertension or diabetes. The greatest risk reduction was found in people with the most prescriptions during the study period. Those with 21-50 prescriptions had a 44% lower risk for AD (aHR, 0.56; 95% CI, 0.43-0.73) and those with more than 50 were 35% less likely to be diagnosed with AD (aHR, 0.65; 95% CI, 0.49-0.87).

There was no association with AD risk in individuals who received fewer than 20 prescriptions. 

Investigators also analyzed associations after introducing a 1- and 3-year lag period after cohort entry to address the latent period between AD onset and diagnosis. The primary findings held with a 1-year lag period but lost significance with the inclusion of a 3-year lag period.

In subgroup analyses, investigators found evidence of reduced AD risk in those who received prescriptions for sildenafil (aHR, 0.81; 95% CI, 0.71-0.93), but there was no evidence for reduced risk compared with nonusers in those who received tadalafil and vardenafil.

Lower AD risk was found in patients with hypertension, diabetes, and in men aged 70 years or older, but there was no association in younger men or those with no history of hypertension or diabetes. 

Although investigators controlled for a wide range of potential risk factors, Dr. Brauer noted that unmeasured confounders such as physical and sexual activity, which were not tracked and may predict PDE5I exposure, may have affected the results. 

Interpret With Caution

Commenting on the findings, Ozama Ismail, PhD, Alzheimer’s Association director of scientific programs, noted that in addition to the limitations cited by the study authors, AD diagnoses were not made with the “gold standard” testing that typically includes imaging biomarkers and postmortem assessments. 

“While this study is interesting and adds to a potential association, there is no evidence that these drugs are able to treat Alzheimer’s disease,” said Dr. Brauer, who was not part of the current study. 

“People should not use over-the-counter phosphodiesterase type 5 inhibitors for prevention of Alzheimer’s or other dementias based on this very preliminary finding. Always consult with your physician before starting or changing your medications,” he cautioned.

However, Dr. Ismael added that the study does highlight a potential new avenue for drug repurposing. 

“Repurposing of existing, already-approved treatments can be a valuable part of drug development because, through already-completed testing, we know much about their safety and side effects,” which can decrease cost and time needed for studies, he said. 

“When considering repurposing an existing drug to an Alzheimer’s treatment, however, it is often important to conduct new studies over longer periods of time and in older people that reflect the diversity of individuals living with Alzheimer’s disease,” Dr. Ismael said.

Randomized Trials Needed

Dr. Brauer agreed, offering that such a trial should also include people with mild cognitive impairment and measure the effects of PDE5Is given in predefined doses plus an acetylcholinesterase inhibitor or placebo plus an acetylcholinesterase inhibitor. 

“The primary outcome would be the change in baseline cognitive function,” she said. “This approach would provide a comprehensive understanding of the potential therapeutic benefits of PDE5I and AD.”

Studies are also needed to better understand the mechanisms by which these drugs might influence AD risk, Sevil Yasar, MD, PhD, and Lolita Nidadavolu, MD, PhD, from the Division of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, noted in an accompanying editorial.

The strong association between PDE5I use and AD risk in people with a history of hypertension or diabetes suggests “a potential neuroprotective effect through a vascular pathway,” they wrote.

In vitro studies on the role of inflammation and clearance of beta-amyloid could strengthen findings from studies like this one, and in vivo studies could help explain the mechanisms behind PDE5I use and lower AD risk, Dr. Yasar and Dr. Nidadavolu noted. 

“In the end, however, further observational studies exploring mechanisms will not prove a causal association,” they wrote. “A well-designed randomized controlled trial is needed before PDE5I drugs can be prescribed for AD prevention.”

The study was unfunded. The study and editorial authors and Dr. Ismail report no relevant financial conflicts. 
 

A version of this article appeared on Medscape.com.

Clinical efforts to get patients with a history of gout to reach specific target serum urate (SU) levels less than either 5 or 6 mg/dL could prevent the great majority of gout flares and hospitalizations for them, according to a new study that tracked patients for a mean of 8.3 years.

The findings, which appeared February 6 in JAMA, “support the value of target serum urate levels in gout flare prevention in primary care, where most gout patients are treated,” rheumatologist and study coauthor Hyon K. Choi, MD, DrPH, of Harvard Medical School and Massachusetts General Hospital, Boston, told this news organization. However, Dr. Choi noted that “the value of relying on target urate levels is not accepted in primary care practice,” and the author of an accompanying commentary said that the jury is still out about the best strategy to prevent flares.

Gout is caused by monosodium urate crystallization within the joints, which occurs when SU levels exceed the saturation point for uric acid crystallization in the body: approximately 6.8 mg/dL. “Studies have found strongly graded associations between serum urate levels above the saturation point and the risk of developing new cases of gout among individuals without gout at baseline,” Dr. Choi said. “However, associations between serum urate levels and the risk of recurrent flares among preexisting gout patients, which is relevant to clinical gout care practice, has not been established.”

Dr. Choi added that “despite the emphasis in US and European rheumatology guidelines on the use of urate-lowering therapy to treat-to-target serum urate level — eg, under 6 or 5 mg/dL — the proportions of flares associated with such target urate levels remained unknown.”
 

Study Shows Relationship Between SU Levels and Recurrent Flares

For the study, researchers tracked 3613 patients aged 40-69 with gout in the UK Biobank database from 2006-2010 to 2017 or 2020. The patients, 86% of whom were men, had a mean age of 60 years and about 96% were White.

Among the patients, 1773 new episodes of acute gout occurred in 27% of the patients (16% had one episode, 6% had two episodes, and 5% had at least three episodes). These were treated in primary care or required hospitalizations. The other 73% of patients had no new acute gout episodes.

Overall, 95% of flares occurred in those with baseline SU levels ≥ 6 mg/dL, and 98% occurred in those with levels ≥ 5 mg/dL.

Patients with baseline SU levels < 6.0 mg/dL had an acute gout flare rate of 10.6 per 1000 person-years. In comparison, relative risks for acute gout flares per 1000 person-years were 3.16 at baseline SU levels of 6.0-6.9 mg/dL, 6.20 for 7.0-7.9 mg/dL, 7.70 for 8.0-8.9 mg/dL, 9.80 for 9.0-9.9 mg/dL, and 11.26 for > 10 mg/dL after adjustment for various possible confounders (P < .001).

The researchers identified 64 hospitalizations with gout as the main discharge diagnosis, and 97% occurred in patients with baseline SU levels ≥ 6 mg/dL. All were in patients with baseline SU levels ≥ 5 mg/dL.

“An important feature of this study was that serum urate measurements were obtained from all gout patients at the study baseline, irrespective of clinical needs or flare status,” Dr. Choi said. “Prior studies failed to reveal the truly compelling nature of relations between serum urate levels and recurrent flares among preexisting gout patients.”

As for the cost of SU tests, Dr. Choi said they can run as low as $2. “Portable tests similar to home glucose measurement for diabetes patients are also being adopted by certain gout care practices,” he said.

The findings matter, Dr. Choi said, because SU is not tracked in the “vast majority of gout patients” in primary care. Instead, primary care doctors — as per the guidelines of the American College of Physicians — often adopt an approach that treats symptoms as needed instead of tracking and lowering SU levels, he said. In fact, “95% and 98% of gout flares can be potentially preventable at the population level if serum urate levels < 6 and < 5 mg/dL can be met, respectively, and 100% of hospitalizations for gout could be preventable with serum urate < 5 mg/dL,” he said.

As for limitations, the authors noted that participants in the UK Biobank “typically have a better socioeconomic status and are healthier than the UK general population,” and they added that “these data may underestimate the number of acute gout flares in the cohort.” Also, 55% of the total 502,490 patients in the UK Biobank were excluded owing to lack of primary care data.
 

Study ‘Offers the Kind of Evidence That We Need’

In an accompanying commentary, University of Alabama at Birmingham rheumatologist Angelo L. Gaffo, MD, MSPH, also noted that the study population was overwhelmingly White, had a low mean SU level (6.9 mg/dL), and had a low level of comorbidities, making the sample “poorly representative of the most commonly described gout populations.”

However, he also noted that there is “growing evidence linking serum urate levels with clinical outcomes,” with a pair of studies — one from 2021 and the other from 2022 — linking reductions in SU to < 6 md/dL to lower flare rates.

Dr. Gaffo told this news organization that although rheumatology guidelines support a treat-to-target strategy, “we haven›t generated a whole lot of important evidence to support it.”

The new study “offers the kind of evidence that we need,” he said, “but this is not going to be the ultimate answer.” That will only come from randomized clinical trials in the works that will pit the treat-to-target approach vs the primary care–favored strategy of titrating treatment until flares are controlled, he said.

Even though evidence is sparse, Dr. Gaffo said he still believes in the treat-to-target strategy: “I believe it is the best way to treat gout.”

What’s next? Researchers hope to understand how to better reach target SU goals in clinical practice, Dr. Choi said. “Involving nurses, pharmacists, or interactive online or app systems — as in other chronic treat-to-target care such as anticoagulation care, blood pressure, or lipid care — is actively being researched.”

He added that “we are trying to find the effective and safe medications and nonpharmacologic measures to reduce the urate burden, which can also simultaneously take care of gout’s frequent cardiovascular-kidney comorbidities.”

The US National Institutes of Health supported the study. Dr. Choi reports receiving grants from Horizon and serving on a board or committee for LG Chem, Shanton, and ANI Pharmaceuticals. Some other authors report an employment and stockholder relationship with Regeneron and support from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, and Rheumatology Research Foundation. Dr. Gaffo reports personal fees from PK MED, SOBI/Selecta, Atom, and UpToDate.

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

Clinical efforts to get patients with a history of gout to reach specific target serum urate (SU) levels less than either 5 or 6 mg/dL could prevent the great majority of gout flares and hospitalizations for them, according to a new study that tracked patients for a mean of 8.3 years.

The findings, which appeared February 6 in JAMA, “support the value of target serum urate levels in gout flare prevention in primary care, where most gout patients are treated,” rheumatologist and study coauthor Hyon K. Choi, MD, DrPH, of Harvard Medical School and Massachusetts General Hospital, Boston, told this news organization. However, Dr. Choi noted that “the value of relying on target urate levels is not accepted in primary care practice,” and the author of an accompanying commentary said that the jury is still out about the best strategy to prevent flares.

Gout is caused by monosodium urate crystallization within the joints, which occurs when SU levels exceed the saturation point for uric acid crystallization in the body: approximately 6.8 mg/dL. “Studies have found strongly graded associations between serum urate levels above the saturation point and the risk of developing new cases of gout among individuals without gout at baseline,” Dr. Choi said. “However, associations between serum urate levels and the risk of recurrent flares among preexisting gout patients, which is relevant to clinical gout care practice, has not been established.”

Dr. Choi added that “despite the emphasis in US and European rheumatology guidelines on the use of urate-lowering therapy to treat-to-target serum urate level — eg, under 6 or 5 mg/dL — the proportions of flares associated with such target urate levels remained unknown.”
 

Study Shows Relationship Between SU Levels and Recurrent Flares

For the study, researchers tracked 3613 patients aged 40-69 with gout in the UK Biobank database from 2006-2010 to 2017 or 2020. The patients, 86% of whom were men, had a mean age of 60 years and about 96% were White.

Among the patients, 1773 new episodes of acute gout occurred in 27% of the patients (16% had one episode, 6% had two episodes, and 5% had at least three episodes). These were treated in primary care or required hospitalizations. The other 73% of patients had no new acute gout episodes.

Overall, 95% of flares occurred in those with baseline SU levels ≥ 6 mg/dL, and 98% occurred in those with levels ≥ 5 mg/dL.

Patients with baseline SU levels < 6.0 mg/dL had an acute gout flare rate of 10.6 per 1000 person-years. In comparison, relative risks for acute gout flares per 1000 person-years were 3.16 at baseline SU levels of 6.0-6.9 mg/dL, 6.20 for 7.0-7.9 mg/dL, 7.70 for 8.0-8.9 mg/dL, 9.80 for 9.0-9.9 mg/dL, and 11.26 for > 10 mg/dL after adjustment for various possible confounders (P < .001).

The researchers identified 64 hospitalizations with gout as the main discharge diagnosis, and 97% occurred in patients with baseline SU levels ≥ 6 mg/dL. All were in patients with baseline SU levels ≥ 5 mg/dL.

“An important feature of this study was that serum urate measurements were obtained from all gout patients at the study baseline, irrespective of clinical needs or flare status,” Dr. Choi said. “Prior studies failed to reveal the truly compelling nature of relations between serum urate levels and recurrent flares among preexisting gout patients.”

As for the cost of SU tests, Dr. Choi said they can run as low as $2. “Portable tests similar to home glucose measurement for diabetes patients are also being adopted by certain gout care practices,” he said.

The findings matter, Dr. Choi said, because SU is not tracked in the “vast majority of gout patients” in primary care. Instead, primary care doctors — as per the guidelines of the American College of Physicians — often adopt an approach that treats symptoms as needed instead of tracking and lowering SU levels, he said. In fact, “95% and 98% of gout flares can be potentially preventable at the population level if serum urate levels < 6 and < 5 mg/dL can be met, respectively, and 100% of hospitalizations for gout could be preventable with serum urate < 5 mg/dL,” he said.

As for limitations, the authors noted that participants in the UK Biobank “typically have a better socioeconomic status and are healthier than the UK general population,” and they added that “these data may underestimate the number of acute gout flares in the cohort.” Also, 55% of the total 502,490 patients in the UK Biobank were excluded owing to lack of primary care data.
 

Study ‘Offers the Kind of Evidence That We Need’

In an accompanying commentary, University of Alabama at Birmingham rheumatologist Angelo L. Gaffo, MD, MSPH, also noted that the study population was overwhelmingly White, had a low mean SU level (6.9 mg/dL), and had a low level of comorbidities, making the sample “poorly representative of the most commonly described gout populations.”

However, he also noted that there is “growing evidence linking serum urate levels with clinical outcomes,” with a pair of studies — one from 2021 and the other from 2022 — linking reductions in SU to < 6 md/dL to lower flare rates.

Dr. Gaffo told this news organization that although rheumatology guidelines support a treat-to-target strategy, “we haven›t generated a whole lot of important evidence to support it.”

The new study “offers the kind of evidence that we need,” he said, “but this is not going to be the ultimate answer.” That will only come from randomized clinical trials in the works that will pit the treat-to-target approach vs the primary care–favored strategy of titrating treatment until flares are controlled, he said.

Even though evidence is sparse, Dr. Gaffo said he still believes in the treat-to-target strategy: “I believe it is the best way to treat gout.”

What’s next? Researchers hope to understand how to better reach target SU goals in clinical practice, Dr. Choi said. “Involving nurses, pharmacists, or interactive online or app systems — as in other chronic treat-to-target care such as anticoagulation care, blood pressure, or lipid care — is actively being researched.”

He added that “we are trying to find the effective and safe medications and nonpharmacologic measures to reduce the urate burden, which can also simultaneously take care of gout’s frequent cardiovascular-kidney comorbidities.”

The US National Institutes of Health supported the study. Dr. Choi reports receiving grants from Horizon and serving on a board or committee for LG Chem, Shanton, and ANI Pharmaceuticals. Some other authors report an employment and stockholder relationship with Regeneron and support from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, and Rheumatology Research Foundation. Dr. Gaffo reports personal fees from PK MED, SOBI/Selecta, Atom, and UpToDate.

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

Clinical efforts to get patients with a history of gout to reach specific target serum urate (SU) levels less than either 5 or 6 mg/dL could prevent the great majority of gout flares and hospitalizations for them, according to a new study that tracked patients for a mean of 8.3 years.

The findings, which appeared February 6 in JAMA, “support the value of target serum urate levels in gout flare prevention in primary care, where most gout patients are treated,” rheumatologist and study coauthor Hyon K. Choi, MD, DrPH, of Harvard Medical School and Massachusetts General Hospital, Boston, told this news organization. However, Dr. Choi noted that “the value of relying on target urate levels is not accepted in primary care practice,” and the author of an accompanying commentary said that the jury is still out about the best strategy to prevent flares.

Gout is caused by monosodium urate crystallization within the joints, which occurs when SU levels exceed the saturation point for uric acid crystallization in the body: approximately 6.8 mg/dL. “Studies have found strongly graded associations between serum urate levels above the saturation point and the risk of developing new cases of gout among individuals without gout at baseline,” Dr. Choi said. “However, associations between serum urate levels and the risk of recurrent flares among preexisting gout patients, which is relevant to clinical gout care practice, has not been established.”

Dr. Choi added that “despite the emphasis in US and European rheumatology guidelines on the use of urate-lowering therapy to treat-to-target serum urate level — eg, under 6 or 5 mg/dL — the proportions of flares associated with such target urate levels remained unknown.”
 

Study Shows Relationship Between SU Levels and Recurrent Flares

For the study, researchers tracked 3613 patients aged 40-69 with gout in the UK Biobank database from 2006-2010 to 2017 or 2020. The patients, 86% of whom were men, had a mean age of 60 years and about 96% were White.

Among the patients, 1773 new episodes of acute gout occurred in 27% of the patients (16% had one episode, 6% had two episodes, and 5% had at least three episodes). These were treated in primary care or required hospitalizations. The other 73% of patients had no new acute gout episodes.

Overall, 95% of flares occurred in those with baseline SU levels ≥ 6 mg/dL, and 98% occurred in those with levels ≥ 5 mg/dL.

Patients with baseline SU levels < 6.0 mg/dL had an acute gout flare rate of 10.6 per 1000 person-years. In comparison, relative risks for acute gout flares per 1000 person-years were 3.16 at baseline SU levels of 6.0-6.9 mg/dL, 6.20 for 7.0-7.9 mg/dL, 7.70 for 8.0-8.9 mg/dL, 9.80 for 9.0-9.9 mg/dL, and 11.26 for > 10 mg/dL after adjustment for various possible confounders (P < .001).

The researchers identified 64 hospitalizations with gout as the main discharge diagnosis, and 97% occurred in patients with baseline SU levels ≥ 6 mg/dL. All were in patients with baseline SU levels ≥ 5 mg/dL.

“An important feature of this study was that serum urate measurements were obtained from all gout patients at the study baseline, irrespective of clinical needs or flare status,” Dr. Choi said. “Prior studies failed to reveal the truly compelling nature of relations between serum urate levels and recurrent flares among preexisting gout patients.”

As for the cost of SU tests, Dr. Choi said they can run as low as $2. “Portable tests similar to home glucose measurement for diabetes patients are also being adopted by certain gout care practices,” he said.

The findings matter, Dr. Choi said, because SU is not tracked in the “vast majority of gout patients” in primary care. Instead, primary care doctors — as per the guidelines of the American College of Physicians — often adopt an approach that treats symptoms as needed instead of tracking and lowering SU levels, he said. In fact, “95% and 98% of gout flares can be potentially preventable at the population level if serum urate levels < 6 and < 5 mg/dL can be met, respectively, and 100% of hospitalizations for gout could be preventable with serum urate < 5 mg/dL,” he said.

As for limitations, the authors noted that participants in the UK Biobank “typically have a better socioeconomic status and are healthier than the UK general population,” and they added that “these data may underestimate the number of acute gout flares in the cohort.” Also, 55% of the total 502,490 patients in the UK Biobank were excluded owing to lack of primary care data.
 

Study ‘Offers the Kind of Evidence That We Need’

In an accompanying commentary, University of Alabama at Birmingham rheumatologist Angelo L. Gaffo, MD, MSPH, also noted that the study population was overwhelmingly White, had a low mean SU level (6.9 mg/dL), and had a low level of comorbidities, making the sample “poorly representative of the most commonly described gout populations.”

However, he also noted that there is “growing evidence linking serum urate levels with clinical outcomes,” with a pair of studies — one from 2021 and the other from 2022 — linking reductions in SU to < 6 md/dL to lower flare rates.

Dr. Gaffo told this news organization that although rheumatology guidelines support a treat-to-target strategy, “we haven›t generated a whole lot of important evidence to support it.”

The new study “offers the kind of evidence that we need,” he said, “but this is not going to be the ultimate answer.” That will only come from randomized clinical trials in the works that will pit the treat-to-target approach vs the primary care–favored strategy of titrating treatment until flares are controlled, he said.

Even though evidence is sparse, Dr. Gaffo said he still believes in the treat-to-target strategy: “I believe it is the best way to treat gout.”

What’s next? Researchers hope to understand how to better reach target SU goals in clinical practice, Dr. Choi said. “Involving nurses, pharmacists, or interactive online or app systems — as in other chronic treat-to-target care such as anticoagulation care, blood pressure, or lipid care — is actively being researched.”

He added that “we are trying to find the effective and safe medications and nonpharmacologic measures to reduce the urate burden, which can also simultaneously take care of gout’s frequent cardiovascular-kidney comorbidities.”

The US National Institutes of Health supported the study. Dr. Choi reports receiving grants from Horizon and serving on a board or committee for LG Chem, Shanton, and ANI Pharmaceuticals. Some other authors report an employment and stockholder relationship with Regeneron and support from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, and Rheumatology Research Foundation. Dr. Gaffo reports personal fees from PK MED, SOBI/Selecta, Atom, and UpToDate.

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

Comorbidities may play a large role in driving poor pregnancy outcomes in pregnant people with certain immune-mediated inflammatory diseases (IMIDs).

In a new study of 12 individual IMIDs, people with rheumatoid arthritis (RA) or inflammatory bowel disease (IBD) did not have signficantly increased risk for preterm birth (PTB) or low birth weight (LBW), compared with people who did not have an IMID, after adjusting for additional chronic conditions and other confounding factors.

The study was published online on February 1 in eClinicalMedicine.

While many studies have explored the relationships between pregnancy outcomes and IMIDs, “the impact of comorbidities on the relation between IMIDs and pregnancy course is insufficiently examined,” the authors wrote. These previous studies also tended to have a small sample size.
 

Pregnancy Outcome Risks Varied Between IMIDs

To remedy this, researchers used electronic health record data from Providence St Joseph Health — a multistate integrated healthcare system — to identify more than 365,000 pregnant people with live births between January 1, 2013, and December 31, 2022. The cohort included more than 5700 people with at least one of 12 IMIDs: Psoriasis, IBD, RA, spondyloarthritis (SpA), multiple sclerosis, systemic lupus erythematosus (SLE), psoriatic arthritis (PsA), antiphospholipid syndrome (APS), Sjögren syndrome (SjS), vasculitis, sarcoidosis, and systemic sclerosis. The study included only live births with a gestational age of 20 weeks or greater.

Researchers compared maternal-fetal health outcomes between the two groups, controlling for comorbidities including diabetes, cardiovascular disease, chronic kidney disease, obesity, and depression. They also accounted for confounding variables including race, age, smoking status, and socioeconomic status.

In total, 83% of people in the IMID group had no immunomodulatory medication prescriptions during their pregnancy. Of the 17% taking medication, 48%-70% continued taking their medication until delivery. Most patients were White, comprising 62.9% of the non-IMID group and 73.1% of the IMID group.

After adjusting for comorbidities, patients with any of the 12 IMIDs had a 10%-20% higher risk for PTB, LBW, small for gestation age (SGA), and cesarean section than did comparators.

But these risks varied between IMIDs. Patients with RA and IBD did not have an increased risk for PTB or LBW. However, when researchers did not control for comorbidities, pregnancy risks were higher and showed statistical significance in these two groups.

“This suggests that for RA and IBD, comorbidities may be a more important factor for adverse outcomes than the underlying autoimmune disease,” senior author Jennifer Hadlock, MD, an associate professor and director of medical data science at the Institute for Systems Biology in Seattle, Washington, said in a video accompanying a press release.

Overall, the analysis found that women with IMIDs were approximately two to three times more likely to have chronic comorbidities than the control group.

Like previous studies, there was a strong association between SLE and APS and poor pregnancy outcomes, even after controlling for confounding factors. Patients with SpA had a 50% increased risk for PTB, while those with SLE and APS had more than a twofold higher risk. Patients with SLE were 90% more likely than comparators to deliver babies with an SGA condition, while RA patients had a 30% higher risk. SLE was the only condition with an increased risk for LBW (relative risk, 3.5). IBD, RA, PsA, SpA, SLE, APS, and SjS were all associated with a higher likelihood of delivery via cesarean section.

“The findings of this study reveal that the associations between IMIDs and adverse pregnancy outcomes are influenced by the specific type of IMIDs and the presence of comorbidities,” the authors wrote.
 

A Large Study, But How Representative Is It?

Asked to comment on the study, Catherine Sims, MD, a rheumatologist at Duke University Medical Center in Durham, North Carolina, noted that the analysis was much larger than many reproductive rheumatology studies, and “their statistics were phenomenal.”

She agreed that “not all autoimmune diseases are created equal when it comes to pregnancy-associated risks.” However, she added that this study’s patient population may not be totally representative of pregnant people with IMIDs or autoimmune diseases.

“We’re making generalizations about autoimmune diseases based on this demographic of White women who are not taking immunosuppression,” she said.

“We know that race and ethnicity play a huge role in pregnancy outcomes, and Black women have higher maternal and fetal morbidity and mortality, which is likely related to systemic racism and biases in the medical system,” she added. “While the study did control for sociodemographic factors, the population studied is not diverse.”

Only 17% of people with IMID in the cohort were on immunosuppressive medication, which could suggest low disease activity in the study population, Dr. Sims said. If the population generally had well-controlled disease, that could have positioned them for better pregnancy outcomes.

The authors noted that their analysis did not have information on IMID disease activity or severity — one of the limitations of the study.

However, the authors argued that the observed low prescription rate during the study may have increased poor pregnancy outcomes.

“Although this reflects real-world care in the population studied, results from this study may show higher risk than might be achieved with recommended care guidelines,” they wrote.

Ultimately, the authors argued that these findings show how co-occurring health conditions can affect pregnancy outcomes in autoimmune diseases, particularly for RA and IBD.

“There is a need to take comorbidities into consideration for guidelines for patients with inflammatory bowel disease and rheumatoid arthritis and when designing future research to investigate maternal health in patients with IMIDs,” they wrote.

The study was funded by the National Institutes of Health. Dr. Sims declared no relevant financial relationships. Dr. Hadlock has received research funding (paid to the institute) from Pfizer, Novartis, Janssen, Bristol-Myers Squibb, and Gilead.

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

Comorbidities may play a large role in driving poor pregnancy outcomes in pregnant people with certain immune-mediated inflammatory diseases (IMIDs).

In a new study of 12 individual IMIDs, people with rheumatoid arthritis (RA) or inflammatory bowel disease (IBD) did not have signficantly increased risk for preterm birth (PTB) or low birth weight (LBW), compared with people who did not have an IMID, after adjusting for additional chronic conditions and other confounding factors.

The study was published online on February 1 in eClinicalMedicine.

While many studies have explored the relationships between pregnancy outcomes and IMIDs, “the impact of comorbidities on the relation between IMIDs and pregnancy course is insufficiently examined,” the authors wrote. These previous studies also tended to have a small sample size.
 

Pregnancy Outcome Risks Varied Between IMIDs

To remedy this, researchers used electronic health record data from Providence St Joseph Health — a multistate integrated healthcare system — to identify more than 365,000 pregnant people with live births between January 1, 2013, and December 31, 2022. The cohort included more than 5700 people with at least one of 12 IMIDs: Psoriasis, IBD, RA, spondyloarthritis (SpA), multiple sclerosis, systemic lupus erythematosus (SLE), psoriatic arthritis (PsA), antiphospholipid syndrome (APS), Sjögren syndrome (SjS), vasculitis, sarcoidosis, and systemic sclerosis. The study included only live births with a gestational age of 20 weeks or greater.

Researchers compared maternal-fetal health outcomes between the two groups, controlling for comorbidities including diabetes, cardiovascular disease, chronic kidney disease, obesity, and depression. They also accounted for confounding variables including race, age, smoking status, and socioeconomic status.

In total, 83% of people in the IMID group had no immunomodulatory medication prescriptions during their pregnancy. Of the 17% taking medication, 48%-70% continued taking their medication until delivery. Most patients were White, comprising 62.9% of the non-IMID group and 73.1% of the IMID group.

After adjusting for comorbidities, patients with any of the 12 IMIDs had a 10%-20% higher risk for PTB, LBW, small for gestation age (SGA), and cesarean section than did comparators.

But these risks varied between IMIDs. Patients with RA and IBD did not have an increased risk for PTB or LBW. However, when researchers did not control for comorbidities, pregnancy risks were higher and showed statistical significance in these two groups.

“This suggests that for RA and IBD, comorbidities may be a more important factor for adverse outcomes than the underlying autoimmune disease,” senior author Jennifer Hadlock, MD, an associate professor and director of medical data science at the Institute for Systems Biology in Seattle, Washington, said in a video accompanying a press release.

Overall, the analysis found that women with IMIDs were approximately two to three times more likely to have chronic comorbidities than the control group.

Like previous studies, there was a strong association between SLE and APS and poor pregnancy outcomes, even after controlling for confounding factors. Patients with SpA had a 50% increased risk for PTB, while those with SLE and APS had more than a twofold higher risk. Patients with SLE were 90% more likely than comparators to deliver babies with an SGA condition, while RA patients had a 30% higher risk. SLE was the only condition with an increased risk for LBW (relative risk, 3.5). IBD, RA, PsA, SpA, SLE, APS, and SjS were all associated with a higher likelihood of delivery via cesarean section.

“The findings of this study reveal that the associations between IMIDs and adverse pregnancy outcomes are influenced by the specific type of IMIDs and the presence of comorbidities,” the authors wrote.
 

A Large Study, But How Representative Is It?

Asked to comment on the study, Catherine Sims, MD, a rheumatologist at Duke University Medical Center in Durham, North Carolina, noted that the analysis was much larger than many reproductive rheumatology studies, and “their statistics were phenomenal.”

She agreed that “not all autoimmune diseases are created equal when it comes to pregnancy-associated risks.” However, she added that this study’s patient population may not be totally representative of pregnant people with IMIDs or autoimmune diseases.

“We’re making generalizations about autoimmune diseases based on this demographic of White women who are not taking immunosuppression,” she said.

“We know that race and ethnicity play a huge role in pregnancy outcomes, and Black women have higher maternal and fetal morbidity and mortality, which is likely related to systemic racism and biases in the medical system,” she added. “While the study did control for sociodemographic factors, the population studied is not diverse.”

Only 17% of people with IMID in the cohort were on immunosuppressive medication, which could suggest low disease activity in the study population, Dr. Sims said. If the population generally had well-controlled disease, that could have positioned them for better pregnancy outcomes.

The authors noted that their analysis did not have information on IMID disease activity or severity — one of the limitations of the study.

However, the authors argued that the observed low prescription rate during the study may have increased poor pregnancy outcomes.

“Although this reflects real-world care in the population studied, results from this study may show higher risk than might be achieved with recommended care guidelines,” they wrote.

Ultimately, the authors argued that these findings show how co-occurring health conditions can affect pregnancy outcomes in autoimmune diseases, particularly for RA and IBD.

“There is a need to take comorbidities into consideration for guidelines for patients with inflammatory bowel disease and rheumatoid arthritis and when designing future research to investigate maternal health in patients with IMIDs,” they wrote.

The study was funded by the National Institutes of Health. Dr. Sims declared no relevant financial relationships. Dr. Hadlock has received research funding (paid to the institute) from Pfizer, Novartis, Janssen, Bristol-Myers Squibb, and Gilead.

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

Comorbidities may play a large role in driving poor pregnancy outcomes in pregnant people with certain immune-mediated inflammatory diseases (IMIDs).

In a new study of 12 individual IMIDs, people with rheumatoid arthritis (RA) or inflammatory bowel disease (IBD) did not have signficantly increased risk for preterm birth (PTB) or low birth weight (LBW), compared with people who did not have an IMID, after adjusting for additional chronic conditions and other confounding factors.

The study was published online on February 1 in eClinicalMedicine.

While many studies have explored the relationships between pregnancy outcomes and IMIDs, “the impact of comorbidities on the relation between IMIDs and pregnancy course is insufficiently examined,” the authors wrote. These previous studies also tended to have a small sample size.
 

Pregnancy Outcome Risks Varied Between IMIDs

To remedy this, researchers used electronic health record data from Providence St Joseph Health — a multistate integrated healthcare system — to identify more than 365,000 pregnant people with live births between January 1, 2013, and December 31, 2022. The cohort included more than 5700 people with at least one of 12 IMIDs: Psoriasis, IBD, RA, spondyloarthritis (SpA), multiple sclerosis, systemic lupus erythematosus (SLE), psoriatic arthritis (PsA), antiphospholipid syndrome (APS), Sjögren syndrome (SjS), vasculitis, sarcoidosis, and systemic sclerosis. The study included only live births with a gestational age of 20 weeks or greater.

Researchers compared maternal-fetal health outcomes between the two groups, controlling for comorbidities including diabetes, cardiovascular disease, chronic kidney disease, obesity, and depression. They also accounted for confounding variables including race, age, smoking status, and socioeconomic status.

In total, 83% of people in the IMID group had no immunomodulatory medication prescriptions during their pregnancy. Of the 17% taking medication, 48%-70% continued taking their medication until delivery. Most patients were White, comprising 62.9% of the non-IMID group and 73.1% of the IMID group.

After adjusting for comorbidities, patients with any of the 12 IMIDs had a 10%-20% higher risk for PTB, LBW, small for gestation age (SGA), and cesarean section than did comparators.

But these risks varied between IMIDs. Patients with RA and IBD did not have an increased risk for PTB or LBW. However, when researchers did not control for comorbidities, pregnancy risks were higher and showed statistical significance in these two groups.

“This suggests that for RA and IBD, comorbidities may be a more important factor for adverse outcomes than the underlying autoimmune disease,” senior author Jennifer Hadlock, MD, an associate professor and director of medical data science at the Institute for Systems Biology in Seattle, Washington, said in a video accompanying a press release.

Overall, the analysis found that women with IMIDs were approximately two to three times more likely to have chronic comorbidities than the control group.

Like previous studies, there was a strong association between SLE and APS and poor pregnancy outcomes, even after controlling for confounding factors. Patients with SpA had a 50% increased risk for PTB, while those with SLE and APS had more than a twofold higher risk. Patients with SLE were 90% more likely than comparators to deliver babies with an SGA condition, while RA patients had a 30% higher risk. SLE was the only condition with an increased risk for LBW (relative risk, 3.5). IBD, RA, PsA, SpA, SLE, APS, and SjS were all associated with a higher likelihood of delivery via cesarean section.

“The findings of this study reveal that the associations between IMIDs and adverse pregnancy outcomes are influenced by the specific type of IMIDs and the presence of comorbidities,” the authors wrote.
 

A Large Study, But How Representative Is It?

Asked to comment on the study, Catherine Sims, MD, a rheumatologist at Duke University Medical Center in Durham, North Carolina, noted that the analysis was much larger than many reproductive rheumatology studies, and “their statistics were phenomenal.”

She agreed that “not all autoimmune diseases are created equal when it comes to pregnancy-associated risks.” However, she added that this study’s patient population may not be totally representative of pregnant people with IMIDs or autoimmune diseases.

“We’re making generalizations about autoimmune diseases based on this demographic of White women who are not taking immunosuppression,” she said.

“We know that race and ethnicity play a huge role in pregnancy outcomes, and Black women have higher maternal and fetal morbidity and mortality, which is likely related to systemic racism and biases in the medical system,” she added. “While the study did control for sociodemographic factors, the population studied is not diverse.”

Only 17% of people with IMID in the cohort were on immunosuppressive medication, which could suggest low disease activity in the study population, Dr. Sims said. If the population generally had well-controlled disease, that could have positioned them for better pregnancy outcomes.

The authors noted that their analysis did not have information on IMID disease activity or severity — one of the limitations of the study.

However, the authors argued that the observed low prescription rate during the study may have increased poor pregnancy outcomes.

“Although this reflects real-world care in the population studied, results from this study may show higher risk than might be achieved with recommended care guidelines,” they wrote.

Ultimately, the authors argued that these findings show how co-occurring health conditions can affect pregnancy outcomes in autoimmune diseases, particularly for RA and IBD.

“There is a need to take comorbidities into consideration for guidelines for patients with inflammatory bowel disease and rheumatoid arthritis and when designing future research to investigate maternal health in patients with IMIDs,” they wrote.

The study was funded by the National Institutes of Health. Dr. Sims declared no relevant financial relationships. Dr. Hadlock has received research funding (paid to the institute) from Pfizer, Novartis, Janssen, Bristol-Myers Squibb, and Gilead.

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

Two years after the end of a randomized trial that showed a benefit of daily vitamin D and omega-3 fatty acid (n-3 FA) supplementation for reducing risk for autoimmune diseases, the salubrious effects of daily vitamin D appear to have waned after the supplement was discontinued, while the protection from n-3 lived on for at least 2 additional years.

As previously reported, the randomized VITAL, which was designed primarily to study the effects of vitamin D and n-3 supplementation on incident cancer and cardiovascular disease, also showed that 5 years of vitamin D supplementation was associated with a 22% reduction in risk for confirmed autoimmune diseases, and 5 years of n-3 FA supplementation was associated with an 18% reduction in confirmed and probable incident autoimmune diseases.

Now, investigators Karen H. Costenbader, MD, MPH, of Brigham & Women’s Hospital in Boston, Massachusetts, and colleagues reported that among 21,592 participants in VITAL who agreed to be followed for an additional 2 years after discontinuation, the protection against autoimmune diseases from daily vitamin D (cholecalciferol; 2000 IU/d) was no longer statistically significant, but the benefits of daily marine n-3 FAs (1 g/d as a fish-oil capsule containing 460 mg of eicosapentaenoic acid and 380 mg of docosahexaenoic acid) remained significant.

“VITAL observational extension results suggest that vitamin D supplementation should be given on a continuous basis for long-term prevention of [autoimmune diseases]. The beneficial effects of n-3 fatty acids, however, may be prolonged for at least 2 years after discontinuation,” they wrote in an article published in Arthritis & Rheumatology.

Dr. Costenbader told this news organization that the results of the observational extension study suggest that the benefits of vitamin D “wear off more quickly, and it should be continued for a longer period of time or indefinitely, rather than only for 5 years.”

In addition to the disparity in the duration of the protective effect, the investigators also saw differences in the effects across different autoimmune diseases.

“The protective effect of vitamin D seemed strongest for psoriasis, while for omega-3 fatty acids, the protective effects were strongest for rheumatoid arthritis and inflammatory bowel disease,” she said.
 

Mixed Effects

In an interview with this news organization, Janet Funk, MD, MS, vice chair of research in the Department of Medicine and professor in the School of Nutritional Science and Wellness at the University of Arizona, Tucson, Arizona, who was not involved in the study, saidthat the results suggest that while each supplement may offer protection against autoimmune diseases, the effects are inconsistent and may not apply to all patients.

“I think the VITAL extension results suggest that either supplement (or both together) may have benefits in reducing risk of autoimmune diseases, including possible persistent effects posttreatment, but that these effects are nuanced (ie, only in normal weight post-vitamin D treatment) and possibly not uniform across all autoimmune diseases (including possible adverse effects for some — eg, inverse association between prior omega-3 and psoriasis and tendency for increased autoimmune thyroid disease for vitamin D), although the study was not powered sufficiently to draw disease-specific conclusions,” she said.

In an editorial accompanying the study, rheumatologist Joel M. Kremer, MD, of Albany Medical College and the Corrona Research Foundation in Delray Beach, Florida, wrote that “[T]he studies by Dr. Costenbader, et al. have shed new light on the possibility that dietary supplements of n-3 FA [fatty acid] may prevent the onset of [autoimmune disease]. The sustained benefits they describe for as long as 2 years after the supplements are discontinued are consistent with the chronicity of FA species in cellular plasma membranes where they serve as substrates for a diverse array of salient metabolic and inflammatory pathways.”
 

VITAL Then

To test whether vitamin D or marine-derived long-chain n-3 FA supplementation could protect against autoimmune disease over time, Dr. Costenbader and colleagues piggybacked an ancillary study onto the VITAL trial, which had primary outcomes of cancer and cardiovascular disease incidence.

A total of 25,871 participants were enrolled, including 12,786 men aged 50 and older and 13,085 women aged 55 and older. The study had a 2 × 2 factorial design, with patients randomly assigned to vitamin D 2000 IU/d or placebo and then further randomized to either 1 g/d n-3 FAs or placebo in both the vitamin D and placebo primary randomization arms.

In multivariate analysis adjusted for age, sex, race, and other supplement arm, vitamin D alone was associated with a hazard ratio (HR) of 0.68 (P = .02) for incident autoimmune disease, n-3 alone was associated with a nonsignificant HR of 0.74, and the combination was associated with an HR of 0.69 (P = .03). However, when probable incident autoimmune disease cases were included, the effect of n-3 became significant, with an HR of 0.82.
 

VITAL Now

In the current analysis, Dr. Costenbader and colleagues reported observational data on 21,592 VITAL participants, a sample representing 83.5% of those who were initially randomized, and 87.9% of those who were alive and could be contacted at the end of the study.

As in the initial trial, the investigators used annual questionnaires to assess incident autoimmune diseases during the randomized follow-up. Participants were asked about new-onset, doctor-diagnosed rheumatoid arthritis, polymyalgia rheumatica, psoriasis, autoimmune thyroid disease, and inflammatory bowel disease. Participants could also write in any other new autoimmune disease diagnoses.

There were 236 new cases of confirmed autoimmune disease that occurred since the initial publication of the trial results, as well as 65 probable cases identified during the median 5.3 years of the randomized portion, and 42 probable cases diagnosed during the 2-year observational phase.

The investigators found that after the 2-year observation period, 255 participants initially randomized to receive vitamin D had a newly developed confirmed autoimmune disease, compared with 259 of those initially randomized to a vitamin D placebo. This translated into a nonsignificant HR of 0.98.

Adding probable autoimmune cases to the confirmed cases made little difference, resulting in a nonsignificant adjusted HR of 0.95.

In contrast, there were 234 confirmed autoimmune disease cases among patients initially assigned to n-3, compared with 280 among patients randomized to the n-3 placebo, translating into a statistically significant HR of 0.83 for new-onset autoimmune disease with n-3.

Dr. Costenbader and colleagues acknowledged that the study was limited by the use of doses intended to prevent cancer or cardiovascular disease and that higher doses intended for high-risk or nutritionally deficient populations might reveal larger effects of supplementation. In addition, they noted the difficulty of identifying the timing and onset of incident disease, and that the small number of cases that occurred during the 2-year observational period precluded detailed analyses of individual autoimmune diseases.

The study was funded by grants from the National Institutes of Health. Dr. Costenbader, Dr. Funk, and Dr. Kremer reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Two years after the end of a randomized trial that showed a benefit of daily vitamin D and omega-3 fatty acid (n-3 FA) supplementation for reducing risk for autoimmune diseases, the salubrious effects of daily vitamin D appear to have waned after the supplement was discontinued, while the protection from n-3 lived on for at least 2 additional years.

As previously reported, the randomized VITAL, which was designed primarily to study the effects of vitamin D and n-3 supplementation on incident cancer and cardiovascular disease, also showed that 5 years of vitamin D supplementation was associated with a 22% reduction in risk for confirmed autoimmune diseases, and 5 years of n-3 FA supplementation was associated with an 18% reduction in confirmed and probable incident autoimmune diseases.

Now, investigators Karen H. Costenbader, MD, MPH, of Brigham & Women’s Hospital in Boston, Massachusetts, and colleagues reported that among 21,592 participants in VITAL who agreed to be followed for an additional 2 years after discontinuation, the protection against autoimmune diseases from daily vitamin D (cholecalciferol; 2000 IU/d) was no longer statistically significant, but the benefits of daily marine n-3 FAs (1 g/d as a fish-oil capsule containing 460 mg of eicosapentaenoic acid and 380 mg of docosahexaenoic acid) remained significant.

“VITAL observational extension results suggest that vitamin D supplementation should be given on a continuous basis for long-term prevention of [autoimmune diseases]. The beneficial effects of n-3 fatty acids, however, may be prolonged for at least 2 years after discontinuation,” they wrote in an article published in Arthritis & Rheumatology.

Dr. Costenbader told this news organization that the results of the observational extension study suggest that the benefits of vitamin D “wear off more quickly, and it should be continued for a longer period of time or indefinitely, rather than only for 5 years.”

In addition to the disparity in the duration of the protective effect, the investigators also saw differences in the effects across different autoimmune diseases.

“The protective effect of vitamin D seemed strongest for psoriasis, while for omega-3 fatty acids, the protective effects were strongest for rheumatoid arthritis and inflammatory bowel disease,” she said.
 

Mixed Effects

In an interview with this news organization, Janet Funk, MD, MS, vice chair of research in the Department of Medicine and professor in the School of Nutritional Science and Wellness at the University of Arizona, Tucson, Arizona, who was not involved in the study, saidthat the results suggest that while each supplement may offer protection against autoimmune diseases, the effects are inconsistent and may not apply to all patients.

“I think the VITAL extension results suggest that either supplement (or both together) may have benefits in reducing risk of autoimmune diseases, including possible persistent effects posttreatment, but that these effects are nuanced (ie, only in normal weight post-vitamin D treatment) and possibly not uniform across all autoimmune diseases (including possible adverse effects for some — eg, inverse association between prior omega-3 and psoriasis and tendency for increased autoimmune thyroid disease for vitamin D), although the study was not powered sufficiently to draw disease-specific conclusions,” she said.

In an editorial accompanying the study, rheumatologist Joel M. Kremer, MD, of Albany Medical College and the Corrona Research Foundation in Delray Beach, Florida, wrote that “[T]he studies by Dr. Costenbader, et al. have shed new light on the possibility that dietary supplements of n-3 FA [fatty acid] may prevent the onset of [autoimmune disease]. The sustained benefits they describe for as long as 2 years after the supplements are discontinued are consistent with the chronicity of FA species in cellular plasma membranes where they serve as substrates for a diverse array of salient metabolic and inflammatory pathways.”
 

VITAL Then

To test whether vitamin D or marine-derived long-chain n-3 FA supplementation could protect against autoimmune disease over time, Dr. Costenbader and colleagues piggybacked an ancillary study onto the VITAL trial, which had primary outcomes of cancer and cardiovascular disease incidence.

A total of 25,871 participants were enrolled, including 12,786 men aged 50 and older and 13,085 women aged 55 and older. The study had a 2 × 2 factorial design, with patients randomly assigned to vitamin D 2000 IU/d or placebo and then further randomized to either 1 g/d n-3 FAs or placebo in both the vitamin D and placebo primary randomization arms.

In multivariate analysis adjusted for age, sex, race, and other supplement arm, vitamin D alone was associated with a hazard ratio (HR) of 0.68 (P = .02) for incident autoimmune disease, n-3 alone was associated with a nonsignificant HR of 0.74, and the combination was associated with an HR of 0.69 (P = .03). However, when probable incident autoimmune disease cases were included, the effect of n-3 became significant, with an HR of 0.82.
 

VITAL Now

In the current analysis, Dr. Costenbader and colleagues reported observational data on 21,592 VITAL participants, a sample representing 83.5% of those who were initially randomized, and 87.9% of those who were alive and could be contacted at the end of the study.

As in the initial trial, the investigators used annual questionnaires to assess incident autoimmune diseases during the randomized follow-up. Participants were asked about new-onset, doctor-diagnosed rheumatoid arthritis, polymyalgia rheumatica, psoriasis, autoimmune thyroid disease, and inflammatory bowel disease. Participants could also write in any other new autoimmune disease diagnoses.

There were 236 new cases of confirmed autoimmune disease that occurred since the initial publication of the trial results, as well as 65 probable cases identified during the median 5.3 years of the randomized portion, and 42 probable cases diagnosed during the 2-year observational phase.

The investigators found that after the 2-year observation period, 255 participants initially randomized to receive vitamin D had a newly developed confirmed autoimmune disease, compared with 259 of those initially randomized to a vitamin D placebo. This translated into a nonsignificant HR of 0.98.

Adding probable autoimmune cases to the confirmed cases made little difference, resulting in a nonsignificant adjusted HR of 0.95.

In contrast, there were 234 confirmed autoimmune disease cases among patients initially assigned to n-3, compared with 280 among patients randomized to the n-3 placebo, translating into a statistically significant HR of 0.83 for new-onset autoimmune disease with n-3.

Dr. Costenbader and colleagues acknowledged that the study was limited by the use of doses intended to prevent cancer or cardiovascular disease and that higher doses intended for high-risk or nutritionally deficient populations might reveal larger effects of supplementation. In addition, they noted the difficulty of identifying the timing and onset of incident disease, and that the small number of cases that occurred during the 2-year observational period precluded detailed analyses of individual autoimmune diseases.

The study was funded by grants from the National Institutes of Health. Dr. Costenbader, Dr. Funk, and Dr. Kremer reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Two years after the end of a randomized trial that showed a benefit of daily vitamin D and omega-3 fatty acid (n-3 FA) supplementation for reducing risk for autoimmune diseases, the salubrious effects of daily vitamin D appear to have waned after the supplement was discontinued, while the protection from n-3 lived on for at least 2 additional years.

As previously reported, the randomized VITAL, which was designed primarily to study the effects of vitamin D and n-3 supplementation on incident cancer and cardiovascular disease, also showed that 5 years of vitamin D supplementation was associated with a 22% reduction in risk for confirmed autoimmune diseases, and 5 years of n-3 FA supplementation was associated with an 18% reduction in confirmed and probable incident autoimmune diseases.

Now, investigators Karen H. Costenbader, MD, MPH, of Brigham & Women’s Hospital in Boston, Massachusetts, and colleagues reported that among 21,592 participants in VITAL who agreed to be followed for an additional 2 years after discontinuation, the protection against autoimmune diseases from daily vitamin D (cholecalciferol; 2000 IU/d) was no longer statistically significant, but the benefits of daily marine n-3 FAs (1 g/d as a fish-oil capsule containing 460 mg of eicosapentaenoic acid and 380 mg of docosahexaenoic acid) remained significant.

“VITAL observational extension results suggest that vitamin D supplementation should be given on a continuous basis for long-term prevention of [autoimmune diseases]. The beneficial effects of n-3 fatty acids, however, may be prolonged for at least 2 years after discontinuation,” they wrote in an article published in Arthritis & Rheumatology.

Dr. Costenbader told this news organization that the results of the observational extension study suggest that the benefits of vitamin D “wear off more quickly, and it should be continued for a longer period of time or indefinitely, rather than only for 5 years.”

In addition to the disparity in the duration of the protective effect, the investigators also saw differences in the effects across different autoimmune diseases.

“The protective effect of vitamin D seemed strongest for psoriasis, while for omega-3 fatty acids, the protective effects were strongest for rheumatoid arthritis and inflammatory bowel disease,” she said.
 

Mixed Effects

In an interview with this news organization, Janet Funk, MD, MS, vice chair of research in the Department of Medicine and professor in the School of Nutritional Science and Wellness at the University of Arizona, Tucson, Arizona, who was not involved in the study, saidthat the results suggest that while each supplement may offer protection against autoimmune diseases, the effects are inconsistent and may not apply to all patients.

“I think the VITAL extension results suggest that either supplement (or both together) may have benefits in reducing risk of autoimmune diseases, including possible persistent effects posttreatment, but that these effects are nuanced (ie, only in normal weight post-vitamin D treatment) and possibly not uniform across all autoimmune diseases (including possible adverse effects for some — eg, inverse association between prior omega-3 and psoriasis and tendency for increased autoimmune thyroid disease for vitamin D), although the study was not powered sufficiently to draw disease-specific conclusions,” she said.

In an editorial accompanying the study, rheumatologist Joel M. Kremer, MD, of Albany Medical College and the Corrona Research Foundation in Delray Beach, Florida, wrote that “[T]he studies by Dr. Costenbader, et al. have shed new light on the possibility that dietary supplements of n-3 FA [fatty acid] may prevent the onset of [autoimmune disease]. The sustained benefits they describe for as long as 2 years after the supplements are discontinued are consistent with the chronicity of FA species in cellular plasma membranes where they serve as substrates for a diverse array of salient metabolic and inflammatory pathways.”
 

VITAL Then

To test whether vitamin D or marine-derived long-chain n-3 FA supplementation could protect against autoimmune disease over time, Dr. Costenbader and colleagues piggybacked an ancillary study onto the VITAL trial, which had primary outcomes of cancer and cardiovascular disease incidence.

A total of 25,871 participants were enrolled, including 12,786 men aged 50 and older and 13,085 women aged 55 and older. The study had a 2 × 2 factorial design, with patients randomly assigned to vitamin D 2000 IU/d or placebo and then further randomized to either 1 g/d n-3 FAs or placebo in both the vitamin D and placebo primary randomization arms.

In multivariate analysis adjusted for age, sex, race, and other supplement arm, vitamin D alone was associated with a hazard ratio (HR) of 0.68 (P = .02) for incident autoimmune disease, n-3 alone was associated with a nonsignificant HR of 0.74, and the combination was associated with an HR of 0.69 (P = .03). However, when probable incident autoimmune disease cases were included, the effect of n-3 became significant, with an HR of 0.82.
 

VITAL Now

In the current analysis, Dr. Costenbader and colleagues reported observational data on 21,592 VITAL participants, a sample representing 83.5% of those who were initially randomized, and 87.9% of those who were alive and could be contacted at the end of the study.

As in the initial trial, the investigators used annual questionnaires to assess incident autoimmune diseases during the randomized follow-up. Participants were asked about new-onset, doctor-diagnosed rheumatoid arthritis, polymyalgia rheumatica, psoriasis, autoimmune thyroid disease, and inflammatory bowel disease. Participants could also write in any other new autoimmune disease diagnoses.

There were 236 new cases of confirmed autoimmune disease that occurred since the initial publication of the trial results, as well as 65 probable cases identified during the median 5.3 years of the randomized portion, and 42 probable cases diagnosed during the 2-year observational phase.

The investigators found that after the 2-year observation period, 255 participants initially randomized to receive vitamin D had a newly developed confirmed autoimmune disease, compared with 259 of those initially randomized to a vitamin D placebo. This translated into a nonsignificant HR of 0.98.

Adding probable autoimmune cases to the confirmed cases made little difference, resulting in a nonsignificant adjusted HR of 0.95.

In contrast, there were 234 confirmed autoimmune disease cases among patients initially assigned to n-3, compared with 280 among patients randomized to the n-3 placebo, translating into a statistically significant HR of 0.83 for new-onset autoimmune disease with n-3.

Dr. Costenbader and colleagues acknowledged that the study was limited by the use of doses intended to prevent cancer or cardiovascular disease and that higher doses intended for high-risk or nutritionally deficient populations might reveal larger effects of supplementation. In addition, they noted the difficulty of identifying the timing and onset of incident disease, and that the small number of cases that occurred during the 2-year observational period precluded detailed analyses of individual autoimmune diseases.

The study was funded by grants from the National Institutes of Health. Dr. Costenbader, Dr. Funk, and Dr. Kremer reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

It’s not always great to be tops among your peers.

For physicians with student debt, half carry more than $200,000 and 26% carry more than $300,000, according to Medscape Medical News’ 2023 Residents Salary and Debt Report.

I’m smack in that upper percentile. I amassed nearly a half million dollars in student debt and currently stand at roughly $400,000. Yay me.

As a naive twentysomething making a major life decision, I never thought my loans would amount to this inconceivable figure, the proverbial “mortgage without a roof” you hear student debt experts talk about.

This isn’t a story about how the student loan industry needs to be reformed or how education has become increasingly expensive or regrets about going to medical school.

It’s also not a story about how you should be handling basics like consolidating and refinancing and paying extra toward your principal.

It’s about my experience as a physician 13 years after signing that first promissory note. In short: I completely miscalculated the impact loans would have on my life.

I bought money to go to school. I can’t undo that. But over the past decade, I have learned a lot, particularly how those with their own mountain of debt — or who will inevitably wind up with one — can manage things better than I have.

Mistake #1: Loan Forgiveness Is More Complicated Than it Seems

My parents and I were aware of the Public Service Loan Forgiveness (PSLF) program which began in 2007 shortly before I started exploring medical school options. I wanted to help people, so working in the nonprofit sector sounded like a no-brainer. Making 120 payments while practicing at a qualifying institution didn’t sound hard.

Newsflash: Not all healthcare organizations are 501(c)3 programs that qualify as nonprofit for the PSLF program. You can’t just snap your fingers and land at one. I graduated from fellowship just as the COVID-19 pandemic began, which meant I was launching my medical career in the midst of hiring freezes and an overnight disappearance of job opportunities.

I had to take a 2-year hiatus from the nonprofit sector and found a part-time position with a local private practice group. It still stings. Had I been working for a qualified employer, I could have benefited from the student loan payment pause and been closer to applying for loan forgiveness.

Avoid it: Be brutally honest with yourself about what kind of medicine you want to practice — especially within the opportunities you have on hand. Private practice is very different from working for the nonprofit sector. I didn›t know that. When weighing career choices, immediately ask, “How will this impact how I pay my loans?” You may not like the answer, but you›ll always know where you stand financially.

Mistake #2: I Forgot to Factor in Life Goals

To be fair, some things were out of my control: Not getting into a state school with cheaper tuition rates, graduating at the start of a once-in-a-lifetime global pandemic. I wasn’t prepared for a changing job landscape. But there were also “expected” life events like getting married, developing a geographical preference, and having a child. I didn’t consider those either.

How about the “expected” goal of buying a home? For years I didn’t feel financially comfortable enough to take on a mortgage. For so long, my attitude has been don’t take on any more debt. (A special shout-out to my 6.8% interest rate which has contributed over a third of my total loan amount.)

This even affected how my husband and I would talk about what a future home might look like. There’s always a giant unwelcome guest casting a shadow over my thoughts.

Avoid it: Don’t compartmentalize your personal and professional lives. Your student loans will hang over both, and you need to be honest with yourself about what “upward mobility” really means to you while in debt. There’s a reason people say “live like a resident” until your loans are paid off. My husband and I finally worked our numbers to where we bought our first home this past year — a moment years in the making. I still drive around in my beloved Honda CR-V like it’s a Mercedes G-Wagon.

Mistake #3: I Didn’t Ask Questions

I regret not talking to a practicing physician about their experience with student loans. I didn’t know any. There weren’t any physicians in my extended family or my community network. I was a first-generation Pakistani American kid trying to figure it out.

It’s difficult because even today, many physicians aren’t comfortable discussing their financial circumstances. The lack of financial transparency and even financial literacy is astounding among young medical professionals. We live in a medical culture where no one talks about the money. I was too diffident and nervous to even try.

Avoid it: Don’t be afraid to have uncomfortable conversations about money. Don’t allow yourself to make even one passive decision. It’s your life.

If you can’t find someone in medicine to talk to about their financial journey, there are plenty of credible resources. Medscape Medical News has a Physician Business Academy with hot topics like personal finance. The White Coat Investor is literally bookmarked on all my electronic devices. KevinMD.com has a ton of resources and articles answering common financial questions about retirement, savings, and house buying. And Travis Hornsby with www.studentloanplanner.com has wonderful advice on all kinds of different loans.

There are no stupid questions. Just ask. You might be surprised by what people are willing to share.

Mistake #4: Playing it Casual With My Lenders

If $400,000 in debt doesn’t sound bad enough, imagine lots more. It turns out my loan carrier had me at a much higher loan balance because they’d inadvertently duplicated one of my loans in the total. I didn’t know that until I transferred my loans to another handler and it came to light.

Imagine my relief at having a lower total. Imagine my anger at myself for not checking sooner.

Avoid it: Do a thorough self-audit on all your loans more than once a year. Pretend they’re a patient with odd symptoms you can’t pin down and you have the luxury of doing every diagnostic test available. It’s not fun studying your own debt, but it’s the only way to really know how much you have.

Mistake #5: Not Leaving Room to Change My Mind

I underestimated how I would evolve and how my goals would change after having the letters “MD” after my name. I never dreamed that a nonprofit salary might not be enough.

A lot of us assume that the bedside is where we will find professional satisfaction. But you might be surprised. In a climate where we’re constantly being pushed to do more in a broken healthcare system, a landscape where misinformation and technology are forcing medicine to change, there might be little joy in working clinically full time. Then what do you do?

Because I elected to go the PSLF route, I’m tied to this decision. And while it still makes the most economic sense for me personally, it now limits my professional exploration and freedom.

Avoid it: Consider how much time you really want to spend in clinical medicine. Be mindful that you have to work at least 0.8 full time equivalent to qualify for the PSLF program. It’s very hard to predict the future, let alone your future, but just know you›ll have moments where you ask, “Do I really want to stay on this career track?” Will you be able to pivot? Can you live with it if the answer is no?

Looking Ahead

Let me be clear about one thing. Despite all the negativity I feel toward my student loans — guilt about the burden I brought to my marriage and my adult life, disappointment about the cost of becoming a successful physician, and frustration that this has turned out to be the most influential factor shaping my professional and personal choices — the one thing I don’t feel is shame.

I worked hard to get to this point in my life. I am proud of being a physician.

My student loan burden will follow me to the grave. But progress is also possible. I have friends that have paid their loans down by hustling, working hard, and dropping every penny toward them.

I also have friends that have had their loans forgiven. There are options. Everyone’s experience looks a little different. But don’t be naive: Student loans will color every financial decision you make.

I’m finding solace now in recently moving and finding work at a nonprofit institution. I’m back at it; 77 payments made, and 43 to go.

Well, technically I’ve made 93 payments. I’m still waiting for my loan servicer to get around to updating my account.

You really have to stay on top of those folks.

A version of this article appeared on Medscape.com.

It’s not always great to be tops among your peers.

For physicians with student debt, half carry more than $200,000 and 26% carry more than $300,000, according to Medscape Medical News’ 2023 Residents Salary and Debt Report.

I’m smack in that upper percentile. I amassed nearly a half million dollars in student debt and currently stand at roughly $400,000. Yay me.

As a naive twentysomething making a major life decision, I never thought my loans would amount to this inconceivable figure, the proverbial “mortgage without a roof” you hear student debt experts talk about.

This isn’t a story about how the student loan industry needs to be reformed or how education has become increasingly expensive or regrets about going to medical school.

It’s also not a story about how you should be handling basics like consolidating and refinancing and paying extra toward your principal.

It’s about my experience as a physician 13 years after signing that first promissory note. In short: I completely miscalculated the impact loans would have on my life.

I bought money to go to school. I can’t undo that. But over the past decade, I have learned a lot, particularly how those with their own mountain of debt — or who will inevitably wind up with one — can manage things better than I have.

Mistake #1: Loan Forgiveness Is More Complicated Than it Seems

My parents and I were aware of the Public Service Loan Forgiveness (PSLF) program which began in 2007 shortly before I started exploring medical school options. I wanted to help people, so working in the nonprofit sector sounded like a no-brainer. Making 120 payments while practicing at a qualifying institution didn’t sound hard.

Newsflash: Not all healthcare organizations are 501(c)3 programs that qualify as nonprofit for the PSLF program. You can’t just snap your fingers and land at one. I graduated from fellowship just as the COVID-19 pandemic began, which meant I was launching my medical career in the midst of hiring freezes and an overnight disappearance of job opportunities.

I had to take a 2-year hiatus from the nonprofit sector and found a part-time position with a local private practice group. It still stings. Had I been working for a qualified employer, I could have benefited from the student loan payment pause and been closer to applying for loan forgiveness.

Avoid it: Be brutally honest with yourself about what kind of medicine you want to practice — especially within the opportunities you have on hand. Private practice is very different from working for the nonprofit sector. I didn›t know that. When weighing career choices, immediately ask, “How will this impact how I pay my loans?” You may not like the answer, but you›ll always know where you stand financially.

Mistake #2: I Forgot to Factor in Life Goals

To be fair, some things were out of my control: Not getting into a state school with cheaper tuition rates, graduating at the start of a once-in-a-lifetime global pandemic. I wasn’t prepared for a changing job landscape. But there were also “expected” life events like getting married, developing a geographical preference, and having a child. I didn’t consider those either.

How about the “expected” goal of buying a home? For years I didn’t feel financially comfortable enough to take on a mortgage. For so long, my attitude has been don’t take on any more debt. (A special shout-out to my 6.8% interest rate which has contributed over a third of my total loan amount.)

This even affected how my husband and I would talk about what a future home might look like. There’s always a giant unwelcome guest casting a shadow over my thoughts.

Avoid it: Don’t compartmentalize your personal and professional lives. Your student loans will hang over both, and you need to be honest with yourself about what “upward mobility” really means to you while in debt. There’s a reason people say “live like a resident” until your loans are paid off. My husband and I finally worked our numbers to where we bought our first home this past year — a moment years in the making. I still drive around in my beloved Honda CR-V like it’s a Mercedes G-Wagon.

Mistake #3: I Didn’t Ask Questions

I regret not talking to a practicing physician about their experience with student loans. I didn’t know any. There weren’t any physicians in my extended family or my community network. I was a first-generation Pakistani American kid trying to figure it out.

It’s difficult because even today, many physicians aren’t comfortable discussing their financial circumstances. The lack of financial transparency and even financial literacy is astounding among young medical professionals. We live in a medical culture where no one talks about the money. I was too diffident and nervous to even try.

Avoid it: Don’t be afraid to have uncomfortable conversations about money. Don’t allow yourself to make even one passive decision. It’s your life.

If you can’t find someone in medicine to talk to about their financial journey, there are plenty of credible resources. Medscape Medical News has a Physician Business Academy with hot topics like personal finance. The White Coat Investor is literally bookmarked on all my electronic devices. KevinMD.com has a ton of resources and articles answering common financial questions about retirement, savings, and house buying. And Travis Hornsby with www.studentloanplanner.com has wonderful advice on all kinds of different loans.

There are no stupid questions. Just ask. You might be surprised by what people are willing to share.

Mistake #4: Playing it Casual With My Lenders

If $400,000 in debt doesn’t sound bad enough, imagine lots more. It turns out my loan carrier had me at a much higher loan balance because they’d inadvertently duplicated one of my loans in the total. I didn’t know that until I transferred my loans to another handler and it came to light.

Imagine my relief at having a lower total. Imagine my anger at myself for not checking sooner.

Avoid it: Do a thorough self-audit on all your loans more than once a year. Pretend they’re a patient with odd symptoms you can’t pin down and you have the luxury of doing every diagnostic test available. It’s not fun studying your own debt, but it’s the only way to really know how much you have.

Mistake #5: Not Leaving Room to Change My Mind

I underestimated how I would evolve and how my goals would change after having the letters “MD” after my name. I never dreamed that a nonprofit salary might not be enough.

A lot of us assume that the bedside is where we will find professional satisfaction. But you might be surprised. In a climate where we’re constantly being pushed to do more in a broken healthcare system, a landscape where misinformation and technology are forcing medicine to change, there might be little joy in working clinically full time. Then what do you do?

Because I elected to go the PSLF route, I’m tied to this decision. And while it still makes the most economic sense for me personally, it now limits my professional exploration and freedom.

Avoid it: Consider how much time you really want to spend in clinical medicine. Be mindful that you have to work at least 0.8 full time equivalent to qualify for the PSLF program. It’s very hard to predict the future, let alone your future, but just know you›ll have moments where you ask, “Do I really want to stay on this career track?” Will you be able to pivot? Can you live with it if the answer is no?

Looking Ahead

Let me be clear about one thing. Despite all the negativity I feel toward my student loans — guilt about the burden I brought to my marriage and my adult life, disappointment about the cost of becoming a successful physician, and frustration that this has turned out to be the most influential factor shaping my professional and personal choices — the one thing I don’t feel is shame.

I worked hard to get to this point in my life. I am proud of being a physician.

My student loan burden will follow me to the grave. But progress is also possible. I have friends that have paid their loans down by hustling, working hard, and dropping every penny toward them.

I also have friends that have had their loans forgiven. There are options. Everyone’s experience looks a little different. But don’t be naive: Student loans will color every financial decision you make.

I’m finding solace now in recently moving and finding work at a nonprofit institution. I’m back at it; 77 payments made, and 43 to go.

Well, technically I’ve made 93 payments. I’m still waiting for my loan servicer to get around to updating my account.

You really have to stay on top of those folks.

A version of this article appeared on Medscape.com.

It’s not always great to be tops among your peers.

For physicians with student debt, half carry more than $200,000 and 26% carry more than $300,000, according to Medscape Medical News’ 2023 Residents Salary and Debt Report.

I’m smack in that upper percentile. I amassed nearly a half million dollars in student debt and currently stand at roughly $400,000. Yay me.

As a naive twentysomething making a major life decision, I never thought my loans would amount to this inconceivable figure, the proverbial “mortgage without a roof” you hear student debt experts talk about.

This isn’t a story about how the student loan industry needs to be reformed or how education has become increasingly expensive or regrets about going to medical school.

It’s also not a story about how you should be handling basics like consolidating and refinancing and paying extra toward your principal.

It’s about my experience as a physician 13 years after signing that first promissory note. In short: I completely miscalculated the impact loans would have on my life.

I bought money to go to school. I can’t undo that. But over the past decade, I have learned a lot, particularly how those with their own mountain of debt — or who will inevitably wind up with one — can manage things better than I have.

Mistake #1: Loan Forgiveness Is More Complicated Than it Seems

My parents and I were aware of the Public Service Loan Forgiveness (PSLF) program which began in 2007 shortly before I started exploring medical school options. I wanted to help people, so working in the nonprofit sector sounded like a no-brainer. Making 120 payments while practicing at a qualifying institution didn’t sound hard.

Newsflash: Not all healthcare organizations are 501(c)3 programs that qualify as nonprofit for the PSLF program. You can’t just snap your fingers and land at one. I graduated from fellowship just as the COVID-19 pandemic began, which meant I was launching my medical career in the midst of hiring freezes and an overnight disappearance of job opportunities.

I had to take a 2-year hiatus from the nonprofit sector and found a part-time position with a local private practice group. It still stings. Had I been working for a qualified employer, I could have benefited from the student loan payment pause and been closer to applying for loan forgiveness.

Avoid it: Be brutally honest with yourself about what kind of medicine you want to practice — especially within the opportunities you have on hand. Private practice is very different from working for the nonprofit sector. I didn›t know that. When weighing career choices, immediately ask, “How will this impact how I pay my loans?” You may not like the answer, but you›ll always know where you stand financially.

Mistake #2: I Forgot to Factor in Life Goals

To be fair, some things were out of my control: Not getting into a state school with cheaper tuition rates, graduating at the start of a once-in-a-lifetime global pandemic. I wasn’t prepared for a changing job landscape. But there were also “expected” life events like getting married, developing a geographical preference, and having a child. I didn’t consider those either.

How about the “expected” goal of buying a home? For years I didn’t feel financially comfortable enough to take on a mortgage. For so long, my attitude has been don’t take on any more debt. (A special shout-out to my 6.8% interest rate which has contributed over a third of my total loan amount.)

This even affected how my husband and I would talk about what a future home might look like. There’s always a giant unwelcome guest casting a shadow over my thoughts.

Avoid it: Don’t compartmentalize your personal and professional lives. Your student loans will hang over both, and you need to be honest with yourself about what “upward mobility” really means to you while in debt. There’s a reason people say “live like a resident” until your loans are paid off. My husband and I finally worked our numbers to where we bought our first home this past year — a moment years in the making. I still drive around in my beloved Honda CR-V like it’s a Mercedes G-Wagon.

Mistake #3: I Didn’t Ask Questions

I regret not talking to a practicing physician about their experience with student loans. I didn’t know any. There weren’t any physicians in my extended family or my community network. I was a first-generation Pakistani American kid trying to figure it out.

It’s difficult because even today, many physicians aren’t comfortable discussing their financial circumstances. The lack of financial transparency and even financial literacy is astounding among young medical professionals. We live in a medical culture where no one talks about the money. I was too diffident and nervous to even try.

Avoid it: Don’t be afraid to have uncomfortable conversations about money. Don’t allow yourself to make even one passive decision. It’s your life.

If you can’t find someone in medicine to talk to about their financial journey, there are plenty of credible resources. Medscape Medical News has a Physician Business Academy with hot topics like personal finance. The White Coat Investor is literally bookmarked on all my electronic devices. KevinMD.com has a ton of resources and articles answering common financial questions about retirement, savings, and house buying. And Travis Hornsby with www.studentloanplanner.com has wonderful advice on all kinds of different loans.

There are no stupid questions. Just ask. You might be surprised by what people are willing to share.

Mistake #4: Playing it Casual With My Lenders

If $400,000 in debt doesn’t sound bad enough, imagine lots more. It turns out my loan carrier had me at a much higher loan balance because they’d inadvertently duplicated one of my loans in the total. I didn’t know that until I transferred my loans to another handler and it came to light.

Imagine my relief at having a lower total. Imagine my anger at myself for not checking sooner.

Avoid it: Do a thorough self-audit on all your loans more than once a year. Pretend they’re a patient with odd symptoms you can’t pin down and you have the luxury of doing every diagnostic test available. It’s not fun studying your own debt, but it’s the only way to really know how much you have.

Mistake #5: Not Leaving Room to Change My Mind

I underestimated how I would evolve and how my goals would change after having the letters “MD” after my name. I never dreamed that a nonprofit salary might not be enough.

A lot of us assume that the bedside is where we will find professional satisfaction. But you might be surprised. In a climate where we’re constantly being pushed to do more in a broken healthcare system, a landscape where misinformation and technology are forcing medicine to change, there might be little joy in working clinically full time. Then what do you do?

Because I elected to go the PSLF route, I’m tied to this decision. And while it still makes the most economic sense for me personally, it now limits my professional exploration and freedom.

Avoid it: Consider how much time you really want to spend in clinical medicine. Be mindful that you have to work at least 0.8 full time equivalent to qualify for the PSLF program. It’s very hard to predict the future, let alone your future, but just know you›ll have moments where you ask, “Do I really want to stay on this career track?” Will you be able to pivot? Can you live with it if the answer is no?

Looking Ahead

Let me be clear about one thing. Despite all the negativity I feel toward my student loans — guilt about the burden I brought to my marriage and my adult life, disappointment about the cost of becoming a successful physician, and frustration that this has turned out to be the most influential factor shaping my professional and personal choices — the one thing I don’t feel is shame.

I worked hard to get to this point in my life. I am proud of being a physician.

My student loan burden will follow me to the grave. But progress is also possible. I have friends that have paid their loans down by hustling, working hard, and dropping every penny toward them.

I also have friends that have had their loans forgiven. There are options. Everyone’s experience looks a little different. But don’t be naive: Student loans will color every financial decision you make.

I’m finding solace now in recently moving and finding work at a nonprofit institution. I’m back at it; 77 payments made, and 43 to go.

Well, technically I’ve made 93 payments. I’m still waiting for my loan servicer to get around to updating my account.

You really have to stay on top of those folks.

A version of this article appeared on Medscape.com.

Patients with calcium pyrophosphate deposition (CPPD) disease, also known as pseudogout, have an 80% higher risk for fracture than individuals who do not have the disease, according to a new analysis.

This trend was driven by wrist fractures, where there was a more than threefold increased risk.

Previous studies identified an association between CPPD and low bone mineral density, and there is growing evidence suggesting that the dysregulation of osteoprotegerin — a molecule that is important in the regulation of osteoclasts — may be associated with early-onset CPPD, noted Sara K. Tedeschi, MD, MPH, the lead author of the study and head of crystal-induced arthritic diseases at Brigham and Women’s Hospital, Boston, Massachusetts.

However, CPPD’s association with fracture risk has yet to be explored.

In the study, Dr. Tedeschi and colleagues used Mass General Brigham electronic health record (EHR) data from 1991 to 2023 to identify 1148 individuals with acute calcium pyrophosphate (CPP) crystal arthritis. The index date was defined as the first documentation of pseudogout or synovial fluid CPP crystals. These patients were matched to 3730 comparators based on healthcare encounters within 30 days of the index date of a patient with CPPD. Patients were also matched based on the year of their first EHR encounter. Patients with a fracture documented prior to the index date were excluded from the analysis.

The primary outcome was the first fracture of the humerus, knee, wrist, hip, or pelvis, detected via published algorithms using diagnostic and procedural codes.

The research was published on January 14 in Arthritis & Rheumatology.

Although participants were not matched on age or sex, the average age was 73, and most participants were female. In total, 83.1% of participants in the CPPD group and 80.0% of those in the control group were White.

After adjustment for confounding factors including age, sex, comorbidities, and glucocorticoid use, CPPD was associated with an 80% higher risk for any fracture (hazard risk [HR], 1.8). Fracture risk was highest for the wrist (HR, 3.6).

Patients with CPPD had a 40% higher risk to experience a humerus or pelvis fracture and a 30% higher risk for hip fractures, but the results were not statistically significant.

The results were similar for sensitivity analyses that excluded patients who were prescribed glucocorticoids, treatment for osteoporosis, or had a diagnosis of rheumatoid arthritis.

Asked to comment, John D. FitzGerald, MD, PhD, clinical chief of rheumatology at the University of California, Los Angeles, noted that these associations were “convincing and strong. I thought it was a very good study and important work. CPPD is common and osteoporosis is common, so better understanding the connection is important.”

It’s still not clear why the risk for wrist fractures was highest, but Dr. Tedeschi had two hypotheses. The researchers were unable to assess for falls in this dataset, but it’s possible that patients with CPPD experiencing joint pain could fall and try to brace themselves with an outstretched arm, leading to a wrist fracture.

CPPD also commonly affects the wrist, “so it’s possible that if CPPD is affecting the wrist and if there is an association between CPPD and low bone density, maybe there’s particularly low bone density at the wrist,” she said.

Dr. FitzGerald agreed that both hypotheses were plausible, but “with the retrospective study, there could be a lot of things that are unobserved or unexplained,” he added.

Dr. Tedeschi is interested in exploring what could be causing the association with an increased fracture risk in future research.

“I hope this draws attention to the fact that people with CPPD can have related medical problems that are outside of their joints,” added Dr. Tedeschi. “Thinking about routine screening for osteopenia and osteoporosis could be a good first step in patients with CPPD.”

The study was funded by grants from the US National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Tedeschi has worked as a consultant for Novartis. Dr. FitzGerald reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Patients with calcium pyrophosphate deposition (CPPD) disease, also known as pseudogout, have an 80% higher risk for fracture than individuals who do not have the disease, according to a new analysis.

This trend was driven by wrist fractures, where there was a more than threefold increased risk.

Previous studies identified an association between CPPD and low bone mineral density, and there is growing evidence suggesting that the dysregulation of osteoprotegerin — a molecule that is important in the regulation of osteoclasts — may be associated with early-onset CPPD, noted Sara K. Tedeschi, MD, MPH, the lead author of the study and head of crystal-induced arthritic diseases at Brigham and Women’s Hospital, Boston, Massachusetts.

However, CPPD’s association with fracture risk has yet to be explored.

In the study, Dr. Tedeschi and colleagues used Mass General Brigham electronic health record (EHR) data from 1991 to 2023 to identify 1148 individuals with acute calcium pyrophosphate (CPP) crystal arthritis. The index date was defined as the first documentation of pseudogout or synovial fluid CPP crystals. These patients were matched to 3730 comparators based on healthcare encounters within 30 days of the index date of a patient with CPPD. Patients were also matched based on the year of their first EHR encounter. Patients with a fracture documented prior to the index date were excluded from the analysis.

The primary outcome was the first fracture of the humerus, knee, wrist, hip, or pelvis, detected via published algorithms using diagnostic and procedural codes.

The research was published on January 14 in Arthritis & Rheumatology.

Although participants were not matched on age or sex, the average age was 73, and most participants were female. In total, 83.1% of participants in the CPPD group and 80.0% of those in the control group were White.

After adjustment for confounding factors including age, sex, comorbidities, and glucocorticoid use, CPPD was associated with an 80% higher risk for any fracture (hazard risk [HR], 1.8). Fracture risk was highest for the wrist (HR, 3.6).

Patients with CPPD had a 40% higher risk to experience a humerus or pelvis fracture and a 30% higher risk for hip fractures, but the results were not statistically significant.

The results were similar for sensitivity analyses that excluded patients who were prescribed glucocorticoids, treatment for osteoporosis, or had a diagnosis of rheumatoid arthritis.

Asked to comment, John D. FitzGerald, MD, PhD, clinical chief of rheumatology at the University of California, Los Angeles, noted that these associations were “convincing and strong. I thought it was a very good study and important work. CPPD is common and osteoporosis is common, so better understanding the connection is important.”

It’s still not clear why the risk for wrist fractures was highest, but Dr. Tedeschi had two hypotheses. The researchers were unable to assess for falls in this dataset, but it’s possible that patients with CPPD experiencing joint pain could fall and try to brace themselves with an outstretched arm, leading to a wrist fracture.

CPPD also commonly affects the wrist, “so it’s possible that if CPPD is affecting the wrist and if there is an association between CPPD and low bone density, maybe there’s particularly low bone density at the wrist,” she said.

Dr. FitzGerald agreed that both hypotheses were plausible, but “with the retrospective study, there could be a lot of things that are unobserved or unexplained,” he added.

Dr. Tedeschi is interested in exploring what could be causing the association with an increased fracture risk in future research.

“I hope this draws attention to the fact that people with CPPD can have related medical problems that are outside of their joints,” added Dr. Tedeschi. “Thinking about routine screening for osteopenia and osteoporosis could be a good first step in patients with CPPD.”

The study was funded by grants from the US National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Tedeschi has worked as a consultant for Novartis. Dr. FitzGerald reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Patients with calcium pyrophosphate deposition (CPPD) disease, also known as pseudogout, have an 80% higher risk for fracture than individuals who do not have the disease, according to a new analysis.

This trend was driven by wrist fractures, where there was a more than threefold increased risk.

Previous studies identified an association between CPPD and low bone mineral density, and there is growing evidence suggesting that the dysregulation of osteoprotegerin — a molecule that is important in the regulation of osteoclasts — may be associated with early-onset CPPD, noted Sara K. Tedeschi, MD, MPH, the lead author of the study and head of crystal-induced arthritic diseases at Brigham and Women’s Hospital, Boston, Massachusetts.

However, CPPD’s association with fracture risk has yet to be explored.

In the study, Dr. Tedeschi and colleagues used Mass General Brigham electronic health record (EHR) data from 1991 to 2023 to identify 1148 individuals with acute calcium pyrophosphate (CPP) crystal arthritis. The index date was defined as the first documentation of pseudogout or synovial fluid CPP crystals. These patients were matched to 3730 comparators based on healthcare encounters within 30 days of the index date of a patient with CPPD. Patients were also matched based on the year of their first EHR encounter. Patients with a fracture documented prior to the index date were excluded from the analysis.

The primary outcome was the first fracture of the humerus, knee, wrist, hip, or pelvis, detected via published algorithms using diagnostic and procedural codes.

The research was published on January 14 in Arthritis & Rheumatology.

Although participants were not matched on age or sex, the average age was 73, and most participants were female. In total, 83.1% of participants in the CPPD group and 80.0% of those in the control group were White.

After adjustment for confounding factors including age, sex, comorbidities, and glucocorticoid use, CPPD was associated with an 80% higher risk for any fracture (hazard risk [HR], 1.8). Fracture risk was highest for the wrist (HR, 3.6).

Patients with CPPD had a 40% higher risk to experience a humerus or pelvis fracture and a 30% higher risk for hip fractures, but the results were not statistically significant.

The results were similar for sensitivity analyses that excluded patients who were prescribed glucocorticoids, treatment for osteoporosis, or had a diagnosis of rheumatoid arthritis.

Asked to comment, John D. FitzGerald, MD, PhD, clinical chief of rheumatology at the University of California, Los Angeles, noted that these associations were “convincing and strong. I thought it was a very good study and important work. CPPD is common and osteoporosis is common, so better understanding the connection is important.”

It’s still not clear why the risk for wrist fractures was highest, but Dr. Tedeschi had two hypotheses. The researchers were unable to assess for falls in this dataset, but it’s possible that patients with CPPD experiencing joint pain could fall and try to brace themselves with an outstretched arm, leading to a wrist fracture.

CPPD also commonly affects the wrist, “so it’s possible that if CPPD is affecting the wrist and if there is an association between CPPD and low bone density, maybe there’s particularly low bone density at the wrist,” she said.

Dr. FitzGerald agreed that both hypotheses were plausible, but “with the retrospective study, there could be a lot of things that are unobserved or unexplained,” he added.

Dr. Tedeschi is interested in exploring what could be causing the association with an increased fracture risk in future research.

“I hope this draws attention to the fact that people with CPPD can have related medical problems that are outside of their joints,” added Dr. Tedeschi. “Thinking about routine screening for osteopenia and osteoporosis could be a good first step in patients with CPPD.”

The study was funded by grants from the US National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Tedeschi has worked as a consultant for Novartis. Dr. FitzGerald reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

Adults with axial spondyloarthritis (axSpA) with longstanding back pain symptoms had response rates to nonsteroidal anti-inflammatory drugs (NSAIDs) that were no different from patients with non-axSpA back pain of similar duration, according to findings from a prospective study.

METHODOLOGY:

The researchers recruited 233 consecutive outpatients with chronic back pain, including 68 with axSpA and 165 with non-axSpA back pain.

The mean ages of the participants in the axSpA and non-axSpA groups were 42.7 years and 49.3 years, respectively; symptom durations were approximately 15 years in both groups.

Participants were given NSAIDs and “any response” was defined as back pain improvement of more than two units on the Numerical Rating Scale, while “good response” was defined as an improvement of > 50% compared with baseline.

TAKEAWAY: 

After 4 weeks, 30.9% of patients with axSpA and 29.1% of patients with non-axSpA back pain had any response, and 23.5% and 16.4% of patients with axSpA and non-axSpA back pain, respectively, had a good response.

The proportion of patients showing improvement ranged from 19% to 31% in both groups after 4 weeks of treatment.

No significant differences in response appeared in subgroups of patients based on inflammatory back pain stage or in different axSpA stages.

IN PRACTICE:

“We think that this information has an effect on clinical practice since a response to NSAIDs is an important criterion in the ASAS [Assessment of SpondyloArthritis international Society]/European Alliance of Associations for Rheumatology treatment recommendations that may influence decisions to initiate treatment with biologic or targeted-synthetic DMARDs [disease-modifying antirheumatic drugs]. Further, a good response to NSAIDs is also an important clinical feature in the ASAS classification criteria,” the researchers wrote.

SOURCE: 

The lead author on the study was Xenofon Baraliakos, MD, of Ruhr University Bochum, Germany. The study was published online on January 15, 2024, in The Journal of Rheumatology.

LIMITATIONS:

The uneven sex match in the diagnoses and the history of NSAID treatment among patients in both groups were potential limiting factors. The researchers also noted that a similarly conducted study in patients with early disease could have findings that are “much different.”

DISCLOSURES:

The study was sponsored in part by Novartis. The researchers reported no relevant financial relationships. 
 

A version of this article appeared on Medscape.com.

TOPLINE:

Adults with axial spondyloarthritis (axSpA) with longstanding back pain symptoms had response rates to nonsteroidal anti-inflammatory drugs (NSAIDs) that were no different from patients with non-axSpA back pain of similar duration, according to findings from a prospective study.

METHODOLOGY:

The researchers recruited 233 consecutive outpatients with chronic back pain, including 68 with axSpA and 165 with non-axSpA back pain.

The mean ages of the participants in the axSpA and non-axSpA groups were 42.7 years and 49.3 years, respectively; symptom durations were approximately 15 years in both groups.

Participants were given NSAIDs and “any response” was defined as back pain improvement of more than two units on the Numerical Rating Scale, while “good response” was defined as an improvement of > 50% compared with baseline.

TAKEAWAY: 

After 4 weeks, 30.9% of patients with axSpA and 29.1% of patients with non-axSpA back pain had any response, and 23.5% and 16.4% of patients with axSpA and non-axSpA back pain, respectively, had a good response.

The proportion of patients showing improvement ranged from 19% to 31% in both groups after 4 weeks of treatment.

No significant differences in response appeared in subgroups of patients based on inflammatory back pain stage or in different axSpA stages.

IN PRACTICE:

“We think that this information has an effect on clinical practice since a response to NSAIDs is an important criterion in the ASAS [Assessment of SpondyloArthritis international Society]/European Alliance of Associations for Rheumatology treatment recommendations that may influence decisions to initiate treatment with biologic or targeted-synthetic DMARDs [disease-modifying antirheumatic drugs]. Further, a good response to NSAIDs is also an important clinical feature in the ASAS classification criteria,” the researchers wrote.

SOURCE: 

The lead author on the study was Xenofon Baraliakos, MD, of Ruhr University Bochum, Germany. The study was published online on January 15, 2024, in The Journal of Rheumatology.

LIMITATIONS:

The uneven sex match in the diagnoses and the history of NSAID treatment among patients in both groups were potential limiting factors. The researchers also noted that a similarly conducted study in patients with early disease could have findings that are “much different.”

DISCLOSURES:

The study was sponsored in part by Novartis. The researchers reported no relevant financial relationships. 
 

A version of this article appeared on Medscape.com.

TOPLINE:

Adults with axial spondyloarthritis (axSpA) with longstanding back pain symptoms had response rates to nonsteroidal anti-inflammatory drugs (NSAIDs) that were no different from patients with non-axSpA back pain of similar duration, according to findings from a prospective study.

METHODOLOGY:

The researchers recruited 233 consecutive outpatients with chronic back pain, including 68 with axSpA and 165 with non-axSpA back pain.

The mean ages of the participants in the axSpA and non-axSpA groups were 42.7 years and 49.3 years, respectively; symptom durations were approximately 15 years in both groups.

Participants were given NSAIDs and “any response” was defined as back pain improvement of more than two units on the Numerical Rating Scale, while “good response” was defined as an improvement of > 50% compared with baseline.

TAKEAWAY: 

After 4 weeks, 30.9% of patients with axSpA and 29.1% of patients with non-axSpA back pain had any response, and 23.5% and 16.4% of patients with axSpA and non-axSpA back pain, respectively, had a good response.

The proportion of patients showing improvement ranged from 19% to 31% in both groups after 4 weeks of treatment.

No significant differences in response appeared in subgroups of patients based on inflammatory back pain stage or in different axSpA stages.

IN PRACTICE:

“We think that this information has an effect on clinical practice since a response to NSAIDs is an important criterion in the ASAS [Assessment of SpondyloArthritis international Society]/European Alliance of Associations for Rheumatology treatment recommendations that may influence decisions to initiate treatment with biologic or targeted-synthetic DMARDs [disease-modifying antirheumatic drugs]. Further, a good response to NSAIDs is also an important clinical feature in the ASAS classification criteria,” the researchers wrote.

SOURCE: 

The lead author on the study was Xenofon Baraliakos, MD, of Ruhr University Bochum, Germany. The study was published online on January 15, 2024, in The Journal of Rheumatology.

LIMITATIONS:

The uneven sex match in the diagnoses and the history of NSAID treatment among patients in both groups were potential limiting factors. The researchers also noted that a similarly conducted study in patients with early disease could have findings that are “much different.”

DISCLOSURES:

The study was sponsored in part by Novartis. The researchers reported no relevant financial relationships. 
 

A version of this article appeared on Medscape.com.

There is insufficient evidence that drugs targeting the Janus kinase–signal transducer and activator of transcription (JAK-STAT) pathway increase the risk of cardiovascular or thrombotic complications in people undergoing treatment for a variety of dermatological conditions, at least in the short term, say the authors of a new meta-analysis published in JAMA Dermatology.

Considering data on over 17,000 patients with different dermatoses from 45 placebo-controlled randomized clinical trials with an average follow up of 16 weeks, they found there was no significant increase in the occurrence of major adverse cardiovascular events (MACE) or venous thromboembolism (VTE) in people with dermatoses treated with JAK-STAT inhibitors, compared with placebo.

The I² statistic was 0.00% for both MACE and VTE comparing the two arms, indicating that the results were unlikely to be due to chance. There was no increased risk in MACE between those on placebo and those on JAK-STAT inhibitors, with a risk ratio (RR) of 0.47; or for VTE risk, with an RR of 0.46.

Similar findings were obtained when data were analyzed according to the dermatological condition being treated, mechanism of action of the medication, or whether the medication carried a boxed warning.

These data “suggest inconsistency with established sentiments,” that JAK-STAT inhibitors increase the risk for cardiovascular events, Patrick Ireland, MD, of the University of New South Wales, Randwick, Australia, and coauthors wrote in the article. “This may be owing to the limited time frames in which these rare events could be adequately captured, or the ages of enrolled patients being too young to realize the well established heightened risks of developing MACE and VTE,” they suggested.

However, the findings challenge the notion that the cardiovascular complications of these drugs are the same in all patients; dermatological use may not be associated with the same risks as with use for rheumatologic indications.
 

Class-Wide Boxed Warning

“JAK-STAT [inhibitors] have had some pretty indemnifying data against their use, with the ORAL [Surveillance] study demonstrating increased all-cause mortality, cardiovascular events, venous thromboembolism, and malignancy,” Dr. Ireland said in an interview.

ORAL Surveillance was an open-label, postmarketing trial conducted in patients with rheumatoid arthritis treated with tofacitinib or a tumor necrosis factor (TNF) inhibitor. The results led the US Food and Drug Administration to require information about the risks of serious heart-related events, cancer, blood clots, and death in a boxed warning for JAK-STAT inhibitors in 2022.

“I think it’s important to recognize that these [ORAL Surveillance participants] are very different patients to the typical dermatological patient being treated with a JAK-STAT [inhibitors], with newer studies demonstrating a much safer profile than initially thought,” Dr. Ireland said.
 

Examining Risk in Dermatological Conditions

The meta-analysis performed by Dr. Ireland and associates focused specifically on the risk for MACE and VTE in patients being treated for dermatological conditions, and included trials published up until June 2023. Only trials that had included a placebo arm were considered; pooled analyses, long-term extension trial data, post hoc analyses, and pediatric-specific trials were excluded.

Most (25) of the trials were phase 2b or phase 3 trials, 18 were phase 2 to 2b, and two were phase 1 trials. The studies included 12,996 participants, mostly with atopic dermatitis or psoriasis, who were treated with JAK-STAT inhibitors, which included baricitinib (2846 patients), tofacitinib (2470), upadacitinib (2218), abrocitinib (1904), and deucravacitinib (1492), among others. There were 4925 patients on placebo.

Overall, MACE — defined as a combined endpoint of acute myocardial infarction, stroke, cardiovascular mortality, heart failure, and unstable angina, as well as arterial embolism — occurred in 13 of the JAK-STAT inhibitor-treated patients and in four of those on placebo. VTE — defined as deep vein thrombosis, pulmonary embolism, and any unusual site thrombosis — was reported in eight JAK-STAT inhibitor-treated patients and in one patient on placebo.

The pooled incidence ratios for MACE and VTE were calculated as 0.20 per 100 person exposure years (PEY) for JAK-STAT inhibitor treatment and 0.13 PEY for placebo. The pooled RRs comparing the two treatment groups were a respective 1.13 for MACE and 2.79 for VTE, but neither RR reached statistical significance.

No difference was seen between the treatment arms in terms of treatment emergent adverse events (RR, 1.05), serious adverse events (RR, 0.92), or study discontinuation because of adverse events (RR, 0.94).
 

Reassuring Results?

Dr. Ireland and coauthors said the finding should help to reassure clinicians that the short-term use of JAK-STAT inhibitors in patients with dermatological conditions with low cardiovascular risk profiles “appears to be both safe and well tolerated.” They cautioned, however, that “clinicians must remain judicious” when using these medications for longer periods and in high-risk patient populations.

This was a pragmatic meta-analysis that provides useful information for dermatologists, Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, DC, said in an interview.

“When there are safety concerns, I think that’s where data like this are so important to not just allay the fears of practitioners, but also to arm the practitioner with information for when they discuss a possible treatment with a patient,” said Dr. Friedman, who was not involved in the study.

“What’s unique here is that they’re looking at any possible use of JAK inhibitors for dermatological disease,” so this represents patients that dermatologists would be seeing, he added.

“The limitation here is time, we only can say so much about the safety of the medication with the data that we have,” Dr. Friedman said. Almost 4 months is “a good amount of time” to know about the cardiovascular risks, he said, but added, what happens then? Will the risk increase and will patients need to be switched to another medication?

“There’s no line in the sand,” with regard to using a JAK-STAT inhibitor. “If you look at the label, they’re not meant to be used incrementally,” but as ongoing treatment, while considering the needs of the patient and the relative risks and benefits, he said.

With that in mind, “the open label extension studies for all these [JAK-STAT inhibitors] are really, really important to get a sense of ‘do new signals emerge down the road.’ ”

The meta-analysis received no commercial funding. One author of the work reported personal fees from several pharmaceutical companies which were done outside of analysis. Dr. Friedman has received research funding from or acted as a consultant for several pharmaceutical companies including, Incyte, Pfizer, Eli Lily, and AbbVie.

There is insufficient evidence that drugs targeting the Janus kinase–signal transducer and activator of transcription (JAK-STAT) pathway increase the risk of cardiovascular or thrombotic complications in people undergoing treatment for a variety of dermatological conditions, at least in the short term, say the authors of a new meta-analysis published in JAMA Dermatology.

Considering data on over 17,000 patients with different dermatoses from 45 placebo-controlled randomized clinical trials with an average follow up of 16 weeks, they found there was no significant increase in the occurrence of major adverse cardiovascular events (MACE) or venous thromboembolism (VTE) in people with dermatoses treated with JAK-STAT inhibitors, compared with placebo.

The I² statistic was 0.00% for both MACE and VTE comparing the two arms, indicating that the results were unlikely to be due to chance. There was no increased risk in MACE between those on placebo and those on JAK-STAT inhibitors, with a risk ratio (RR) of 0.47; or for VTE risk, with an RR of 0.46.

Similar findings were obtained when data were analyzed according to the dermatological condition being treated, mechanism of action of the medication, or whether the medication carried a boxed warning.

These data “suggest inconsistency with established sentiments,” that JAK-STAT inhibitors increase the risk for cardiovascular events, Patrick Ireland, MD, of the University of New South Wales, Randwick, Australia, and coauthors wrote in the article. “This may be owing to the limited time frames in which these rare events could be adequately captured, or the ages of enrolled patients being too young to realize the well established heightened risks of developing MACE and VTE,” they suggested.

However, the findings challenge the notion that the cardiovascular complications of these drugs are the same in all patients; dermatological use may not be associated with the same risks as with use for rheumatologic indications.
 

Class-Wide Boxed Warning

“JAK-STAT [inhibitors] have had some pretty indemnifying data against their use, with the ORAL [Surveillance] study demonstrating increased all-cause mortality, cardiovascular events, venous thromboembolism, and malignancy,” Dr. Ireland said in an interview.

ORAL Surveillance was an open-label, postmarketing trial conducted in patients with rheumatoid arthritis treated with tofacitinib or a tumor necrosis factor (TNF) inhibitor. The results led the US Food and Drug Administration to require information about the risks of serious heart-related events, cancer, blood clots, and death in a boxed warning for JAK-STAT inhibitors in 2022.

“I think it’s important to recognize that these [ORAL Surveillance participants] are very different patients to the typical dermatological patient being treated with a JAK-STAT [inhibitors], with newer studies demonstrating a much safer profile than initially thought,” Dr. Ireland said.
 

Examining Risk in Dermatological Conditions

The meta-analysis performed by Dr. Ireland and associates focused specifically on the risk for MACE and VTE in patients being treated for dermatological conditions, and included trials published up until June 2023. Only trials that had included a placebo arm were considered; pooled analyses, long-term extension trial data, post hoc analyses, and pediatric-specific trials were excluded.

Most (25) of the trials were phase 2b or phase 3 trials, 18 were phase 2 to 2b, and two were phase 1 trials. The studies included 12,996 participants, mostly with atopic dermatitis or psoriasis, who were treated with JAK-STAT inhibitors, which included baricitinib (2846 patients), tofacitinib (2470), upadacitinib (2218), abrocitinib (1904), and deucravacitinib (1492), among others. There were 4925 patients on placebo.

Overall, MACE — defined as a combined endpoint of acute myocardial infarction, stroke, cardiovascular mortality, heart failure, and unstable angina, as well as arterial embolism — occurred in 13 of the JAK-STAT inhibitor-treated patients and in four of those on placebo. VTE — defined as deep vein thrombosis, pulmonary embolism, and any unusual site thrombosis — was reported in eight JAK-STAT inhibitor-treated patients and in one patient on placebo.

The pooled incidence ratios for MACE and VTE were calculated as 0.20 per 100 person exposure years (PEY) for JAK-STAT inhibitor treatment and 0.13 PEY for placebo. The pooled RRs comparing the two treatment groups were a respective 1.13 for MACE and 2.79 for VTE, but neither RR reached statistical significance.

No difference was seen between the treatment arms in terms of treatment emergent adverse events (RR, 1.05), serious adverse events (RR, 0.92), or study discontinuation because of adverse events (RR, 0.94).
 

Reassuring Results?

Dr. Ireland and coauthors said the finding should help to reassure clinicians that the short-term use of JAK-STAT inhibitors in patients with dermatological conditions with low cardiovascular risk profiles “appears to be both safe and well tolerated.” They cautioned, however, that “clinicians must remain judicious” when using these medications for longer periods and in high-risk patient populations.

This was a pragmatic meta-analysis that provides useful information for dermatologists, Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, DC, said in an interview.

“When there are safety concerns, I think that’s where data like this are so important to not just allay the fears of practitioners, but also to arm the practitioner with information for when they discuss a possible treatment with a patient,” said Dr. Friedman, who was not involved in the study.

“What’s unique here is that they’re looking at any possible use of JAK inhibitors for dermatological disease,” so this represents patients that dermatologists would be seeing, he added.

“The limitation here is time, we only can say so much about the safety of the medication with the data that we have,” Dr. Friedman said. Almost 4 months is “a good amount of time” to know about the cardiovascular risks, he said, but added, what happens then? Will the risk increase and will patients need to be switched to another medication?

“There’s no line in the sand,” with regard to using a JAK-STAT inhibitor. “If you look at the label, they’re not meant to be used incrementally,” but as ongoing treatment, while considering the needs of the patient and the relative risks and benefits, he said.

With that in mind, “the open label extension studies for all these [JAK-STAT inhibitors] are really, really important to get a sense of ‘do new signals emerge down the road.’ ”

The meta-analysis received no commercial funding. One author of the work reported personal fees from several pharmaceutical companies which were done outside of analysis. Dr. Friedman has received research funding from or acted as a consultant for several pharmaceutical companies including, Incyte, Pfizer, Eli Lily, and AbbVie.

There is insufficient evidence that drugs targeting the Janus kinase–signal transducer and activator of transcription (JAK-STAT) pathway increase the risk of cardiovascular or thrombotic complications in people undergoing treatment for a variety of dermatological conditions, at least in the short term, say the authors of a new meta-analysis published in JAMA Dermatology.

Considering data on over 17,000 patients with different dermatoses from 45 placebo-controlled randomized clinical trials with an average follow up of 16 weeks, they found there was no significant increase in the occurrence of major adverse cardiovascular events (MACE) or venous thromboembolism (VTE) in people with dermatoses treated with JAK-STAT inhibitors, compared with placebo.

The I² statistic was 0.00% for both MACE and VTE comparing the two arms, indicating that the results were unlikely to be due to chance. There was no increased risk in MACE between those on placebo and those on JAK-STAT inhibitors, with a risk ratio (RR) of 0.47; or for VTE risk, with an RR of 0.46.

Similar findings were obtained when data were analyzed according to the dermatological condition being treated, mechanism of action of the medication, or whether the medication carried a boxed warning.

These data “suggest inconsistency with established sentiments,” that JAK-STAT inhibitors increase the risk for cardiovascular events, Patrick Ireland, MD, of the University of New South Wales, Randwick, Australia, and coauthors wrote in the article. “This may be owing to the limited time frames in which these rare events could be adequately captured, or the ages of enrolled patients being too young to realize the well established heightened risks of developing MACE and VTE,” they suggested.

However, the findings challenge the notion that the cardiovascular complications of these drugs are the same in all patients; dermatological use may not be associated with the same risks as with use for rheumatologic indications.
 

Class-Wide Boxed Warning

“JAK-STAT [inhibitors] have had some pretty indemnifying data against their use, with the ORAL [Surveillance] study demonstrating increased all-cause mortality, cardiovascular events, venous thromboembolism, and malignancy,” Dr. Ireland said in an interview.

ORAL Surveillance was an open-label, postmarketing trial conducted in patients with rheumatoid arthritis treated with tofacitinib or a tumor necrosis factor (TNF) inhibitor. The results led the US Food and Drug Administration to require information about the risks of serious heart-related events, cancer, blood clots, and death in a boxed warning for JAK-STAT inhibitors in 2022.

“I think it’s important to recognize that these [ORAL Surveillance participants] are very different patients to the typical dermatological patient being treated with a JAK-STAT [inhibitors], with newer studies demonstrating a much safer profile than initially thought,” Dr. Ireland said.
 

Examining Risk in Dermatological Conditions

The meta-analysis performed by Dr. Ireland and associates focused specifically on the risk for MACE and VTE in patients being treated for dermatological conditions, and included trials published up until June 2023. Only trials that had included a placebo arm were considered; pooled analyses, long-term extension trial data, post hoc analyses, and pediatric-specific trials were excluded.

Most (25) of the trials were phase 2b or phase 3 trials, 18 were phase 2 to 2b, and two were phase 1 trials. The studies included 12,996 participants, mostly with atopic dermatitis or psoriasis, who were treated with JAK-STAT inhibitors, which included baricitinib (2846 patients), tofacitinib (2470), upadacitinib (2218), abrocitinib (1904), and deucravacitinib (1492), among others. There were 4925 patients on placebo.

Overall, MACE — defined as a combined endpoint of acute myocardial infarction, stroke, cardiovascular mortality, heart failure, and unstable angina, as well as arterial embolism — occurred in 13 of the JAK-STAT inhibitor-treated patients and in four of those on placebo. VTE — defined as deep vein thrombosis, pulmonary embolism, and any unusual site thrombosis — was reported in eight JAK-STAT inhibitor-treated patients and in one patient on placebo.

The pooled incidence ratios for MACE and VTE were calculated as 0.20 per 100 person exposure years (PEY) for JAK-STAT inhibitor treatment and 0.13 PEY for placebo. The pooled RRs comparing the two treatment groups were a respective 1.13 for MACE and 2.79 for VTE, but neither RR reached statistical significance.

No difference was seen between the treatment arms in terms of treatment emergent adverse events (RR, 1.05), serious adverse events (RR, 0.92), or study discontinuation because of adverse events (RR, 0.94).
 

Reassuring Results?

Dr. Ireland and coauthors said the finding should help to reassure clinicians that the short-term use of JAK-STAT inhibitors in patients with dermatological conditions with low cardiovascular risk profiles “appears to be both safe and well tolerated.” They cautioned, however, that “clinicians must remain judicious” when using these medications for longer periods and in high-risk patient populations.

This was a pragmatic meta-analysis that provides useful information for dermatologists, Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, DC, said in an interview.

“When there are safety concerns, I think that’s where data like this are so important to not just allay the fears of practitioners, but also to arm the practitioner with information for when they discuss a possible treatment with a patient,” said Dr. Friedman, who was not involved in the study.

“What’s unique here is that they’re looking at any possible use of JAK inhibitors for dermatological disease,” so this represents patients that dermatologists would be seeing, he added.

“The limitation here is time, we only can say so much about the safety of the medication with the data that we have,” Dr. Friedman said. Almost 4 months is “a good amount of time” to know about the cardiovascular risks, he said, but added, what happens then? Will the risk increase and will patients need to be switched to another medication?

“There’s no line in the sand,” with regard to using a JAK-STAT inhibitor. “If you look at the label, they’re not meant to be used incrementally,” but as ongoing treatment, while considering the needs of the patient and the relative risks and benefits, he said.

With that in mind, “the open label extension studies for all these [JAK-STAT inhibitors] are really, really important to get a sense of ‘do new signals emerge down the road.’ ”

The meta-analysis received no commercial funding. One author of the work reported personal fees from several pharmaceutical companies which were done outside of analysis. Dr. Friedman has received research funding from or acted as a consultant for several pharmaceutical companies including, Incyte, Pfizer, Eli Lily, and AbbVie.

TOPLINE:

Higher scores on the dietary inflammatory index in patients with knee osteoarthritis (KOA) were associated with an increased risk of experiencing greater pain over 10 years of follow-up.

METHODOLOGY:

• The researchers recruited 944 adults aged 50-80 years from the community; the mean age at baseline was 62.9 years, 51% were female, the mean body mass index was 27.9 kg/m2, and 60% had radiographic KOA at baseline.
• Magnetic resonance imaging was used to identify structural changes in the knee based on cartilage volume and bone marrow lesions at baseline and follow-up; knee pain was assessed using the Western Ontario and McMaster Universities Osteoarthritis Index pain questionnaire.
• Dietary inflammation was measured using energy-adjusted dietary inflammatory index (E-DII) scores based on nutritional information from the Food-Frequency Questionnaire (FFQ).

TAKEAWAY: 

• Over a follow-up period of 10.7 years, higher E-DII scores were positively associated with increased pain scores (beta = 0.21) after adjustment for age, sex, body mass index, steps per day, education, emotional problems, employment status, comorbidities, and radiographic KOA.
• E-DII scores were not associated with tibial cartilage volume loss or overall bone marrow loss.
• Patients with higher E-DII scores had a significantly higher risk of being on a moderate pain trajectory (relative risk ratio, 1.19), compared with those who followed a minimal pain trajectory over the follow-up period.

IN PRACTICE:

“An anti-inflammatory diet may reduce pain among KOA patients. Future trials investigating the potential of an anti-inflammatory diet for pain relief in KOA are warranted,” the researchers wrote. 

SOURCE:

The lead author on the study was Canchen Ma, PhD, of the University of Tasmania, Hobart, Australia. The study was published online in Arthritis Care & Research. 

LIMITATIONS:

The study used a relatively small number of nutrients from the FFQ to calculate the E-DII scores; participants also exhibited a narrower range of E-DII scores than previous studies. The researchers were unable to account for pharmacologic or preventive treatments. 

DISCLOSURES:

The study was supported by the National Health and Medical Research Council of Australia (NHMRC) and Arthritis Australia. Several authors received support from the National Heart Foundation Fellowship, the NHMRC Leadership Fellowship, the NHMRC Practitioner Fellowship, and the NHMRC Early Career Fellowship. The researchers had no financial conflicts to disclose.

A version of this article appeared on Medscape.com.