Rheumatology News

PORTLAND, ORE. – Some pernio-like/chilblains-like lesions on the toes – which became widely known as “COVID toes” – and other acral sites that have occurred during the COVID-19 pandemic are related to COVID-19 infection, while others are not, according to Lindy P. Fox, MD, professor of dermatology and director of the hospital consultation service at the University of California, San Francisco.

“We’re learning a lot about pernio because of COVID,” Dr. Fox, a member of the American Academy of Dermatology’s Ad Hoc Task Force on COVID-19, said at the annual meeting of the Pacific Dermatologic Association. “Patients with pernio tend to either have bright red or purple individual lesions or an erythromelalgia-like presentation, often waking up in the middle of the night saying ‘my feet hurt. I can’t put sheets over my feet.’ In my experience, the patients with an erythromelalgia-like presentation tend to be a lot harder to treat.”

courtesy UCSF

Establishing terminology to describe pernio-like lesions was a challenge in the early stages of the COVID-19 pandemic, Dr. Fox added, with clinicians using terms like erythema multiforme-like, coxsackie-like, or even necrotic to describe the lesions. “I don’t think pernio is truly necrotic; I think it’s really inflammatory and purpuric,” she said.

Early in the pandemic, studies suggesting a link with these cases and COVID-19 infection include a case series of 318 patients with pernio-like skin lesions who had confirmed or suspected COVID-19. Most of these patients were generally young and healthy and most had relatively mild COVID-19; 7% were laboratory-confirmed COVID-19 positive, and 6% were close contacts of patients with confirmed COVID-19. Pernio-like lesions were the only symptoms in 55% of the patients.

In another study, researchers in France evaluated the clinical, laboratory, and pathologic characteristics of 40 patients who developed chilblain-like lesions (mostly involving the toes) during the COVID-19 pandemic and were seen as outpatients in April 2020 . All were polymerase chain reaction (PCR) negative, 30% were SARS-CoV-2 serology positive, and 60% had elevated D-dimers. Histology obtained from 19 of the patients revealed lymphocytic inflammation and vascular damage, and 8 had IgA positivity.

In a retrospective analysis of seven pediatric chilblains cases during the pandemic, researchers examined the skin biopsies to evaluate histopathological features and explored the presence of SARS-CoV-2 in the tissue. All patients were PCR negative. The authors observed cytoplasmic granular positivity for SARS-CoV-2 spike protein in endothelial cells, a feature that they said showed coronavirus-like particles, consistent with SARS-CoV-2.

Not all studies in the medical literature have demonstrated an association between pernio-like/chilblains-like lesions and COVID-19, though. An analysis of 23 patients, with skin eruptions considered associated with SARS-CoV-2 infections (including 21 cases of chilblains) during the first wave of the pandemic found that the antibody and T-cell response in patients with pandemic chilblains was the same as in negative controls.

“What’s remarkably interesting about this study is that they did autopsies of samples from patients who had died prepandemic, so there was no such thing as COVID-19,” said Dr. Fox, who was not involved with the study. “They stained for viral particles in those patients, and they were positive in a subset of patients. This makes me wonder about what the significance of that staining positivity is.”

Yet another group of investigators looked at what was happening with pernio during the waves of COVID in a study of chilblains cases in children in Spain, and found a stronger association between lockdown and cold temperature, which argues against a direct association between pernio and COVID infection.

In Dr. Fox’s experience, COVID toes can recur, especially upon exposure to cold. “What taught me this in real life is a patient who I saw remotely by video,” she recalled. “It was early on in the pandemic. I could not prove he had COVID no matter how hard I tried, but I do think he had COVID toes at that time.” When he later was confirmed to have COVID, “he got pernio in the same exact location as his original suspected COVID toes.”

According to an analysis of long COVID in the skin, based on cases reported to the American Academy of Dermatology–International League of Dermatological Societies registry from April 8 to Oct. 8, 2020, pernio-like lesions lasted a median of 12 days in patients with lab-confirmed COVID-19 and a median of 15 days in those with suspected COVID-19. But almost 7% of the 103 pernio cases were long-haulers, defined as those with dermatologic signs of COVID that lasted beyond 60 days.

“There are some patients who are resistant to treatment,” Dr. Fox said. “In addition, recurrent lesions make me think that maybe all pernio is triggered by some viral cause. This causes an immunologic phenomenon that’s responding to a viral trigger you’re trying to deal with. That may be the better way to think about COVID toes.”

Different variants of COVID also appear to be changing the characteristics of dermatologic manifestations associated with infection. Results from a large retrospective analysis of nearly 350,000 users of a COVID study App in the United Kingdom found that skin lesions were more predictive of a positive test in the Delta wave, compared with the Omicron wave, while pernio-like lesions were predictive of infection in the Delta wave but not in the Omicron wave.

“And, whether you were vaccinated or unvaccinated really did not influence whether or not you were going to have a skin rash as a presenting sign of COVID, except for the burning rash, which was less in vaccinated patients,” said Dr. Fox, who was not involved with the study.

Dr. Fox reported having no relevant disclosures.

PORTLAND, ORE. – Some pernio-like/chilblains-like lesions on the toes – which became widely known as “COVID toes” – and other acral sites that have occurred during the COVID-19 pandemic are related to COVID-19 infection, while others are not, according to Lindy P. Fox, MD, professor of dermatology and director of the hospital consultation service at the University of California, San Francisco.

“We’re learning a lot about pernio because of COVID,” Dr. Fox, a member of the American Academy of Dermatology’s Ad Hoc Task Force on COVID-19, said at the annual meeting of the Pacific Dermatologic Association. “Patients with pernio tend to either have bright red or purple individual lesions or an erythromelalgia-like presentation, often waking up in the middle of the night saying ‘my feet hurt. I can’t put sheets over my feet.’ In my experience, the patients with an erythromelalgia-like presentation tend to be a lot harder to treat.”

courtesy UCSF

Establishing terminology to describe pernio-like lesions was a challenge in the early stages of the COVID-19 pandemic, Dr. Fox added, with clinicians using terms like erythema multiforme-like, coxsackie-like, or even necrotic to describe the lesions. “I don’t think pernio is truly necrotic; I think it’s really inflammatory and purpuric,” she said.

Early in the pandemic, studies suggesting a link with these cases and COVID-19 infection include a case series of 318 patients with pernio-like skin lesions who had confirmed or suspected COVID-19. Most of these patients were generally young and healthy and most had relatively mild COVID-19; 7% were laboratory-confirmed COVID-19 positive, and 6% were close contacts of patients with confirmed COVID-19. Pernio-like lesions were the only symptoms in 55% of the patients.

In another study, researchers in France evaluated the clinical, laboratory, and pathologic characteristics of 40 patients who developed chilblain-like lesions (mostly involving the toes) during the COVID-19 pandemic and were seen as outpatients in April 2020 . All were polymerase chain reaction (PCR) negative, 30% were SARS-CoV-2 serology positive, and 60% had elevated D-dimers. Histology obtained from 19 of the patients revealed lymphocytic inflammation and vascular damage, and 8 had IgA positivity.

In a retrospective analysis of seven pediatric chilblains cases during the pandemic, researchers examined the skin biopsies to evaluate histopathological features and explored the presence of SARS-CoV-2 in the tissue. All patients were PCR negative. The authors observed cytoplasmic granular positivity for SARS-CoV-2 spike protein in endothelial cells, a feature that they said showed coronavirus-like particles, consistent with SARS-CoV-2.

Not all studies in the medical literature have demonstrated an association between pernio-like/chilblains-like lesions and COVID-19, though. An analysis of 23 patients, with skin eruptions considered associated with SARS-CoV-2 infections (including 21 cases of chilblains) during the first wave of the pandemic found that the antibody and T-cell response in patients with pandemic chilblains was the same as in negative controls.

“What’s remarkably interesting about this study is that they did autopsies of samples from patients who had died prepandemic, so there was no such thing as COVID-19,” said Dr. Fox, who was not involved with the study. “They stained for viral particles in those patients, and they were positive in a subset of patients. This makes me wonder about what the significance of that staining positivity is.”

Yet another group of investigators looked at what was happening with pernio during the waves of COVID in a study of chilblains cases in children in Spain, and found a stronger association between lockdown and cold temperature, which argues against a direct association between pernio and COVID infection.

In Dr. Fox’s experience, COVID toes can recur, especially upon exposure to cold. “What taught me this in real life is a patient who I saw remotely by video,” she recalled. “It was early on in the pandemic. I could not prove he had COVID no matter how hard I tried, but I do think he had COVID toes at that time.” When he later was confirmed to have COVID, “he got pernio in the same exact location as his original suspected COVID toes.”

According to an analysis of long COVID in the skin, based on cases reported to the American Academy of Dermatology–International League of Dermatological Societies registry from April 8 to Oct. 8, 2020, pernio-like lesions lasted a median of 12 days in patients with lab-confirmed COVID-19 and a median of 15 days in those with suspected COVID-19. But almost 7% of the 103 pernio cases were long-haulers, defined as those with dermatologic signs of COVID that lasted beyond 60 days.

“There are some patients who are resistant to treatment,” Dr. Fox said. “In addition, recurrent lesions make me think that maybe all pernio is triggered by some viral cause. This causes an immunologic phenomenon that’s responding to a viral trigger you’re trying to deal with. That may be the better way to think about COVID toes.”

Different variants of COVID also appear to be changing the characteristics of dermatologic manifestations associated with infection. Results from a large retrospective analysis of nearly 350,000 users of a COVID study App in the United Kingdom found that skin lesions were more predictive of a positive test in the Delta wave, compared with the Omicron wave, while pernio-like lesions were predictive of infection in the Delta wave but not in the Omicron wave.

“And, whether you were vaccinated or unvaccinated really did not influence whether or not you were going to have a skin rash as a presenting sign of COVID, except for the burning rash, which was less in vaccinated patients,” said Dr. Fox, who was not involved with the study.

Dr. Fox reported having no relevant disclosures.

PORTLAND, ORE. – Some pernio-like/chilblains-like lesions on the toes – which became widely known as “COVID toes” – and other acral sites that have occurred during the COVID-19 pandemic are related to COVID-19 infection, while others are not, according to Lindy P. Fox, MD, professor of dermatology and director of the hospital consultation service at the University of California, San Francisco.

“We’re learning a lot about pernio because of COVID,” Dr. Fox, a member of the American Academy of Dermatology’s Ad Hoc Task Force on COVID-19, said at the annual meeting of the Pacific Dermatologic Association. “Patients with pernio tend to either have bright red or purple individual lesions or an erythromelalgia-like presentation, often waking up in the middle of the night saying ‘my feet hurt. I can’t put sheets over my feet.’ In my experience, the patients with an erythromelalgia-like presentation tend to be a lot harder to treat.”

courtesy UCSF

Establishing terminology to describe pernio-like lesions was a challenge in the early stages of the COVID-19 pandemic, Dr. Fox added, with clinicians using terms like erythema multiforme-like, coxsackie-like, or even necrotic to describe the lesions. “I don’t think pernio is truly necrotic; I think it’s really inflammatory and purpuric,” she said.

Early in the pandemic, studies suggesting a link with these cases and COVID-19 infection include a case series of 318 patients with pernio-like skin lesions who had confirmed or suspected COVID-19. Most of these patients were generally young and healthy and most had relatively mild COVID-19; 7% were laboratory-confirmed COVID-19 positive, and 6% were close contacts of patients with confirmed COVID-19. Pernio-like lesions were the only symptoms in 55% of the patients.

In another study, researchers in France evaluated the clinical, laboratory, and pathologic characteristics of 40 patients who developed chilblain-like lesions (mostly involving the toes) during the COVID-19 pandemic and were seen as outpatients in April 2020 . All were polymerase chain reaction (PCR) negative, 30% were SARS-CoV-2 serology positive, and 60% had elevated D-dimers. Histology obtained from 19 of the patients revealed lymphocytic inflammation and vascular damage, and 8 had IgA positivity.

In a retrospective analysis of seven pediatric chilblains cases during the pandemic, researchers examined the skin biopsies to evaluate histopathological features and explored the presence of SARS-CoV-2 in the tissue. All patients were PCR negative. The authors observed cytoplasmic granular positivity for SARS-CoV-2 spike protein in endothelial cells, a feature that they said showed coronavirus-like particles, consistent with SARS-CoV-2.

Not all studies in the medical literature have demonstrated an association between pernio-like/chilblains-like lesions and COVID-19, though. An analysis of 23 patients, with skin eruptions considered associated with SARS-CoV-2 infections (including 21 cases of chilblains) during the first wave of the pandemic found that the antibody and T-cell response in patients with pandemic chilblains was the same as in negative controls.

“What’s remarkably interesting about this study is that they did autopsies of samples from patients who had died prepandemic, so there was no such thing as COVID-19,” said Dr. Fox, who was not involved with the study. “They stained for viral particles in those patients, and they were positive in a subset of patients. This makes me wonder about what the significance of that staining positivity is.”

Yet another group of investigators looked at what was happening with pernio during the waves of COVID in a study of chilblains cases in children in Spain, and found a stronger association between lockdown and cold temperature, which argues against a direct association between pernio and COVID infection.

In Dr. Fox’s experience, COVID toes can recur, especially upon exposure to cold. “What taught me this in real life is a patient who I saw remotely by video,” she recalled. “It was early on in the pandemic. I could not prove he had COVID no matter how hard I tried, but I do think he had COVID toes at that time.” When he later was confirmed to have COVID, “he got pernio in the same exact location as his original suspected COVID toes.”

According to an analysis of long COVID in the skin, based on cases reported to the American Academy of Dermatology–International League of Dermatological Societies registry from April 8 to Oct. 8, 2020, pernio-like lesions lasted a median of 12 days in patients with lab-confirmed COVID-19 and a median of 15 days in those with suspected COVID-19. But almost 7% of the 103 pernio cases were long-haulers, defined as those with dermatologic signs of COVID that lasted beyond 60 days.

“There are some patients who are resistant to treatment,” Dr. Fox said. “In addition, recurrent lesions make me think that maybe all pernio is triggered by some viral cause. This causes an immunologic phenomenon that’s responding to a viral trigger you’re trying to deal with. That may be the better way to think about COVID toes.”

Different variants of COVID also appear to be changing the characteristics of dermatologic manifestations associated with infection. Results from a large retrospective analysis of nearly 350,000 users of a COVID study App in the United Kingdom found that skin lesions were more predictive of a positive test in the Delta wave, compared with the Omicron wave, while pernio-like lesions were predictive of infection in the Delta wave but not in the Omicron wave.

“And, whether you were vaccinated or unvaccinated really did not influence whether or not you were going to have a skin rash as a presenting sign of COVID, except for the burning rash, which was less in vaccinated patients,” said Dr. Fox, who was not involved with the study.

Dr. Fox reported having no relevant disclosures.

Patients with a rheumatic immune-mediated inflammatory disease (IMID) had worse outcomes, especially for mortality, after a myocardial infarction than those without an IMID, in a large propensity-matched analysis.

At a median of 2 years after their MI, Medicare beneficiaries with an IMID had adjusted risks that were:

• 15% higher for all-cause death (hazard ratio, 1.15);
• 12% higher for heart failure (HR, 1.12);
• 8% higher for recurrent MI (HR, 1.08); and
• 6% higher risk for coronary reintervention (HR, 1.06; P < .05 for all).

In addition, interventions known to improve outcomes in this context, such as coronary revascularization, were less common in patients with IMID.

“This could be because they usually are sicker and have more risk factors when they present, like kidney disease, so maybe they’re not eligible for the therapy. But by itself, it was surprising they’re not offered these interventions as common[ly] as people who don’t have the disease,” Amgad Mentias, MD, a clinical cardiologist at the Cleveland Clinic, said in an interview.

The study was published Sept. 14 in the Journal of the American Heart Association, with Dr. Mentias as senior author and Heba Wassif, MD, MPH, also with Cleveland Clinic, as first author.

IMIDs, such as rheumatoid arthritis, psoriasis, lupus, and inflammatory bowel disease, are known to be associated with significantly higher cardiovascular disease (CVD) risk due to a greater prevalence of traditional CVD risk factors and chronic systemic inflammation.

Certain disease-modifying agents may also increase patients’ cardiovascular risk. This has been a long-simmering issue for the arthritis and ulcerative colitis drug tofacitinib (Xeljanz, Xeljanz XR), resulting in an updated boxed warning in 2021.

Many of these patients also have joint disease, pain, and fatigue, which can limit physical activity, Dr. Mentias said. “So these small nuances of how to manage these patients, or balance between controlling the inflammation but also improv[ing] cardiac risk factors, is not an easy task.”

Evidence regarding post-MI events has been inconsistent and limited to smaller single-center studies, he said. After propensity-score matching, the present study included 59,820 patients with and 178,547 patients without rheumatic IMIDs followed for a maximum of 6 years.

They were drawn from a cohort of 1.6 million persons aged 65 or older in the Medicare Provider Analysis and Review (MedPAR) file who had been admitted for an MI between 2014 and 2019. Of these, 60,072 had a prior history of rheumatic IMIDs, most commonly rheumatoid arthritis (77.8%), followed by systemic lupus erythematosus (12.2%), psoriasis (5.1%), systemic sclerosis (2.8%), and myositis/dermatomyositis (1.8%).

Patients with an IMID were more often women; had a higher prevalence of valve disease, pulmonary hypertension, hypothyroidism, and anemia; and were more likely to present with non–ST-segment MI (NSTEMI).

Rates of coronary angiography (46.1% vs. 51.5%), percutaneous coronary intervention (31.6% vs. 33.6%), and coronary artery bypass grafting (7.7% vs. 10.7%) were significantly lower in patients with IMIDs who had NSTEMI, compared with patients without an IMID who had NSTEMI. Rates of these interventions were also lower in patients with IMIDs who presented with STEMI versus their peers without an IMID, at 78.2% vs. 80.7%, 70.2% vs. 71.5%, and 4.9% vs. 6.4%, respectively.

Dr. Mentias pointed out that the emerging subspecialty of cardiorheumatology is gaining traction, especially at large hospitals and academic centers, but that less than one-third of persons in the United States with an IMID are likely to be under the care of such specialists.

“It’s important before developing an MI to try and control the different risk factors and improve the risk profile for these patients as much as possible by both specialties, and then, after an unfortunate event like MI happens, it’s important to make sure we offer therapies and treatments that are known to improve outcomes,” he said.

Commenting for this article, Jon Tyler Giles, MD, a clinical researcher who focuses on cardiovascular diseases in rheumatology at Columbia University Vagelos College of Physicians and Surgeons, New York, said that “at least for rheumatoid arthritis, this is something that we already knew. People with rheumatic arthritis, when they have a heart attack, are less likely to get the standard kind of treatments and have worse outcomes. This is a little larger sample, but it’s not a surprise, not a surprise at all.”

He noted that the study could have answered questions regarding potential drivers, but “they didn’t dig down into any of the factors that were associated with the poorer outcomes in the patients with rheumatoid arthritis and lupus and scleroderma.”

Indeed, the investigators acknowledge that the study lacked information on coronary anatomy, duration and severity of the autoimmune disease, imaging data, and medications such as anti-inflammatory or immune-targeted therapies.

Dr. Giles highlighted several factors that can contribute to a poorer post-MI prognosis in patients with rheumatic diseases; these include frailty, being more hypercoaguable, increased rates of myocardial dysfunction and other heart and blood vessel diseases, and chronic treatment with steroids and nonsteroidal anti-inflammatory drugs that often interferes with anticoagulation after a MI or when putting in a stent. “So, there’s lot of moving parts, and not one single thing that is likely the answer.”

In addition, he said, “there’s always going to be a portion of these patients who, despite doing the best that we can with treatment, are going to have very severe disease. That may or may not be the subset of patients that did the worst, but likely they’re overrepresented in those patients.”

Finally, the inability to move the needle may lie with the lack of evidence-based screening and management guidelines for cardiovascular disease in any rheumatic disease, Dr. Giles observed. “There’s no guideline for us to use to decide who needs screening over and above what’s recommended for the general population, and then, even if you do screen, what do you do other than what you would normally?”

Rheumatologists are often reluctant to take up the cardiovascular screening side of things because visits are short, and a lot of that time is spent trying to manage the inflammatory components of a patient’s disease, he said. There’s also a barrier in getting some patients to add a cardiologist to the mix of physicians they already see, especially if they don’t have any symptoms.

“If someone has had an event, it’s a lot easier for people to be convinced to go see the cardiologist, obviously, but prior to having an event, the preventative side of things is something that often gets missed or goes to the wayside,” Dr. Giles said.

The study was partly funded by philanthropic gifts by the Haslam family, Bailey family, and Khouri family to the Cleveland Clinic for coauthor Dr. Milind Desai’s research. Dr. Desai is a consultant for Medtronic and Bristol Myers Squibb and serves on an executive steering committee of a BMS-sponsored trial. The remaining authors report having no relevant disclosures. Dr. Giles is a consultant on drug cardiovascular safety for Pfizer, AbbVie, and Eli Lilly.

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

Patients with a rheumatic immune-mediated inflammatory disease (IMID) had worse outcomes, especially for mortality, after a myocardial infarction than those without an IMID, in a large propensity-matched analysis.

At a median of 2 years after their MI, Medicare beneficiaries with an IMID had adjusted risks that were:

• 15% higher for all-cause death (hazard ratio, 1.15);
• 12% higher for heart failure (HR, 1.12);
• 8% higher for recurrent MI (HR, 1.08); and
• 6% higher risk for coronary reintervention (HR, 1.06; P < .05 for all).

In addition, interventions known to improve outcomes in this context, such as coronary revascularization, were less common in patients with IMID.

“This could be because they usually are sicker and have more risk factors when they present, like kidney disease, so maybe they’re not eligible for the therapy. But by itself, it was surprising they’re not offered these interventions as common[ly] as people who don’t have the disease,” Amgad Mentias, MD, a clinical cardiologist at the Cleveland Clinic, said in an interview.

The study was published Sept. 14 in the Journal of the American Heart Association, with Dr. Mentias as senior author and Heba Wassif, MD, MPH, also with Cleveland Clinic, as first author.

IMIDs, such as rheumatoid arthritis, psoriasis, lupus, and inflammatory bowel disease, are known to be associated with significantly higher cardiovascular disease (CVD) risk due to a greater prevalence of traditional CVD risk factors and chronic systemic inflammation.

Certain disease-modifying agents may also increase patients’ cardiovascular risk. This has been a long-simmering issue for the arthritis and ulcerative colitis drug tofacitinib (Xeljanz, Xeljanz XR), resulting in an updated boxed warning in 2021.

Many of these patients also have joint disease, pain, and fatigue, which can limit physical activity, Dr. Mentias said. “So these small nuances of how to manage these patients, or balance between controlling the inflammation but also improv[ing] cardiac risk factors, is not an easy task.”

Evidence regarding post-MI events has been inconsistent and limited to smaller single-center studies, he said. After propensity-score matching, the present study included 59,820 patients with and 178,547 patients without rheumatic IMIDs followed for a maximum of 6 years.

They were drawn from a cohort of 1.6 million persons aged 65 or older in the Medicare Provider Analysis and Review (MedPAR) file who had been admitted for an MI between 2014 and 2019. Of these, 60,072 had a prior history of rheumatic IMIDs, most commonly rheumatoid arthritis (77.8%), followed by systemic lupus erythematosus (12.2%), psoriasis (5.1%), systemic sclerosis (2.8%), and myositis/dermatomyositis (1.8%).

Patients with an IMID were more often women; had a higher prevalence of valve disease, pulmonary hypertension, hypothyroidism, and anemia; and were more likely to present with non–ST-segment MI (NSTEMI).

Rates of coronary angiography (46.1% vs. 51.5%), percutaneous coronary intervention (31.6% vs. 33.6%), and coronary artery bypass grafting (7.7% vs. 10.7%) were significantly lower in patients with IMIDs who had NSTEMI, compared with patients without an IMID who had NSTEMI. Rates of these interventions were also lower in patients with IMIDs who presented with STEMI versus their peers without an IMID, at 78.2% vs. 80.7%, 70.2% vs. 71.5%, and 4.9% vs. 6.4%, respectively.

Dr. Mentias pointed out that the emerging subspecialty of cardiorheumatology is gaining traction, especially at large hospitals and academic centers, but that less than one-third of persons in the United States with an IMID are likely to be under the care of such specialists.

“It’s important before developing an MI to try and control the different risk factors and improve the risk profile for these patients as much as possible by both specialties, and then, after an unfortunate event like MI happens, it’s important to make sure we offer therapies and treatments that are known to improve outcomes,” he said.

Commenting for this article, Jon Tyler Giles, MD, a clinical researcher who focuses on cardiovascular diseases in rheumatology at Columbia University Vagelos College of Physicians and Surgeons, New York, said that “at least for rheumatoid arthritis, this is something that we already knew. People with rheumatic arthritis, when they have a heart attack, are less likely to get the standard kind of treatments and have worse outcomes. This is a little larger sample, but it’s not a surprise, not a surprise at all.”

He noted that the study could have answered questions regarding potential drivers, but “they didn’t dig down into any of the factors that were associated with the poorer outcomes in the patients with rheumatoid arthritis and lupus and scleroderma.”

Indeed, the investigators acknowledge that the study lacked information on coronary anatomy, duration and severity of the autoimmune disease, imaging data, and medications such as anti-inflammatory or immune-targeted therapies.

Dr. Giles highlighted several factors that can contribute to a poorer post-MI prognosis in patients with rheumatic diseases; these include frailty, being more hypercoaguable, increased rates of myocardial dysfunction and other heart and blood vessel diseases, and chronic treatment with steroids and nonsteroidal anti-inflammatory drugs that often interferes with anticoagulation after a MI or when putting in a stent. “So, there’s lot of moving parts, and not one single thing that is likely the answer.”

In addition, he said, “there’s always going to be a portion of these patients who, despite doing the best that we can with treatment, are going to have very severe disease. That may or may not be the subset of patients that did the worst, but likely they’re overrepresented in those patients.”

Finally, the inability to move the needle may lie with the lack of evidence-based screening and management guidelines for cardiovascular disease in any rheumatic disease, Dr. Giles observed. “There’s no guideline for us to use to decide who needs screening over and above what’s recommended for the general population, and then, even if you do screen, what do you do other than what you would normally?”

Rheumatologists are often reluctant to take up the cardiovascular screening side of things because visits are short, and a lot of that time is spent trying to manage the inflammatory components of a patient’s disease, he said. There’s also a barrier in getting some patients to add a cardiologist to the mix of physicians they already see, especially if they don’t have any symptoms.

“If someone has had an event, it’s a lot easier for people to be convinced to go see the cardiologist, obviously, but prior to having an event, the preventative side of things is something that often gets missed or goes to the wayside,” Dr. Giles said.

The study was partly funded by philanthropic gifts by the Haslam family, Bailey family, and Khouri family to the Cleveland Clinic for coauthor Dr. Milind Desai’s research. Dr. Desai is a consultant for Medtronic and Bristol Myers Squibb and serves on an executive steering committee of a BMS-sponsored trial. The remaining authors report having no relevant disclosures. Dr. Giles is a consultant on drug cardiovascular safety for Pfizer, AbbVie, and Eli Lilly.

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

Patients with a rheumatic immune-mediated inflammatory disease (IMID) had worse outcomes, especially for mortality, after a myocardial infarction than those without an IMID, in a large propensity-matched analysis.

At a median of 2 years after their MI, Medicare beneficiaries with an IMID had adjusted risks that were:

• 15% higher for all-cause death (hazard ratio, 1.15);
• 12% higher for heart failure (HR, 1.12);
• 8% higher for recurrent MI (HR, 1.08); and
• 6% higher risk for coronary reintervention (HR, 1.06; P < .05 for all).

In addition, interventions known to improve outcomes in this context, such as coronary revascularization, were less common in patients with IMID.

“This could be because they usually are sicker and have more risk factors when they present, like kidney disease, so maybe they’re not eligible for the therapy. But by itself, it was surprising they’re not offered these interventions as common[ly] as people who don’t have the disease,” Amgad Mentias, MD, a clinical cardiologist at the Cleveland Clinic, said in an interview.

The study was published Sept. 14 in the Journal of the American Heart Association, with Dr. Mentias as senior author and Heba Wassif, MD, MPH, also with Cleveland Clinic, as first author.

IMIDs, such as rheumatoid arthritis, psoriasis, lupus, and inflammatory bowel disease, are known to be associated with significantly higher cardiovascular disease (CVD) risk due to a greater prevalence of traditional CVD risk factors and chronic systemic inflammation.

Certain disease-modifying agents may also increase patients’ cardiovascular risk. This has been a long-simmering issue for the arthritis and ulcerative colitis drug tofacitinib (Xeljanz, Xeljanz XR), resulting in an updated boxed warning in 2021.

Many of these patients also have joint disease, pain, and fatigue, which can limit physical activity, Dr. Mentias said. “So these small nuances of how to manage these patients, or balance between controlling the inflammation but also improv[ing] cardiac risk factors, is not an easy task.”

Evidence regarding post-MI events has been inconsistent and limited to smaller single-center studies, he said. After propensity-score matching, the present study included 59,820 patients with and 178,547 patients without rheumatic IMIDs followed for a maximum of 6 years.

They were drawn from a cohort of 1.6 million persons aged 65 or older in the Medicare Provider Analysis and Review (MedPAR) file who had been admitted for an MI between 2014 and 2019. Of these, 60,072 had a prior history of rheumatic IMIDs, most commonly rheumatoid arthritis (77.8%), followed by systemic lupus erythematosus (12.2%), psoriasis (5.1%), systemic sclerosis (2.8%), and myositis/dermatomyositis (1.8%).

Patients with an IMID were more often women; had a higher prevalence of valve disease, pulmonary hypertension, hypothyroidism, and anemia; and were more likely to present with non–ST-segment MI (NSTEMI).

Rates of coronary angiography (46.1% vs. 51.5%), percutaneous coronary intervention (31.6% vs. 33.6%), and coronary artery bypass grafting (7.7% vs. 10.7%) were significantly lower in patients with IMIDs who had NSTEMI, compared with patients without an IMID who had NSTEMI. Rates of these interventions were also lower in patients with IMIDs who presented with STEMI versus their peers without an IMID, at 78.2% vs. 80.7%, 70.2% vs. 71.5%, and 4.9% vs. 6.4%, respectively.

Dr. Mentias pointed out that the emerging subspecialty of cardiorheumatology is gaining traction, especially at large hospitals and academic centers, but that less than one-third of persons in the United States with an IMID are likely to be under the care of such specialists.

“It’s important before developing an MI to try and control the different risk factors and improve the risk profile for these patients as much as possible by both specialties, and then, after an unfortunate event like MI happens, it’s important to make sure we offer therapies and treatments that are known to improve outcomes,” he said.

Commenting for this article, Jon Tyler Giles, MD, a clinical researcher who focuses on cardiovascular diseases in rheumatology at Columbia University Vagelos College of Physicians and Surgeons, New York, said that “at least for rheumatoid arthritis, this is something that we already knew. People with rheumatic arthritis, when they have a heart attack, are less likely to get the standard kind of treatments and have worse outcomes. This is a little larger sample, but it’s not a surprise, not a surprise at all.”

He noted that the study could have answered questions regarding potential drivers, but “they didn’t dig down into any of the factors that were associated with the poorer outcomes in the patients with rheumatoid arthritis and lupus and scleroderma.”

Indeed, the investigators acknowledge that the study lacked information on coronary anatomy, duration and severity of the autoimmune disease, imaging data, and medications such as anti-inflammatory or immune-targeted therapies.

Dr. Giles highlighted several factors that can contribute to a poorer post-MI prognosis in patients with rheumatic diseases; these include frailty, being more hypercoaguable, increased rates of myocardial dysfunction and other heart and blood vessel diseases, and chronic treatment with steroids and nonsteroidal anti-inflammatory drugs that often interferes with anticoagulation after a MI or when putting in a stent. “So, there’s lot of moving parts, and not one single thing that is likely the answer.”

In addition, he said, “there’s always going to be a portion of these patients who, despite doing the best that we can with treatment, are going to have very severe disease. That may or may not be the subset of patients that did the worst, but likely they’re overrepresented in those patients.”

Finally, the inability to move the needle may lie with the lack of evidence-based screening and management guidelines for cardiovascular disease in any rheumatic disease, Dr. Giles observed. “There’s no guideline for us to use to decide who needs screening over and above what’s recommended for the general population, and then, even if you do screen, what do you do other than what you would normally?”

Rheumatologists are often reluctant to take up the cardiovascular screening side of things because visits are short, and a lot of that time is spent trying to manage the inflammatory components of a patient’s disease, he said. There’s also a barrier in getting some patients to add a cardiologist to the mix of physicians they already see, especially if they don’t have any symptoms.

“If someone has had an event, it’s a lot easier for people to be convinced to go see the cardiologist, obviously, but prior to having an event, the preventative side of things is something that often gets missed or goes to the wayside,” Dr. Giles said.

The study was partly funded by philanthropic gifts by the Haslam family, Bailey family, and Khouri family to the Cleveland Clinic for coauthor Dr. Milind Desai’s research. Dr. Desai is a consultant for Medtronic and Bristol Myers Squibb and serves on an executive steering committee of a BMS-sponsored trial. The remaining authors report having no relevant disclosures. Dr. Giles is a consultant on drug cardiovascular safety for Pfizer, AbbVie, and Eli Lilly.

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

MILAN – The day after deucravacitinib became the first TYK2 inhibitor approved for the treatment of moderate to severe psoriasis, long-term data were presented at the annual congress of the European Academy of Dermatology and Venereology, suggesting that a high degree of benefit persists for at least 2 years, making this oral drug a potential competitor for biologics.

As a once-daily drug, deucravacitinib has “the potential to be a treatment of choice and a new standard of care for patients who require systemic therapy for their moderate to severe plaque psoriasis,” said Mark G. Lebwohl, MD, professor of dermatology and dean of clinical therapeutics, Icahn School of Medicine at Mount Sinai, New York.

Just 2 months after the 52-week data from the phase 3 POETYK PSO-1 trial were published online in the Journal of the American Academy of Dermatology, a long-term extension study found essentially no loss of benefit at 112 weeks, according to Dr. Lebwohl.

One of the two co-primary endpoints was a 75% clearance on the Psoriasis and Severity Index (PASI75) score. At 52 weeks, 80.2% of patients on deucravacitinib had met this criterion of benefit. At 112 weeks, the proportion was 84.4%.

The other primary endpoint was a static Physician’s Global Assessment (sPGA) score of clear or almost clear skin. The proportion of patients meeting this criterion at weeks 52 and 112 weeks were 65.6% and 67.6%, respectively.

When assessed by Treatment Failure Rule (TFR) or modified nonresponder imputation (mNRI), results were similar. For both, the primary endpoints at every time interval were just one or two percentage points lower but not clinically meaningfully different, according to Dr. Lebwohl.

The same type of sustained response out to 112 weeks was observed in multiple analyses. When the researchers isolated the subgroup of patients who had achieved a PASI 75 response at 16 weeks (100%), there was a modest decline in the PASI 75 rate at week 52 (90.2%) but then no additional decline at week 112 (91.3%).

There were essentially no changes in the PASI 90 rates at week 16 (63%), week 52 (65.3%), and week 112 (63.1%), Dr. Lebwohl reported. PASI 100 rates, once achieved, were sustained long term.

The target, TYK2, is one of four Janus kinase (JAK) inhibitors. Until now, almost all JAK inhibitors have had greater relative specificity for JAK 1, JAK 2, and JAK 3, but several inhibitors of TYK2 inhibitors other than deucravacitinib are in development for inflammatory diseases. Deucravacitinib (Sotyktu), approved by the Food and Drug Administration on Sept. 9, is the only TYK2 inhibitor with regulatory approval for plaque psoriasis.

In the POETYK PSO-1 trial, 666 patients were initially randomized in a 2:1:1 ratio to 6 mg deucravacitinib (now the approved dose), placebo, or the oral phosphodiesterase 4 inhibitor apremilast. At week 16, patients on placebo were switched over to deucravacitinib. At week 24, patients who did not achieve a PASI 50 on apremilast (which had been titrated to 10 mg daily to 30 mg twice a day over the first 5 days of dosing) were switched to deucravacitinib.

In the previously reported data, deucravacitinib was superior for all efficacy endpoints at week 16, including an analysis of quality of life when compared with placebo (P < .0001) or apremilast (P = .0088). At week 52, after having been switched to deucravacitinib at week 16, patients on placebo achieved comparable responses on the efficacy measures in this study, including PASI75.

Relative to JAK inhibitors commonly used in rheumatoid arthritis and other inflammatory diseases, the greater specificity of deucravacitinib for TYK2 appears to have meaningful safety advantages, according to Dr. Lebwohl. Targeted mostly on the TYK2 regulatory domain, deucravacitinib largely avoids inhibition of the JAK 1, 2, and 3 subtypes. Dr. Lebwohl said this explains why deucravacitinib labeling does not share the boxed warnings about off-target effects, such as those on the cardiovascular system, that can be found in the labeling of other JAK inhibitors.

In the published 52-week data, the discontinuation rate for adverse events was lower in the group randomized to deucravacitinib arm than in the placebo arm. In the extended follow-up, there were no new signals for adverse events, including those involving the CV system or immune function.

The key message so far from the long-term follow-up, which is ongoing, is that “continuous treatment with deucravacitinib is associated with durable efficacy,” Dr. Lebwohl said. It is this combination of sustained efficacy and safety that led Dr. Lebwohl to suggest it as a reasonable oral competitor to injectable biologics.

“Patients now have a choice,” he said.

Jashin J. Wu, MD, a board member of the National Psoriasis Foundation and an associate professor in the department of dermatology, University of Miami, has been following the development of deucravacitinib. He said that the recent FDA approval validates the clinical evidence of benefit and safety, while the long-term data presented at the EADV congress support its role in expanding treatment options.

“Deucravacitinib is a very effective oral agent for moderate to severe plaque psoriasis with strong maintenance of effect through week 112,” he said. Differentiating it from other JAK inhibitors, the FDA approval “confirms the safety of this agent as there is no boxed warning,” he added.

Dr. Lebwohl reports financial relationships with more than 30 pharmaceutical companies, including Bristol-Myers Squibb, the manufacturer of deucravacitinib. Dr. Wu has financial relationships with 14 pharmaceutical companies, including Bristol-Myers Squibb, but he was not an investigator for the phase 3 trials of deucravacitinib.

MILAN – The day after deucravacitinib became the first TYK2 inhibitor approved for the treatment of moderate to severe psoriasis, long-term data were presented at the annual congress of the European Academy of Dermatology and Venereology, suggesting that a high degree of benefit persists for at least 2 years, making this oral drug a potential competitor for biologics.

As a once-daily drug, deucravacitinib has “the potential to be a treatment of choice and a new standard of care for patients who require systemic therapy for their moderate to severe plaque psoriasis,” said Mark G. Lebwohl, MD, professor of dermatology and dean of clinical therapeutics, Icahn School of Medicine at Mount Sinai, New York.

Just 2 months after the 52-week data from the phase 3 POETYK PSO-1 trial were published online in the Journal of the American Academy of Dermatology, a long-term extension study found essentially no loss of benefit at 112 weeks, according to Dr. Lebwohl.

One of the two co-primary endpoints was a 75% clearance on the Psoriasis and Severity Index (PASI75) score. At 52 weeks, 80.2% of patients on deucravacitinib had met this criterion of benefit. At 112 weeks, the proportion was 84.4%.

The other primary endpoint was a static Physician’s Global Assessment (sPGA) score of clear or almost clear skin. The proportion of patients meeting this criterion at weeks 52 and 112 weeks were 65.6% and 67.6%, respectively.

When assessed by Treatment Failure Rule (TFR) or modified nonresponder imputation (mNRI), results were similar. For both, the primary endpoints at every time interval were just one or two percentage points lower but not clinically meaningfully different, according to Dr. Lebwohl.

The same type of sustained response out to 112 weeks was observed in multiple analyses. When the researchers isolated the subgroup of patients who had achieved a PASI 75 response at 16 weeks (100%), there was a modest decline in the PASI 75 rate at week 52 (90.2%) but then no additional decline at week 112 (91.3%).

There were essentially no changes in the PASI 90 rates at week 16 (63%), week 52 (65.3%), and week 112 (63.1%), Dr. Lebwohl reported. PASI 100 rates, once achieved, were sustained long term.

The target, TYK2, is one of four Janus kinase (JAK) inhibitors. Until now, almost all JAK inhibitors have had greater relative specificity for JAK 1, JAK 2, and JAK 3, but several inhibitors of TYK2 inhibitors other than deucravacitinib are in development for inflammatory diseases. Deucravacitinib (Sotyktu), approved by the Food and Drug Administration on Sept. 9, is the only TYK2 inhibitor with regulatory approval for plaque psoriasis.

In the POETYK PSO-1 trial, 666 patients were initially randomized in a 2:1:1 ratio to 6 mg deucravacitinib (now the approved dose), placebo, or the oral phosphodiesterase 4 inhibitor apremilast. At week 16, patients on placebo were switched over to deucravacitinib. At week 24, patients who did not achieve a PASI 50 on apremilast (which had been titrated to 10 mg daily to 30 mg twice a day over the first 5 days of dosing) were switched to deucravacitinib.

In the previously reported data, deucravacitinib was superior for all efficacy endpoints at week 16, including an analysis of quality of life when compared with placebo (P < .0001) or apremilast (P = .0088). At week 52, after having been switched to deucravacitinib at week 16, patients on placebo achieved comparable responses on the efficacy measures in this study, including PASI75.

Relative to JAK inhibitors commonly used in rheumatoid arthritis and other inflammatory diseases, the greater specificity of deucravacitinib for TYK2 appears to have meaningful safety advantages, according to Dr. Lebwohl. Targeted mostly on the TYK2 regulatory domain, deucravacitinib largely avoids inhibition of the JAK 1, 2, and 3 subtypes. Dr. Lebwohl said this explains why deucravacitinib labeling does not share the boxed warnings about off-target effects, such as those on the cardiovascular system, that can be found in the labeling of other JAK inhibitors.

In the published 52-week data, the discontinuation rate for adverse events was lower in the group randomized to deucravacitinib arm than in the placebo arm. In the extended follow-up, there were no new signals for adverse events, including those involving the CV system or immune function.

The key message so far from the long-term follow-up, which is ongoing, is that “continuous treatment with deucravacitinib is associated with durable efficacy,” Dr. Lebwohl said. It is this combination of sustained efficacy and safety that led Dr. Lebwohl to suggest it as a reasonable oral competitor to injectable biologics.

“Patients now have a choice,” he said.

Jashin J. Wu, MD, a board member of the National Psoriasis Foundation and an associate professor in the department of dermatology, University of Miami, has been following the development of deucravacitinib. He said that the recent FDA approval validates the clinical evidence of benefit and safety, while the long-term data presented at the EADV congress support its role in expanding treatment options.

“Deucravacitinib is a very effective oral agent for moderate to severe plaque psoriasis with strong maintenance of effect through week 112,” he said. Differentiating it from other JAK inhibitors, the FDA approval “confirms the safety of this agent as there is no boxed warning,” he added.

Dr. Lebwohl reports financial relationships with more than 30 pharmaceutical companies, including Bristol-Myers Squibb, the manufacturer of deucravacitinib. Dr. Wu has financial relationships with 14 pharmaceutical companies, including Bristol-Myers Squibb, but he was not an investigator for the phase 3 trials of deucravacitinib.

MILAN – The day after deucravacitinib became the first TYK2 inhibitor approved for the treatment of moderate to severe psoriasis, long-term data were presented at the annual congress of the European Academy of Dermatology and Venereology, suggesting that a high degree of benefit persists for at least 2 years, making this oral drug a potential competitor for biologics.

As a once-daily drug, deucravacitinib has “the potential to be a treatment of choice and a new standard of care for patients who require systemic therapy for their moderate to severe plaque psoriasis,” said Mark G. Lebwohl, MD, professor of dermatology and dean of clinical therapeutics, Icahn School of Medicine at Mount Sinai, New York.

Just 2 months after the 52-week data from the phase 3 POETYK PSO-1 trial were published online in the Journal of the American Academy of Dermatology, a long-term extension study found essentially no loss of benefit at 112 weeks, according to Dr. Lebwohl.

One of the two co-primary endpoints was a 75% clearance on the Psoriasis and Severity Index (PASI75) score. At 52 weeks, 80.2% of patients on deucravacitinib had met this criterion of benefit. At 112 weeks, the proportion was 84.4%.

The other primary endpoint was a static Physician’s Global Assessment (sPGA) score of clear or almost clear skin. The proportion of patients meeting this criterion at weeks 52 and 112 weeks were 65.6% and 67.6%, respectively.

When assessed by Treatment Failure Rule (TFR) or modified nonresponder imputation (mNRI), results were similar. For both, the primary endpoints at every time interval were just one or two percentage points lower but not clinically meaningfully different, according to Dr. Lebwohl.

The same type of sustained response out to 112 weeks was observed in multiple analyses. When the researchers isolated the subgroup of patients who had achieved a PASI 75 response at 16 weeks (100%), there was a modest decline in the PASI 75 rate at week 52 (90.2%) but then no additional decline at week 112 (91.3%).

There were essentially no changes in the PASI 90 rates at week 16 (63%), week 52 (65.3%), and week 112 (63.1%), Dr. Lebwohl reported. PASI 100 rates, once achieved, were sustained long term.

The target, TYK2, is one of four Janus kinase (JAK) inhibitors. Until now, almost all JAK inhibitors have had greater relative specificity for JAK 1, JAK 2, and JAK 3, but several inhibitors of TYK2 inhibitors other than deucravacitinib are in development for inflammatory diseases. Deucravacitinib (Sotyktu), approved by the Food and Drug Administration on Sept. 9, is the only TYK2 inhibitor with regulatory approval for plaque psoriasis.

In the POETYK PSO-1 trial, 666 patients were initially randomized in a 2:1:1 ratio to 6 mg deucravacitinib (now the approved dose), placebo, or the oral phosphodiesterase 4 inhibitor apremilast. At week 16, patients on placebo were switched over to deucravacitinib. At week 24, patients who did not achieve a PASI 50 on apremilast (which had been titrated to 10 mg daily to 30 mg twice a day over the first 5 days of dosing) were switched to deucravacitinib.

In the previously reported data, deucravacitinib was superior for all efficacy endpoints at week 16, including an analysis of quality of life when compared with placebo (P < .0001) or apremilast (P = .0088). At week 52, after having been switched to deucravacitinib at week 16, patients on placebo achieved comparable responses on the efficacy measures in this study, including PASI75.

Relative to JAK inhibitors commonly used in rheumatoid arthritis and other inflammatory diseases, the greater specificity of deucravacitinib for TYK2 appears to have meaningful safety advantages, according to Dr. Lebwohl. Targeted mostly on the TYK2 regulatory domain, deucravacitinib largely avoids inhibition of the JAK 1, 2, and 3 subtypes. Dr. Lebwohl said this explains why deucravacitinib labeling does not share the boxed warnings about off-target effects, such as those on the cardiovascular system, that can be found in the labeling of other JAK inhibitors.

In the published 52-week data, the discontinuation rate for adverse events was lower in the group randomized to deucravacitinib arm than in the placebo arm. In the extended follow-up, there were no new signals for adverse events, including those involving the CV system or immune function.

The key message so far from the long-term follow-up, which is ongoing, is that “continuous treatment with deucravacitinib is associated with durable efficacy,” Dr. Lebwohl said. It is this combination of sustained efficacy and safety that led Dr. Lebwohl to suggest it as a reasonable oral competitor to injectable biologics.

“Patients now have a choice,” he said.

Jashin J. Wu, MD, a board member of the National Psoriasis Foundation and an associate professor in the department of dermatology, University of Miami, has been following the development of deucravacitinib. He said that the recent FDA approval validates the clinical evidence of benefit and safety, while the long-term data presented at the EADV congress support its role in expanding treatment options.

“Deucravacitinib is a very effective oral agent for moderate to severe plaque psoriasis with strong maintenance of effect through week 112,” he said. Differentiating it from other JAK inhibitors, the FDA approval “confirms the safety of this agent as there is no boxed warning,” he added.

Dr. Lebwohl reports financial relationships with more than 30 pharmaceutical companies, including Bristol-Myers Squibb, the manufacturer of deucravacitinib. Dr. Wu has financial relationships with 14 pharmaceutical companies, including Bristol-Myers Squibb, but he was not an investigator for the phase 3 trials of deucravacitinib.

From the earliest days of the COVID-19 pandemic, people of color have been hardest hit by the virus. Now, many doctors and researchers are seeing big disparities come about in who gets care for long COVID.

Long COVID can affect patients from all walks of life. But many of the same issues that have made the virus particularly devastating in communities of color are also shaping who gets diagnosed and treated for long COVID, said Alba Miranda Azola, MD, codirector of the post–acute COVID-19 team at Johns Hopkins University, Baltimore.

Non-White patients are more apt to lack access to primary care, face insurance barriers to see specialists, struggle with time off work or transportation for appointments, and have financial barriers to care as copayments for therapy pile up.

“We are getting a very skewed population of Caucasian wealthy people who are coming to our clinic because they have the ability to access care, they have good insurance, and they are looking on the internet and find us,” Dr. Azola said.

This mix of patients at Dr. Azola’s clinic is out of step with the demographics of Baltimore, where the majority of residents are Black, half of them earn less than $52,000 a year, and one in five live in poverty. And this isn’t unique to Hopkins. Many of the dozens of specialized long COVID clinics that have cropped up around the country are also seeing an unequal share of affluent White patients, experts say.

It’s also a patient mix that very likely doesn’t reflect who is most apt to have long COVID.

During the pandemic, people who identified as Black, Hispanic, American Indian, or Alaska Native were more likely to be diagnosed with COVID than people who identified as White, according to the Centers for Disease Control and Prevention. These people of color were also at least twice as likely to be hospitalized with severe infections, and at least 70% more likely to die.

“Data repeatedly show the disproportionate impact of COVID-19 on racial and ethnic minority populations, as well as other population groups such as people living in rural or frontier areas, people experiencing homelessness, essential and frontline workers, people with disabilities, people with substance use disorders, people who are incarcerated, and non–U.S.-born persons,” John Brooks, MD, chief medical officer for COVID-19 response at the CDC, said during testimony before the U.S. House Energy and Commerce Subcommittee on Health in April 2021.

“While we do not yet have clear data on the impact of post-COVID conditions on racial and ethnic minority populations and other disadvantaged communities, we do believe that they are likely to be disproportionately impacted ... and less likely to be able to access health care services,” Dr. Brooks said at the time.

The picture that’s emerging of long COVID suggests that the condition impacts about one in five adults. It’s more common among Hispanic adults than among people who identify as Black, Asian, or White. It’s also more common among those who identify as other races or multiple races, according survey data collected by the CDC.

It’s hard to say how accurate this snapshot is because researchers need to do a better job of identifying and following people with long COVID, said Monica Verduzco-Gutierrez, MD, chair of rehabilitation medicine and director of the COVID-19 Recovery Clinic at the University of Texas Health Science Center at San Antonio. A major limitation of surveys like the ones done by the CDC to monitor long COVID is that only people who realize they have the condition can get counted.

“Some people from historically marginalized groups may have less health literacy to know about impacts of long COVID,” she said.

Lack of awareness may keep people with persistent symptoms from seeking medical attention, leaving many long COVID cases undiagnosed.

When some patients do seek help, their complaints may not be acknowledged or understood. Often, cultural bias or structural racism can get in the way of diagnosis and treatment, Dr. Azola said.

“I hate to say this, but there is probably bias among providers,” she said. “For example, I am Puerto Rican, and the way we describe symptoms as Latinos may sound exaggerated or may be brushed aside or lost in translation. I think we miss a lot of patients being diagnosed or referred to specialists because the primary care provider they see maybe leans into this cultural bias of thinking this is just a Latino being dramatic.”

There’s some evidence that treatment for long COVID may differ by race even when symptoms are similar. One study of more than 400,000 patients, for example, found no racial differences in the proportion of people who have six common long COVID symptoms: shortness of breath, fatigue, weakness, pain, trouble with thinking skills, and a hard time getting around. Despite this, Black patients were significantly less likely to receive outpatient rehabilitation services to treat these symptoms.

Benjamin Abramoff, MD, who leads the long COVID collaborative for the American Academy of Physical Medicine and Rehabilitation, draws parallels between what happens with long COVID to another common health problem often undertreated among patients of color: pain. With both long COVID and chronic pain, one major barrier to care is “just getting taken seriously by providers,” he said.

“There is significant evidence that racial bias has led to less prescription of pain medications to people of color,” Dr. Abramoff said. “Just as pain can be difficult to get objective measures of, long COVID symptoms can also be difficult to objectively measure and requires trust between the provider and patient.”

Geography can be another barrier to care, said Aaron Friedberg, MD, clinical colead of the post-COVID recovery program at Ohio State University Wexner Medical Center, Columbus. Many communities hardest hit by COVID – particularly in high-poverty urban neighborhoods – have long had limited access to care. The pandemic worsened staffing shortages at many hospitals and clinics in these communities, leaving patients even fewer options close to home.

“I often have patients driving several hours to come to our clinic, and that can create significant challenges both because of the financial burden and time required to coordinate that type of travel, but also because post-COVID symptoms can make it extremely challenging to tolerate that type of travel,” Dr. Friedberg said.

Even though the complete picture of who has long COVID – and who’s getting treated and getting good outcomes – is still emerging, it’s very clear at this point in the pandemic that access isn’t equal among everyone and that many low-income and non-White patients are missing out on needed treatments, Friedberg said.

“One thing that is clear is that there are many people suffering alone from these conditions,” he said.

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

From the earliest days of the COVID-19 pandemic, people of color have been hardest hit by the virus. Now, many doctors and researchers are seeing big disparities come about in who gets care for long COVID.

Long COVID can affect patients from all walks of life. But many of the same issues that have made the virus particularly devastating in communities of color are also shaping who gets diagnosed and treated for long COVID, said Alba Miranda Azola, MD, codirector of the post–acute COVID-19 team at Johns Hopkins University, Baltimore.

Non-White patients are more apt to lack access to primary care, face insurance barriers to see specialists, struggle with time off work or transportation for appointments, and have financial barriers to care as copayments for therapy pile up.

“We are getting a very skewed population of Caucasian wealthy people who are coming to our clinic because they have the ability to access care, they have good insurance, and they are looking on the internet and find us,” Dr. Azola said.

This mix of patients at Dr. Azola’s clinic is out of step with the demographics of Baltimore, where the majority of residents are Black, half of them earn less than $52,000 a year, and one in five live in poverty. And this isn’t unique to Hopkins. Many of the dozens of specialized long COVID clinics that have cropped up around the country are also seeing an unequal share of affluent White patients, experts say.

It’s also a patient mix that very likely doesn’t reflect who is most apt to have long COVID.

During the pandemic, people who identified as Black, Hispanic, American Indian, or Alaska Native were more likely to be diagnosed with COVID than people who identified as White, according to the Centers for Disease Control and Prevention. These people of color were also at least twice as likely to be hospitalized with severe infections, and at least 70% more likely to die.

“Data repeatedly show the disproportionate impact of COVID-19 on racial and ethnic minority populations, as well as other population groups such as people living in rural or frontier areas, people experiencing homelessness, essential and frontline workers, people with disabilities, people with substance use disorders, people who are incarcerated, and non–U.S.-born persons,” John Brooks, MD, chief medical officer for COVID-19 response at the CDC, said during testimony before the U.S. House Energy and Commerce Subcommittee on Health in April 2021.

“While we do not yet have clear data on the impact of post-COVID conditions on racial and ethnic minority populations and other disadvantaged communities, we do believe that they are likely to be disproportionately impacted ... and less likely to be able to access health care services,” Dr. Brooks said at the time.

The picture that’s emerging of long COVID suggests that the condition impacts about one in five adults. It’s more common among Hispanic adults than among people who identify as Black, Asian, or White. It’s also more common among those who identify as other races or multiple races, according survey data collected by the CDC.

It’s hard to say how accurate this snapshot is because researchers need to do a better job of identifying and following people with long COVID, said Monica Verduzco-Gutierrez, MD, chair of rehabilitation medicine and director of the COVID-19 Recovery Clinic at the University of Texas Health Science Center at San Antonio. A major limitation of surveys like the ones done by the CDC to monitor long COVID is that only people who realize they have the condition can get counted.

“Some people from historically marginalized groups may have less health literacy to know about impacts of long COVID,” she said.

Lack of awareness may keep people with persistent symptoms from seeking medical attention, leaving many long COVID cases undiagnosed.

When some patients do seek help, their complaints may not be acknowledged or understood. Often, cultural bias or structural racism can get in the way of diagnosis and treatment, Dr. Azola said.

“I hate to say this, but there is probably bias among providers,” she said. “For example, I am Puerto Rican, and the way we describe symptoms as Latinos may sound exaggerated or may be brushed aside or lost in translation. I think we miss a lot of patients being diagnosed or referred to specialists because the primary care provider they see maybe leans into this cultural bias of thinking this is just a Latino being dramatic.”

There’s some evidence that treatment for long COVID may differ by race even when symptoms are similar. One study of more than 400,000 patients, for example, found no racial differences in the proportion of people who have six common long COVID symptoms: shortness of breath, fatigue, weakness, pain, trouble with thinking skills, and a hard time getting around. Despite this, Black patients were significantly less likely to receive outpatient rehabilitation services to treat these symptoms.

Benjamin Abramoff, MD, who leads the long COVID collaborative for the American Academy of Physical Medicine and Rehabilitation, draws parallels between what happens with long COVID to another common health problem often undertreated among patients of color: pain. With both long COVID and chronic pain, one major barrier to care is “just getting taken seriously by providers,” he said.

“There is significant evidence that racial bias has led to less prescription of pain medications to people of color,” Dr. Abramoff said. “Just as pain can be difficult to get objective measures of, long COVID symptoms can also be difficult to objectively measure and requires trust between the provider and patient.”

Geography can be another barrier to care, said Aaron Friedberg, MD, clinical colead of the post-COVID recovery program at Ohio State University Wexner Medical Center, Columbus. Many communities hardest hit by COVID – particularly in high-poverty urban neighborhoods – have long had limited access to care. The pandemic worsened staffing shortages at many hospitals and clinics in these communities, leaving patients even fewer options close to home.

“I often have patients driving several hours to come to our clinic, and that can create significant challenges both because of the financial burden and time required to coordinate that type of travel, but also because post-COVID symptoms can make it extremely challenging to tolerate that type of travel,” Dr. Friedberg said.

Even though the complete picture of who has long COVID – and who’s getting treated and getting good outcomes – is still emerging, it’s very clear at this point in the pandemic that access isn’t equal among everyone and that many low-income and non-White patients are missing out on needed treatments, Friedberg said.

“One thing that is clear is that there are many people suffering alone from these conditions,” he said.

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

From the earliest days of the COVID-19 pandemic, people of color have been hardest hit by the virus. Now, many doctors and researchers are seeing big disparities come about in who gets care for long COVID.

Long COVID can affect patients from all walks of life. But many of the same issues that have made the virus particularly devastating in communities of color are also shaping who gets diagnosed and treated for long COVID, said Alba Miranda Azola, MD, codirector of the post–acute COVID-19 team at Johns Hopkins University, Baltimore.

Non-White patients are more apt to lack access to primary care, face insurance barriers to see specialists, struggle with time off work or transportation for appointments, and have financial barriers to care as copayments for therapy pile up.

“We are getting a very skewed population of Caucasian wealthy people who are coming to our clinic because they have the ability to access care, they have good insurance, and they are looking on the internet and find us,” Dr. Azola said.

This mix of patients at Dr. Azola’s clinic is out of step with the demographics of Baltimore, where the majority of residents are Black, half of them earn less than $52,000 a year, and one in five live in poverty. And this isn’t unique to Hopkins. Many of the dozens of specialized long COVID clinics that have cropped up around the country are also seeing an unequal share of affluent White patients, experts say.

It’s also a patient mix that very likely doesn’t reflect who is most apt to have long COVID.

During the pandemic, people who identified as Black, Hispanic, American Indian, or Alaska Native were more likely to be diagnosed with COVID than people who identified as White, according to the Centers for Disease Control and Prevention. These people of color were also at least twice as likely to be hospitalized with severe infections, and at least 70% more likely to die.

“Data repeatedly show the disproportionate impact of COVID-19 on racial and ethnic minority populations, as well as other population groups such as people living in rural or frontier areas, people experiencing homelessness, essential and frontline workers, people with disabilities, people with substance use disorders, people who are incarcerated, and non–U.S.-born persons,” John Brooks, MD, chief medical officer for COVID-19 response at the CDC, said during testimony before the U.S. House Energy and Commerce Subcommittee on Health in April 2021.

“While we do not yet have clear data on the impact of post-COVID conditions on racial and ethnic minority populations and other disadvantaged communities, we do believe that they are likely to be disproportionately impacted ... and less likely to be able to access health care services,” Dr. Brooks said at the time.

The picture that’s emerging of long COVID suggests that the condition impacts about one in five adults. It’s more common among Hispanic adults than among people who identify as Black, Asian, or White. It’s also more common among those who identify as other races or multiple races, according survey data collected by the CDC.

It’s hard to say how accurate this snapshot is because researchers need to do a better job of identifying and following people with long COVID, said Monica Verduzco-Gutierrez, MD, chair of rehabilitation medicine and director of the COVID-19 Recovery Clinic at the University of Texas Health Science Center at San Antonio. A major limitation of surveys like the ones done by the CDC to monitor long COVID is that only people who realize they have the condition can get counted.

“Some people from historically marginalized groups may have less health literacy to know about impacts of long COVID,” she said.

Lack of awareness may keep people with persistent symptoms from seeking medical attention, leaving many long COVID cases undiagnosed.

When some patients do seek help, their complaints may not be acknowledged or understood. Often, cultural bias or structural racism can get in the way of diagnosis and treatment, Dr. Azola said.

“I hate to say this, but there is probably bias among providers,” she said. “For example, I am Puerto Rican, and the way we describe symptoms as Latinos may sound exaggerated or may be brushed aside or lost in translation. I think we miss a lot of patients being diagnosed or referred to specialists because the primary care provider they see maybe leans into this cultural bias of thinking this is just a Latino being dramatic.”

There’s some evidence that treatment for long COVID may differ by race even when symptoms are similar. One study of more than 400,000 patients, for example, found no racial differences in the proportion of people who have six common long COVID symptoms: shortness of breath, fatigue, weakness, pain, trouble with thinking skills, and a hard time getting around. Despite this, Black patients were significantly less likely to receive outpatient rehabilitation services to treat these symptoms.

Benjamin Abramoff, MD, who leads the long COVID collaborative for the American Academy of Physical Medicine and Rehabilitation, draws parallels between what happens with long COVID to another common health problem often undertreated among patients of color: pain. With both long COVID and chronic pain, one major barrier to care is “just getting taken seriously by providers,” he said.

“There is significant evidence that racial bias has led to less prescription of pain medications to people of color,” Dr. Abramoff said. “Just as pain can be difficult to get objective measures of, long COVID symptoms can also be difficult to objectively measure and requires trust between the provider and patient.”

Geography can be another barrier to care, said Aaron Friedberg, MD, clinical colead of the post-COVID recovery program at Ohio State University Wexner Medical Center, Columbus. Many communities hardest hit by COVID – particularly in high-poverty urban neighborhoods – have long had limited access to care. The pandemic worsened staffing shortages at many hospitals and clinics in these communities, leaving patients even fewer options close to home.

“I often have patients driving several hours to come to our clinic, and that can create significant challenges both because of the financial burden and time required to coordinate that type of travel, but also because post-COVID symptoms can make it extremely challenging to tolerate that type of travel,” Dr. Friedberg said.

Even though the complete picture of who has long COVID – and who’s getting treated and getting good outcomes – is still emerging, it’s very clear at this point in the pandemic that access isn’t equal among everyone and that many low-income and non-White patients are missing out on needed treatments, Friedberg said.

“One thing that is clear is that there are many people suffering alone from these conditions,” he said.

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

Monkey see, monkey do (advanced medical procedures)

We don’t tend to think too kindly of our prehistoric ancestors. We throw around the word “caveman” – hardly a term of endearment – and depictions of Paleolithic humans rarely flatter their subjects. In many ways, though, our conceptions are correct. Humans of the Stone Age lived short, often brutish lives, but civilization had to start somewhere, and our prehistoric ancestors were often far more capable than we give them credit for.

Tim Maloney/Nature

Case in point is a recent discovery from an archaeological dig in Borneo: A young adult who lived 31,000 years ago was discovered with the lower third of their left leg amputated. Save the clever retort about the person’s untimely death, because this individual did not die from the surgery. The amputation occurred when the individual was a child and the subject lived for several years after the operation.

Amputation is usually unnecessary given our current level of medical technology, but it’s actually quite an advanced procedure, and this example predates the previous first case of amputation by nearly 25,000 years. Not only did the surgeon need to cut at an appropriate place, they needed to understand blood loss, the risk of infection, and the need to preserve skin in order to seal the wound back up. That’s quite a lot for our Paleolithic doctor to know, and it’s even more impressive considering the, shall we say, limited tools they would have had available to perform the operation.

Rocks. They cut off the leg with a rock. And it worked.

This discovery also gives insight into the amputee’s society. Someone knew that amputation was the right move for this person, indicating that it had been done before. In addition, the individual would not have been able to spring back into action hunting mammoths right away, they would require care for the rest of their lives. And clearly the community provided, given the individual’s continued life post operation and their burial in a place of honor.

If only the American health care system was capable of such feats of compassion, but that would require the majority of politicians to be as clever as cavemen. We’re not hopeful on those odds.
 

The first step is admitting you have a crying baby. The second step is … a step

Knock, knock.

Who’s there?

Crying baby.

Crying baby who?

Current Biology/Ohmura et al.

Crying baby who … umm … doesn’t have a punchline. Let’s try this again.

A priest, a rabbi, and a crying baby walk into a bar and … nope, that’s not going to work.

Why did the crying baby cross the road? Ugh, never mind.

Clearly, crying babies are no laughing matter. What crying babies need is science. And the latest innovation – it’s fresh from a study conducted at the RIKEN Center for Brain Science in Saitama, Japan – in the science of crying babies is … walking. Researchers observed 21 unhappy infants and compared their responses to four strategies: being held by their walking mothers, held by their sitting mothers, lying in a motionless crib, or lying in a rocking cot.

The best strategy is for the mother – the experiment only involved mothers, but the results should apply to any caregiver – to pick up the crying baby, walk around for 5 minutes, sit for another 5-8 minutes, and then put the infant back to bed, the researchers said in a written statement.

The walking strategy, however, isn’t perfect. “Walking for 5 minutes promoted sleep, but only for crying infants. Surprisingly, this effect was absent when babies were already calm beforehand,” lead author Kumi O. Kuroda, MD, PhD, explained in a separate statement from the center.

It also doesn’t work on adults. We could not get a crying LOTME writer to fall asleep no matter how long his mother carried him around the office.
 

New way to detect Parkinson’s has already passed the sniff test

We humans aren’t generally known for our superpowers, but a woman from Scotland may just be the Smelling Superhero. Not only was she able to literally smell Parkinson’s disease (PD) on her husband 12 years before his diagnosis; she is also the reason that scientists have found a new way to test for PD.

© Siri Stafford/Thinkstock

Joy Milne, a retired nurse, told the BBC that her husband “had this musty rather unpleasant smell especially round his shoulders and the back of his neck and his skin had definitely changed.” She put two and two together after he had been diagnosed with PD and she came in contact with others with the same scent at a support group.

Researchers at the University of Manchester, working with Ms. Milne, have now created a skin test that uses mass spectroscopy to analyze a sample of the patient’s sebum in just 3 minutes and is 95% accurate. They tested 79 people with Parkinson’s and 71 without using this method and found “specific compounds unique to PD sebum samples when compared to healthy controls. Furthermore, we have identified two classes of lipids, namely, triacylglycerides and diglycerides, as components of human sebum that are significantly differentially expressed in PD,” they said in JACS Au.

This test could be available to general physicians within 2 years, which would provide new opportunities to the people who are waiting in line for neurologic consults. Ms. Milne’s husband passed away in 2015, but her courageous help and amazing nasal abilities may help millions down the line.
 

The power of flirting

It’s a common office stereotype: Women flirt with the boss to get ahead in the workplace, while men in power sexually harass women in subordinate positions. Nobody ever suspects the guys in the cubicles. A recent study takes a different look and paints a different picture.

Mart Production/Pexels

The investigators conducted multiple online and lab experiments in how social sexual identity drives behavior in a workplace setting in relation to job placement. They found that it was most often men in lower-power positions who are insecure about their roles who initiate social sexual behavior, even though they know it’s offensive. Why? Power.

They randomly paired over 200 undergraduate students in a male/female fashion, placed them in subordinate and boss-like roles, and asked them to choose from a series of social sexual questions they wanted to ask their teammate. Male participants who were placed in subordinate positions to a female boss chose social sexual questions more often than did male bosses, female subordinates, and female bosses.

So what does this say about the threat of workplace harassment? The researchers found that men and women differ in their strategy for flirtation. For men, it’s a way to gain more power. But problems arise when they rationalize their behavior with a character trait like being a “big flirt.”

“When we take on that identity, it leads to certain behavioral patterns that reinforce the identity. And then, people use that identity as an excuse,” lead author Laura Kray of the University of California, Berkeley, said in a statement from the school.

The researchers make a point to note that the study isn’t about whether flirting is good or bad, nor are they suggesting that people in powerful positions don’t sexually harass underlings. It’s meant to provide insight to improve corporate sexual harassment training. A comment or conversation held in jest could potentially be a warning sign for future behavior.

Monkey see, monkey do (advanced medical procedures)

We don’t tend to think too kindly of our prehistoric ancestors. We throw around the word “caveman” – hardly a term of endearment – and depictions of Paleolithic humans rarely flatter their subjects. In many ways, though, our conceptions are correct. Humans of the Stone Age lived short, often brutish lives, but civilization had to start somewhere, and our prehistoric ancestors were often far more capable than we give them credit for.

Tim Maloney/Nature

Case in point is a recent discovery from an archaeological dig in Borneo: A young adult who lived 31,000 years ago was discovered with the lower third of their left leg amputated. Save the clever retort about the person’s untimely death, because this individual did not die from the surgery. The amputation occurred when the individual was a child and the subject lived for several years after the operation.

Amputation is usually unnecessary given our current level of medical technology, but it’s actually quite an advanced procedure, and this example predates the previous first case of amputation by nearly 25,000 years. Not only did the surgeon need to cut at an appropriate place, they needed to understand blood loss, the risk of infection, and the need to preserve skin in order to seal the wound back up. That’s quite a lot for our Paleolithic doctor to know, and it’s even more impressive considering the, shall we say, limited tools they would have had available to perform the operation.

Rocks. They cut off the leg with a rock. And it worked.

This discovery also gives insight into the amputee’s society. Someone knew that amputation was the right move for this person, indicating that it had been done before. In addition, the individual would not have been able to spring back into action hunting mammoths right away, they would require care for the rest of their lives. And clearly the community provided, given the individual’s continued life post operation and their burial in a place of honor.

If only the American health care system was capable of such feats of compassion, but that would require the majority of politicians to be as clever as cavemen. We’re not hopeful on those odds.
 

The first step is admitting you have a crying baby. The second step is … a step

Knock, knock.

Who’s there?

Crying baby.

Crying baby who?

Current Biology/Ohmura et al.

Crying baby who … umm … doesn’t have a punchline. Let’s try this again.

A priest, a rabbi, and a crying baby walk into a bar and … nope, that’s not going to work.

Why did the crying baby cross the road? Ugh, never mind.

Clearly, crying babies are no laughing matter. What crying babies need is science. And the latest innovation – it’s fresh from a study conducted at the RIKEN Center for Brain Science in Saitama, Japan – in the science of crying babies is … walking. Researchers observed 21 unhappy infants and compared their responses to four strategies: being held by their walking mothers, held by their sitting mothers, lying in a motionless crib, or lying in a rocking cot.

The best strategy is for the mother – the experiment only involved mothers, but the results should apply to any caregiver – to pick up the crying baby, walk around for 5 minutes, sit for another 5-8 minutes, and then put the infant back to bed, the researchers said in a written statement.

The walking strategy, however, isn’t perfect. “Walking for 5 minutes promoted sleep, but only for crying infants. Surprisingly, this effect was absent when babies were already calm beforehand,” lead author Kumi O. Kuroda, MD, PhD, explained in a separate statement from the center.

It also doesn’t work on adults. We could not get a crying LOTME writer to fall asleep no matter how long his mother carried him around the office.
 

New way to detect Parkinson’s has already passed the sniff test

We humans aren’t generally known for our superpowers, but a woman from Scotland may just be the Smelling Superhero. Not only was she able to literally smell Parkinson’s disease (PD) on her husband 12 years before his diagnosis; she is also the reason that scientists have found a new way to test for PD.

© Siri Stafford/Thinkstock

Joy Milne, a retired nurse, told the BBC that her husband “had this musty rather unpleasant smell especially round his shoulders and the back of his neck and his skin had definitely changed.” She put two and two together after he had been diagnosed with PD and she came in contact with others with the same scent at a support group.

Researchers at the University of Manchester, working with Ms. Milne, have now created a skin test that uses mass spectroscopy to analyze a sample of the patient’s sebum in just 3 minutes and is 95% accurate. They tested 79 people with Parkinson’s and 71 without using this method and found “specific compounds unique to PD sebum samples when compared to healthy controls. Furthermore, we have identified two classes of lipids, namely, triacylglycerides and diglycerides, as components of human sebum that are significantly differentially expressed in PD,” they said in JACS Au.

This test could be available to general physicians within 2 years, which would provide new opportunities to the people who are waiting in line for neurologic consults. Ms. Milne’s husband passed away in 2015, but her courageous help and amazing nasal abilities may help millions down the line.
 

The power of flirting

It’s a common office stereotype: Women flirt with the boss to get ahead in the workplace, while men in power sexually harass women in subordinate positions. Nobody ever suspects the guys in the cubicles. A recent study takes a different look and paints a different picture.

Mart Production/Pexels

The investigators conducted multiple online and lab experiments in how social sexual identity drives behavior in a workplace setting in relation to job placement. They found that it was most often men in lower-power positions who are insecure about their roles who initiate social sexual behavior, even though they know it’s offensive. Why? Power.

They randomly paired over 200 undergraduate students in a male/female fashion, placed them in subordinate and boss-like roles, and asked them to choose from a series of social sexual questions they wanted to ask their teammate. Male participants who were placed in subordinate positions to a female boss chose social sexual questions more often than did male bosses, female subordinates, and female bosses.

So what does this say about the threat of workplace harassment? The researchers found that men and women differ in their strategy for flirtation. For men, it’s a way to gain more power. But problems arise when they rationalize their behavior with a character trait like being a “big flirt.”

“When we take on that identity, it leads to certain behavioral patterns that reinforce the identity. And then, people use that identity as an excuse,” lead author Laura Kray of the University of California, Berkeley, said in a statement from the school.

The researchers make a point to note that the study isn’t about whether flirting is good or bad, nor are they suggesting that people in powerful positions don’t sexually harass underlings. It’s meant to provide insight to improve corporate sexual harassment training. A comment or conversation held in jest could potentially be a warning sign for future behavior.

Monkey see, monkey do (advanced medical procedures)

We don’t tend to think too kindly of our prehistoric ancestors. We throw around the word “caveman” – hardly a term of endearment – and depictions of Paleolithic humans rarely flatter their subjects. In many ways, though, our conceptions are correct. Humans of the Stone Age lived short, often brutish lives, but civilization had to start somewhere, and our prehistoric ancestors were often far more capable than we give them credit for.

Tim Maloney/Nature

Case in point is a recent discovery from an archaeological dig in Borneo: A young adult who lived 31,000 years ago was discovered with the lower third of their left leg amputated. Save the clever retort about the person’s untimely death, because this individual did not die from the surgery. The amputation occurred when the individual was a child and the subject lived for several years after the operation.

Amputation is usually unnecessary given our current level of medical technology, but it’s actually quite an advanced procedure, and this example predates the previous first case of amputation by nearly 25,000 years. Not only did the surgeon need to cut at an appropriate place, they needed to understand blood loss, the risk of infection, and the need to preserve skin in order to seal the wound back up. That’s quite a lot for our Paleolithic doctor to know, and it’s even more impressive considering the, shall we say, limited tools they would have had available to perform the operation.

Rocks. They cut off the leg with a rock. And it worked.

This discovery also gives insight into the amputee’s society. Someone knew that amputation was the right move for this person, indicating that it had been done before. In addition, the individual would not have been able to spring back into action hunting mammoths right away, they would require care for the rest of their lives. And clearly the community provided, given the individual’s continued life post operation and their burial in a place of honor.

If only the American health care system was capable of such feats of compassion, but that would require the majority of politicians to be as clever as cavemen. We’re not hopeful on those odds.
 

The first step is admitting you have a crying baby. The second step is … a step

Knock, knock.

Who’s there?

Crying baby.

Crying baby who?

Current Biology/Ohmura et al.

Crying baby who … umm … doesn’t have a punchline. Let’s try this again.

A priest, a rabbi, and a crying baby walk into a bar and … nope, that’s not going to work.

Why did the crying baby cross the road? Ugh, never mind.

Clearly, crying babies are no laughing matter. What crying babies need is science. And the latest innovation – it’s fresh from a study conducted at the RIKEN Center for Brain Science in Saitama, Japan – in the science of crying babies is … walking. Researchers observed 21 unhappy infants and compared their responses to four strategies: being held by their walking mothers, held by their sitting mothers, lying in a motionless crib, or lying in a rocking cot.

The best strategy is for the mother – the experiment only involved mothers, but the results should apply to any caregiver – to pick up the crying baby, walk around for 5 minutes, sit for another 5-8 minutes, and then put the infant back to bed, the researchers said in a written statement.

The walking strategy, however, isn’t perfect. “Walking for 5 minutes promoted sleep, but only for crying infants. Surprisingly, this effect was absent when babies were already calm beforehand,” lead author Kumi O. Kuroda, MD, PhD, explained in a separate statement from the center.

It also doesn’t work on adults. We could not get a crying LOTME writer to fall asleep no matter how long his mother carried him around the office.
 

New way to detect Parkinson’s has already passed the sniff test

We humans aren’t generally known for our superpowers, but a woman from Scotland may just be the Smelling Superhero. Not only was she able to literally smell Parkinson’s disease (PD) on her husband 12 years before his diagnosis; she is also the reason that scientists have found a new way to test for PD.

© Siri Stafford/Thinkstock

Joy Milne, a retired nurse, told the BBC that her husband “had this musty rather unpleasant smell especially round his shoulders and the back of his neck and his skin had definitely changed.” She put two and two together after he had been diagnosed with PD and she came in contact with others with the same scent at a support group.

Researchers at the University of Manchester, working with Ms. Milne, have now created a skin test that uses mass spectroscopy to analyze a sample of the patient’s sebum in just 3 minutes and is 95% accurate. They tested 79 people with Parkinson’s and 71 without using this method and found “specific compounds unique to PD sebum samples when compared to healthy controls. Furthermore, we have identified two classes of lipids, namely, triacylglycerides and diglycerides, as components of human sebum that are significantly differentially expressed in PD,” they said in JACS Au.

This test could be available to general physicians within 2 years, which would provide new opportunities to the people who are waiting in line for neurologic consults. Ms. Milne’s husband passed away in 2015, but her courageous help and amazing nasal abilities may help millions down the line.
 

The power of flirting

It’s a common office stereotype: Women flirt with the boss to get ahead in the workplace, while men in power sexually harass women in subordinate positions. Nobody ever suspects the guys in the cubicles. A recent study takes a different look and paints a different picture.

Mart Production/Pexels

The investigators conducted multiple online and lab experiments in how social sexual identity drives behavior in a workplace setting in relation to job placement. They found that it was most often men in lower-power positions who are insecure about their roles who initiate social sexual behavior, even though they know it’s offensive. Why? Power.

They randomly paired over 200 undergraduate students in a male/female fashion, placed them in subordinate and boss-like roles, and asked them to choose from a series of social sexual questions they wanted to ask their teammate. Male participants who were placed in subordinate positions to a female boss chose social sexual questions more often than did male bosses, female subordinates, and female bosses.

So what does this say about the threat of workplace harassment? The researchers found that men and women differ in their strategy for flirtation. For men, it’s a way to gain more power. But problems arise when they rationalize their behavior with a character trait like being a “big flirt.”

“When we take on that identity, it leads to certain behavioral patterns that reinforce the identity. And then, people use that identity as an excuse,” lead author Laura Kray of the University of California, Berkeley, said in a statement from the school.

The researchers make a point to note that the study isn’t about whether flirting is good or bad, nor are they suggesting that people in powerful positions don’t sexually harass underlings. It’s meant to provide insight to improve corporate sexual harassment training. A comment or conversation held in jest could potentially be a warning sign for future behavior.

GHENT, BELGIUM – The Ankylosing Spondylitis Disease Activity Score (ASDAS) should be the preferred tool for disease activity assessment in patients with axial spondyloarthritis (axSpA) because it is not influenced by gender, according to new data on gender and patient outcomes as assessed by commonly used scoring methods and indices across the spectrum of SpA disease subtypes.

In contrast, researchers led by Diego Benavent, MD, a rheumatologist at La Paz University Hospital, Madrid, found that gender influenced the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) in all three disease subtypes: axSpA, peripheral SpA (pSpA), and psoriatic arthritis (PsA).

In addition, data show that women with axSpA, pSpA, or PsA reported higher disease activity, functional limitation, and poorer overall health.

Dr. Benavent presented the results at the 13th International Congress on Spondyloarthritides. The study was also published online Sept. 12 in RMD Open.

“The ASDAS is more likely to be the activity score used because we are reassured that it performs well in both men and women. However, there is a need for more appropriate validated indices that are not affected by gender in peripheral spondyloarthropathies and psoriatic arthritis,” Dr. Benavent said.

So far, most data concerning gender differences have been described in patients with axSpA, and with various measurement instruments available to assess disease activity, function, and overall health. Dr. Benavent and his colleagues wanted to investigate the influence of gender on disease outcomes across not only axSpA but pSpA and PsA, too, to see if there were differences in the relationship between gender and these other disease subtypes.

In previous studies, ASDAS has shown better psychometric properties than the BASDAI for disease activity in axSpA. “But there is little validation in pSpA and PsA, and the influence of gender in the outcomes assessed by these instruments is unknown.

“Compared with men, women with an axSpA diagnosis tend to have more frequent peripheral and extramusculoskeletal manifestations, such as enthesitis and inflammatory bowel disease,” Dr. Benavent said in an interview. “However, males with axSpA present more radiographic damage and objective signs of inflammation.”

Martin Rudwaleit, MD, head of the department of internal medicine and rheumatology at Klinikum Bielefeld (Germany), who attended the talk, reflected on the findings.

“Decades ago, ankylosing spondylitis was largely considered a male disease as found in 80%-90% of cases. Later, with MRI, we started to diagnose patients earlier and learned that more females have the disease and that females have less structural damage in the spine than men. As such, male gender is a predictor for worse radiographic progression,” Dr. Rudwaleit said.

“The question is whether the female patients who are considered to have axSpA really have axSpA, or do they have other origins of their back pain?” he continued.

“Also, this study shows us that females report a wider spectrum of symptoms than males. For example, headache, general discomfort, and overall, a broader spectrum of symptoms than men. This might have contributed to the fact that, previously, diagnoses of axSpA might have been made later in females than males.”

Large study across SpA phenotypes and disease-scoring methods

A total of 4,185 patients from 24 countries participated, with 65% having axSpA, 10% pSpA, and 25% PsA. Females totaled 38.8% of patients across all three types of spondyloarthritis. The researchers drew the data from the Assessment of SpondyloArthritis International Society (ASAS)-perSpA study.

The researchers looked for associations between gender and disease activity as measured by ASDAS and BASDAI, C-reactive protein (CRP), physical function with the Bath Ankylosing Spondylitis Functional Index (BASFI), overall health with the ASAS Health Index (ASAS HI), and European Quality of Life Five Dimensions (EQ-5D) outcomes.

In axSpA, there was a split of 68% men vs. 32% women. The researchers observed certain factors that were more common among men: smoking (49% vs. 32%), HLA-B27 positivity (83% vs. 70%), and elevated CRP (75% vs. 66%). Women more often had enthesitis (45% vs. 39%) and fibromyalgia (17% vs. 3%).

In pSpA, the gender split was approximately equal at 47% men and 53% women. But compared with women, men had more inflammatory back pain (62% vs. 50%), HLA-B27 positivity (70% vs. 54%), and elevated CRP (75% vs. 66%). Women more frequently had inflammatory bowel disease (IBD, 8% vs. 3%) and fibromyalgia (18% vs. 3%).

An approximately equal gender split was also found with PsA (48.5% men vs. 51.5% women). Men more frequently reported ever drinking alcohol than did women (63% vs. 26%), whereas women had a greater family history of both spondyloarthritis (41% vs. 32%) and psoriasis (41% vs. 31%). Women also more often reported enthesitis (49% vs. 42%) and fibromyalgia (19% vs. 3%) than men.

“These data strongly suggest that female patients showed significantly more fibromyalgia across all disease subtypes, and the magnitude of the difference with men is notable,” Dr. Benavent said.”Fibromyalgia is associated with pain and worse patient-reported outcomes, which may bias outcomes with disease activity scores.”

When the researchers analyzed outcomes by the different scores and indices for each disease subtype, they found that females had worse scores for most indices (ASDAS, BASDAI, patient’s global assessment (PtGA), BASFI, ASAS HI, and EQ-5D). “However, for CRP, men presented worse scores across axSpA and pSpA, and no differences were found with women in PsA,” Dr. Benavent added.

Although there are differences between the genders according to the scores, these differences may be confounded and this will affect the score outcome: for example, confounding by fibromyalgia in women, he explained.

To avoid the confounding effect, multivariable regression models were used, including the dependent variable as the explored outcome: for example, with BASDAI or ASDAS serving as the dependent variable and gender as the main independent variable, along with adjustments for potential confounders. When the influence of gender on BASDAI was considered, Dr. Benavent and colleagues found that being female increased all scores across the spectrum: axSpA (0.39 units; 95%  confidence interval, 0.2-0.58), pSpA (1.22 units; 95%  CI, 0.77-1.69), and PsA (0.88 units; 95%  CI, 0.59-1.19). When the influence of gender on ASDAS was considered, the researchers found that being female had no effect on axSpA (0.02 units; 95%  CI, –0.07 to 0.11), but did for pSpA (0.36 units; 95%  CI, 0.15-0.58) and PsA (0.25 units; 95%  CI, 0.12-0.38).

“ASDAS is better than BASDAI because it is similar in males and females, but this only holds true in axSpA, not in pSpA or PsA,” Dr. Benavent concluded.

Dr. Benavent declared serving on speakers bureaus for Janssen, Galapagos, and AbbVie, and receiving grant or research support from Novartis outside the submitted work. Dr. Rudwaleit declared financial relationships with AbbVie, UCB, and Lilly.

GHENT, BELGIUM – The Ankylosing Spondylitis Disease Activity Score (ASDAS) should be the preferred tool for disease activity assessment in patients with axial spondyloarthritis (axSpA) because it is not influenced by gender, according to new data on gender and patient outcomes as assessed by commonly used scoring methods and indices across the spectrum of SpA disease subtypes.

In contrast, researchers led by Diego Benavent, MD, a rheumatologist at La Paz University Hospital, Madrid, found that gender influenced the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) in all three disease subtypes: axSpA, peripheral SpA (pSpA), and psoriatic arthritis (PsA).

In addition, data show that women with axSpA, pSpA, or PsA reported higher disease activity, functional limitation, and poorer overall health.

Dr. Benavent presented the results at the 13th International Congress on Spondyloarthritides. The study was also published online Sept. 12 in RMD Open.

“The ASDAS is more likely to be the activity score used because we are reassured that it performs well in both men and women. However, there is a need for more appropriate validated indices that are not affected by gender in peripheral spondyloarthropathies and psoriatic arthritis,” Dr. Benavent said.

So far, most data concerning gender differences have been described in patients with axSpA, and with various measurement instruments available to assess disease activity, function, and overall health. Dr. Benavent and his colleagues wanted to investigate the influence of gender on disease outcomes across not only axSpA but pSpA and PsA, too, to see if there were differences in the relationship between gender and these other disease subtypes.

In previous studies, ASDAS has shown better psychometric properties than the BASDAI for disease activity in axSpA. “But there is little validation in pSpA and PsA, and the influence of gender in the outcomes assessed by these instruments is unknown.

“Compared with men, women with an axSpA diagnosis tend to have more frequent peripheral and extramusculoskeletal manifestations, such as enthesitis and inflammatory bowel disease,” Dr. Benavent said in an interview. “However, males with axSpA present more radiographic damage and objective signs of inflammation.”

Martin Rudwaleit, MD, head of the department of internal medicine and rheumatology at Klinikum Bielefeld (Germany), who attended the talk, reflected on the findings.

“Decades ago, ankylosing spondylitis was largely considered a male disease as found in 80%-90% of cases. Later, with MRI, we started to diagnose patients earlier and learned that more females have the disease and that females have less structural damage in the spine than men. As such, male gender is a predictor for worse radiographic progression,” Dr. Rudwaleit said.

“The question is whether the female patients who are considered to have axSpA really have axSpA, or do they have other origins of their back pain?” he continued.

“Also, this study shows us that females report a wider spectrum of symptoms than males. For example, headache, general discomfort, and overall, a broader spectrum of symptoms than men. This might have contributed to the fact that, previously, diagnoses of axSpA might have been made later in females than males.”

Large study across SpA phenotypes and disease-scoring methods

A total of 4,185 patients from 24 countries participated, with 65% having axSpA, 10% pSpA, and 25% PsA. Females totaled 38.8% of patients across all three types of spondyloarthritis. The researchers drew the data from the Assessment of SpondyloArthritis International Society (ASAS)-perSpA study.

The researchers looked for associations between gender and disease activity as measured by ASDAS and BASDAI, C-reactive protein (CRP), physical function with the Bath Ankylosing Spondylitis Functional Index (BASFI), overall health with the ASAS Health Index (ASAS HI), and European Quality of Life Five Dimensions (EQ-5D) outcomes.

In axSpA, there was a split of 68% men vs. 32% women. The researchers observed certain factors that were more common among men: smoking (49% vs. 32%), HLA-B27 positivity (83% vs. 70%), and elevated CRP (75% vs. 66%). Women more often had enthesitis (45% vs. 39%) and fibromyalgia (17% vs. 3%).

In pSpA, the gender split was approximately equal at 47% men and 53% women. But compared with women, men had more inflammatory back pain (62% vs. 50%), HLA-B27 positivity (70% vs. 54%), and elevated CRP (75% vs. 66%). Women more frequently had inflammatory bowel disease (IBD, 8% vs. 3%) and fibromyalgia (18% vs. 3%).

An approximately equal gender split was also found with PsA (48.5% men vs. 51.5% women). Men more frequently reported ever drinking alcohol than did women (63% vs. 26%), whereas women had a greater family history of both spondyloarthritis (41% vs. 32%) and psoriasis (41% vs. 31%). Women also more often reported enthesitis (49% vs. 42%) and fibromyalgia (19% vs. 3%) than men.

“These data strongly suggest that female patients showed significantly more fibromyalgia across all disease subtypes, and the magnitude of the difference with men is notable,” Dr. Benavent said.”Fibromyalgia is associated with pain and worse patient-reported outcomes, which may bias outcomes with disease activity scores.”

When the researchers analyzed outcomes by the different scores and indices for each disease subtype, they found that females had worse scores for most indices (ASDAS, BASDAI, patient’s global assessment (PtGA), BASFI, ASAS HI, and EQ-5D). “However, for CRP, men presented worse scores across axSpA and pSpA, and no differences were found with women in PsA,” Dr. Benavent added.

Although there are differences between the genders according to the scores, these differences may be confounded and this will affect the score outcome: for example, confounding by fibromyalgia in women, he explained.

To avoid the confounding effect, multivariable regression models were used, including the dependent variable as the explored outcome: for example, with BASDAI or ASDAS serving as the dependent variable and gender as the main independent variable, along with adjustments for potential confounders. When the influence of gender on BASDAI was considered, Dr. Benavent and colleagues found that being female increased all scores across the spectrum: axSpA (0.39 units; 95%  confidence interval, 0.2-0.58), pSpA (1.22 units; 95%  CI, 0.77-1.69), and PsA (0.88 units; 95%  CI, 0.59-1.19). When the influence of gender on ASDAS was considered, the researchers found that being female had no effect on axSpA (0.02 units; 95%  CI, –0.07 to 0.11), but did for pSpA (0.36 units; 95%  CI, 0.15-0.58) and PsA (0.25 units; 95%  CI, 0.12-0.38).

“ASDAS is better than BASDAI because it is similar in males and females, but this only holds true in axSpA, not in pSpA or PsA,” Dr. Benavent concluded.

Dr. Benavent declared serving on speakers bureaus for Janssen, Galapagos, and AbbVie, and receiving grant or research support from Novartis outside the submitted work. Dr. Rudwaleit declared financial relationships with AbbVie, UCB, and Lilly.

GHENT, BELGIUM – The Ankylosing Spondylitis Disease Activity Score (ASDAS) should be the preferred tool for disease activity assessment in patients with axial spondyloarthritis (axSpA) because it is not influenced by gender, according to new data on gender and patient outcomes as assessed by commonly used scoring methods and indices across the spectrum of SpA disease subtypes.

In contrast, researchers led by Diego Benavent, MD, a rheumatologist at La Paz University Hospital, Madrid, found that gender influenced the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) in all three disease subtypes: axSpA, peripheral SpA (pSpA), and psoriatic arthritis (PsA).

In addition, data show that women with axSpA, pSpA, or PsA reported higher disease activity, functional limitation, and poorer overall health.

Dr. Benavent presented the results at the 13th International Congress on Spondyloarthritides. The study was also published online Sept. 12 in RMD Open.

“The ASDAS is more likely to be the activity score used because we are reassured that it performs well in both men and women. However, there is a need for more appropriate validated indices that are not affected by gender in peripheral spondyloarthropathies and psoriatic arthritis,” Dr. Benavent said.

So far, most data concerning gender differences have been described in patients with axSpA, and with various measurement instruments available to assess disease activity, function, and overall health. Dr. Benavent and his colleagues wanted to investigate the influence of gender on disease outcomes across not only axSpA but pSpA and PsA, too, to see if there were differences in the relationship between gender and these other disease subtypes.

In previous studies, ASDAS has shown better psychometric properties than the BASDAI for disease activity in axSpA. “But there is little validation in pSpA and PsA, and the influence of gender in the outcomes assessed by these instruments is unknown.

“Compared with men, women with an axSpA diagnosis tend to have more frequent peripheral and extramusculoskeletal manifestations, such as enthesitis and inflammatory bowel disease,” Dr. Benavent said in an interview. “However, males with axSpA present more radiographic damage and objective signs of inflammation.”

Martin Rudwaleit, MD, head of the department of internal medicine and rheumatology at Klinikum Bielefeld (Germany), who attended the talk, reflected on the findings.

“Decades ago, ankylosing spondylitis was largely considered a male disease as found in 80%-90% of cases. Later, with MRI, we started to diagnose patients earlier and learned that more females have the disease and that females have less structural damage in the spine than men. As such, male gender is a predictor for worse radiographic progression,” Dr. Rudwaleit said.

“The question is whether the female patients who are considered to have axSpA really have axSpA, or do they have other origins of their back pain?” he continued.

“Also, this study shows us that females report a wider spectrum of symptoms than males. For example, headache, general discomfort, and overall, a broader spectrum of symptoms than men. This might have contributed to the fact that, previously, diagnoses of axSpA might have been made later in females than males.”

Large study across SpA phenotypes and disease-scoring methods

A total of 4,185 patients from 24 countries participated, with 65% having axSpA, 10% pSpA, and 25% PsA. Females totaled 38.8% of patients across all three types of spondyloarthritis. The researchers drew the data from the Assessment of SpondyloArthritis International Society (ASAS)-perSpA study.

The researchers looked for associations between gender and disease activity as measured by ASDAS and BASDAI, C-reactive protein (CRP), physical function with the Bath Ankylosing Spondylitis Functional Index (BASFI), overall health with the ASAS Health Index (ASAS HI), and European Quality of Life Five Dimensions (EQ-5D) outcomes.

In axSpA, there was a split of 68% men vs. 32% women. The researchers observed certain factors that were more common among men: smoking (49% vs. 32%), HLA-B27 positivity (83% vs. 70%), and elevated CRP (75% vs. 66%). Women more often had enthesitis (45% vs. 39%) and fibromyalgia (17% vs. 3%).

In pSpA, the gender split was approximately equal at 47% men and 53% women. But compared with women, men had more inflammatory back pain (62% vs. 50%), HLA-B27 positivity (70% vs. 54%), and elevated CRP (75% vs. 66%). Women more frequently had inflammatory bowel disease (IBD, 8% vs. 3%) and fibromyalgia (18% vs. 3%).

An approximately equal gender split was also found with PsA (48.5% men vs. 51.5% women). Men more frequently reported ever drinking alcohol than did women (63% vs. 26%), whereas women had a greater family history of both spondyloarthritis (41% vs. 32%) and psoriasis (41% vs. 31%). Women also more often reported enthesitis (49% vs. 42%) and fibromyalgia (19% vs. 3%) than men.

“These data strongly suggest that female patients showed significantly more fibromyalgia across all disease subtypes, and the magnitude of the difference with men is notable,” Dr. Benavent said.”Fibromyalgia is associated with pain and worse patient-reported outcomes, which may bias outcomes with disease activity scores.”

When the researchers analyzed outcomes by the different scores and indices for each disease subtype, they found that females had worse scores for most indices (ASDAS, BASDAI, patient’s global assessment (PtGA), BASFI, ASAS HI, and EQ-5D). “However, for CRP, men presented worse scores across axSpA and pSpA, and no differences were found with women in PsA,” Dr. Benavent added.

Although there are differences between the genders according to the scores, these differences may be confounded and this will affect the score outcome: for example, confounding by fibromyalgia in women, he explained.

To avoid the confounding effect, multivariable regression models were used, including the dependent variable as the explored outcome: for example, with BASDAI or ASDAS serving as the dependent variable and gender as the main independent variable, along with adjustments for potential confounders. When the influence of gender on BASDAI was considered, Dr. Benavent and colleagues found that being female increased all scores across the spectrum: axSpA (0.39 units; 95%  confidence interval, 0.2-0.58), pSpA (1.22 units; 95%  CI, 0.77-1.69), and PsA (0.88 units; 95%  CI, 0.59-1.19). When the influence of gender on ASDAS was considered, the researchers found that being female had no effect on axSpA (0.02 units; 95%  CI, –0.07 to 0.11), but did for pSpA (0.36 units; 95%  CI, 0.15-0.58) and PsA (0.25 units; 95%  CI, 0.12-0.38).

“ASDAS is better than BASDAI because it is similar in males and females, but this only holds true in axSpA, not in pSpA or PsA,” Dr. Benavent concluded.

Dr. Benavent declared serving on speakers bureaus for Janssen, Galapagos, and AbbVie, and receiving grant or research support from Novartis outside the submitted work. Dr. Rudwaleit declared financial relationships with AbbVie, UCB, and Lilly.

Lots of things can disrupt your gut health over the years. A high-sugar diet, stress, antibiotics – all are linked to bad changes in the gut microbiome, the microbes that live in your intestinal tract. And this can raise the risk of diseases.

But what if you could erase all that damage, restoring your gut to a time when you were younger and healthier?

It could be possible, scientists say, by having people take a sample of their own stool when they are young to be put back into their colons when they are older.

While the science to back this up isn’t quite there yet, some researchers are saying we shouldn’t wait. They are calling on existing stool banks to let people start banking their stool now, so it’s there for them to use if the science becomes available.

But how would that work?

First, you’d go to a stool bank and provide a fresh sample of your poop, which would be screened for diseases, washed, processed, and deposited into a long-term storage facility.

Then, down the road, if you get a condition such as inflammatory bowel disease, heart disease, or type 2 diabetes – or if you have a procedure that wipes out your microbiome, like a course of antibiotics or chemotherapy – doctors could use your preserved stool to “re-colonize” your gut, restoring it to its earlier, healthier state, said Scott Weiss, MD, professor of medicine at Harvard Medical School, Boston, and a coauthor of a recent paper on the topic. They would do that using fecal microbiota transplantation, or FMT.

Timing is everything. You’d want a sample from when you’re healthy – say, between the ages of 18 and 35, or before a chronic condition is likely, said Dr. Weiss. But if you’re still healthy into your late 30s, 40s, or even 50s, providing a sample then could still benefit you later in life.

If we could pull off a banking system like this, it could have the potential to treat autoimmune disease, inflammatory bowel disease, diabetes, obesity, and heart disease – or even reverse the effects of aging. How can we make this happen?
 

Stool banks of today

While stool banks do exist today, the samples inside are destined not for the original donors but rather for sick patients hoping to treat an illness. Using FMT, doctors transfer the fecal material to the patient’s colon, restoring helpful gut microbiota.

Some research shows FMT may help treat inflammatory bowel diseases, such as Crohn’s or ulcerative colitis. Animal studies suggest it could help treat obesity, lengthen lifespan, and reverse some effects of aging, such as age-related decline in brain function. Other clinical trials are looking into its potential as a cancer treatment, said Dr. Weiss.

But outside the lab, FMT is mainly used for one purpose: to treat Clostridioides difficile infection. It works even better than antibiotics, research shows.

But first you need to find a healthy donor, and that’s harder than you might think.
 

Finding healthy stool samples

Banking our bodily substances is nothing new. Blood banks, for example, are common throughout the United States, and cord blood banking – preserving blood from a baby’s umbilical cord to aid possible future medical needs of the child – is becoming more popular. Sperm donors are highly sought after, and doctors regularly transplant kidneys and bone marrow to patients in need.

So why are we so particular about poop?

Part of the reason may be because feces (like blood, for that matter) can harbor disease – which is why it’s so important to find healthy stool donors. Problem is, this can be surprisingly hard to do.

To donate fecal matter, people must go through a rigorous screening process, said Majdi Osman, MD, chief medical officer for OpenBiome, a nonprofit microbiome research organization.

Until recently, OpenBiome operated a stool donation program, though it has since shifted its focus to research. Potential donors were screened for diseases and mental health conditions, pathogens, and antibiotic resistance. The pass rate was less than 3%.

“We take a very cautious approach because the association between diseases and the microbiome is still being understood,” Dr. Osman said.

FMT also carries risks – though so far, they seem mild. Side effects include mild diarrhea, nausea, belly pain, and fatigue. (The reason? Even the healthiest donor stool may not mix perfectly with your own.)

That’s where the idea of using your own stool comes in, said Yang-Yu Liu, PhD, a Harvard researcher who studies the microbiome and the lead author of the paper mentioned above. It’s not just more appealing but may also be a better “match” for your body.
 

Should you bank your stool?

While the researchers say we have reason to be optimistic about the future, it’s important to remember that many challenges remain. FMT is early in development, and there’s a lot about the microbiome we still don’t know.

There’s no guarantee, for example, that restoring a person’s microbiome to its formerly disease-free state will keep diseases at bay forever, said Dr. Weiss. If your genes raise your odds of having Crohn’s, for instance, it’s possible the disease could come back.

We also don’t know how long stool samples can be preserved, said Dr. Liu. Stool banks currently store fecal matter for 1 or 2 years, not decades. To protect the proteins and DNA structures for that long, samples would likely need to be stashed at the liquid nitrogen storage temperature of –196° C. (Currently, samples are stored at about –80° C.) Even then, testing would be needed to confirm if the fragile microorganisms in the stool can survive.

This raises another question: Who’s going to regulate all this?

The FDA regulates the use of FMT as a drug for the treatment of C. diff, but as Dr. Liu pointed out, many gastroenterologists consider the gut microbiota an organ. In that case, human fecal matter could be regulated the same way blood, bone, or even egg cells are.

Cord blood banking may be a helpful model, Dr. Liu said.

“We don’t have to start from scratch.”

Then there’s the question of cost. Cord blood banks could be a point of reference for that too, the researchers say. They charge about $1,500 to $2,820 for the first collection and processing, plus a yearly storage fee of $185 to $370.

Despite the unknowns, one thing is for sure: The interest in fecal banking is real – and growing. At least one microbiome firm, Cordlife Group Limited, based in Singapore, announced that it has started to allow people to bank their stool for future use.

“More people should talk about it and think about it,” said Dr. Liu.

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

Lots of things can disrupt your gut health over the years. A high-sugar diet, stress, antibiotics – all are linked to bad changes in the gut microbiome, the microbes that live in your intestinal tract. And this can raise the risk of diseases.

But what if you could erase all that damage, restoring your gut to a time when you were younger and healthier?

It could be possible, scientists say, by having people take a sample of their own stool when they are young to be put back into their colons when they are older.

While the science to back this up isn’t quite there yet, some researchers are saying we shouldn’t wait. They are calling on existing stool banks to let people start banking their stool now, so it’s there for them to use if the science becomes available.

But how would that work?

First, you’d go to a stool bank and provide a fresh sample of your poop, which would be screened for diseases, washed, processed, and deposited into a long-term storage facility.

Then, down the road, if you get a condition such as inflammatory bowel disease, heart disease, or type 2 diabetes – or if you have a procedure that wipes out your microbiome, like a course of antibiotics or chemotherapy – doctors could use your preserved stool to “re-colonize” your gut, restoring it to its earlier, healthier state, said Scott Weiss, MD, professor of medicine at Harvard Medical School, Boston, and a coauthor of a recent paper on the topic. They would do that using fecal microbiota transplantation, or FMT.

Timing is everything. You’d want a sample from when you’re healthy – say, between the ages of 18 and 35, or before a chronic condition is likely, said Dr. Weiss. But if you’re still healthy into your late 30s, 40s, or even 50s, providing a sample then could still benefit you later in life.

If we could pull off a banking system like this, it could have the potential to treat autoimmune disease, inflammatory bowel disease, diabetes, obesity, and heart disease – or even reverse the effects of aging. How can we make this happen?
 

Stool banks of today

While stool banks do exist today, the samples inside are destined not for the original donors but rather for sick patients hoping to treat an illness. Using FMT, doctors transfer the fecal material to the patient’s colon, restoring helpful gut microbiota.

Some research shows FMT may help treat inflammatory bowel diseases, such as Crohn’s or ulcerative colitis. Animal studies suggest it could help treat obesity, lengthen lifespan, and reverse some effects of aging, such as age-related decline in brain function. Other clinical trials are looking into its potential as a cancer treatment, said Dr. Weiss.

But outside the lab, FMT is mainly used for one purpose: to treat Clostridioides difficile infection. It works even better than antibiotics, research shows.

But first you need to find a healthy donor, and that’s harder than you might think.
 

Finding healthy stool samples

Banking our bodily substances is nothing new. Blood banks, for example, are common throughout the United States, and cord blood banking – preserving blood from a baby’s umbilical cord to aid possible future medical needs of the child – is becoming more popular. Sperm donors are highly sought after, and doctors regularly transplant kidneys and bone marrow to patients in need.

So why are we so particular about poop?

Part of the reason may be because feces (like blood, for that matter) can harbor disease – which is why it’s so important to find healthy stool donors. Problem is, this can be surprisingly hard to do.

To donate fecal matter, people must go through a rigorous screening process, said Majdi Osman, MD, chief medical officer for OpenBiome, a nonprofit microbiome research organization.

Until recently, OpenBiome operated a stool donation program, though it has since shifted its focus to research. Potential donors were screened for diseases and mental health conditions, pathogens, and antibiotic resistance. The pass rate was less than 3%.

“We take a very cautious approach because the association between diseases and the microbiome is still being understood,” Dr. Osman said.

FMT also carries risks – though so far, they seem mild. Side effects include mild diarrhea, nausea, belly pain, and fatigue. (The reason? Even the healthiest donor stool may not mix perfectly with your own.)

That’s where the idea of using your own stool comes in, said Yang-Yu Liu, PhD, a Harvard researcher who studies the microbiome and the lead author of the paper mentioned above. It’s not just more appealing but may also be a better “match” for your body.
 

Should you bank your stool?

While the researchers say we have reason to be optimistic about the future, it’s important to remember that many challenges remain. FMT is early in development, and there’s a lot about the microbiome we still don’t know.

There’s no guarantee, for example, that restoring a person’s microbiome to its formerly disease-free state will keep diseases at bay forever, said Dr. Weiss. If your genes raise your odds of having Crohn’s, for instance, it’s possible the disease could come back.

We also don’t know how long stool samples can be preserved, said Dr. Liu. Stool banks currently store fecal matter for 1 or 2 years, not decades. To protect the proteins and DNA structures for that long, samples would likely need to be stashed at the liquid nitrogen storage temperature of –196° C. (Currently, samples are stored at about –80° C.) Even then, testing would be needed to confirm if the fragile microorganisms in the stool can survive.

This raises another question: Who’s going to regulate all this?

The FDA regulates the use of FMT as a drug for the treatment of C. diff, but as Dr. Liu pointed out, many gastroenterologists consider the gut microbiota an organ. In that case, human fecal matter could be regulated the same way blood, bone, or even egg cells are.

Cord blood banking may be a helpful model, Dr. Liu said.

“We don’t have to start from scratch.”

Then there’s the question of cost. Cord blood banks could be a point of reference for that too, the researchers say. They charge about $1,500 to $2,820 for the first collection and processing, plus a yearly storage fee of $185 to $370.

Despite the unknowns, one thing is for sure: The interest in fecal banking is real – and growing. At least one microbiome firm, Cordlife Group Limited, based in Singapore, announced that it has started to allow people to bank their stool for future use.

“More people should talk about it and think about it,” said Dr. Liu.

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

Lots of things can disrupt your gut health over the years. A high-sugar diet, stress, antibiotics – all are linked to bad changes in the gut microbiome, the microbes that live in your intestinal tract. And this can raise the risk of diseases.

But what if you could erase all that damage, restoring your gut to a time when you were younger and healthier?

It could be possible, scientists say, by having people take a sample of their own stool when they are young to be put back into their colons when they are older.

While the science to back this up isn’t quite there yet, some researchers are saying we shouldn’t wait. They are calling on existing stool banks to let people start banking their stool now, so it’s there for them to use if the science becomes available.

But how would that work?

First, you’d go to a stool bank and provide a fresh sample of your poop, which would be screened for diseases, washed, processed, and deposited into a long-term storage facility.

Then, down the road, if you get a condition such as inflammatory bowel disease, heart disease, or type 2 diabetes – or if you have a procedure that wipes out your microbiome, like a course of antibiotics or chemotherapy – doctors could use your preserved stool to “re-colonize” your gut, restoring it to its earlier, healthier state, said Scott Weiss, MD, professor of medicine at Harvard Medical School, Boston, and a coauthor of a recent paper on the topic. They would do that using fecal microbiota transplantation, or FMT.

Timing is everything. You’d want a sample from when you’re healthy – say, between the ages of 18 and 35, or before a chronic condition is likely, said Dr. Weiss. But if you’re still healthy into your late 30s, 40s, or even 50s, providing a sample then could still benefit you later in life.

If we could pull off a banking system like this, it could have the potential to treat autoimmune disease, inflammatory bowel disease, diabetes, obesity, and heart disease – or even reverse the effects of aging. How can we make this happen?
 

Stool banks of today

While stool banks do exist today, the samples inside are destined not for the original donors but rather for sick patients hoping to treat an illness. Using FMT, doctors transfer the fecal material to the patient’s colon, restoring helpful gut microbiota.

Some research shows FMT may help treat inflammatory bowel diseases, such as Crohn’s or ulcerative colitis. Animal studies suggest it could help treat obesity, lengthen lifespan, and reverse some effects of aging, such as age-related decline in brain function. Other clinical trials are looking into its potential as a cancer treatment, said Dr. Weiss.

But outside the lab, FMT is mainly used for one purpose: to treat Clostridioides difficile infection. It works even better than antibiotics, research shows.

But first you need to find a healthy donor, and that’s harder than you might think.
 

Finding healthy stool samples

Banking our bodily substances is nothing new. Blood banks, for example, are common throughout the United States, and cord blood banking – preserving blood from a baby’s umbilical cord to aid possible future medical needs of the child – is becoming more popular. Sperm donors are highly sought after, and doctors regularly transplant kidneys and bone marrow to patients in need.

So why are we so particular about poop?

Part of the reason may be because feces (like blood, for that matter) can harbor disease – which is why it’s so important to find healthy stool donors. Problem is, this can be surprisingly hard to do.

To donate fecal matter, people must go through a rigorous screening process, said Majdi Osman, MD, chief medical officer for OpenBiome, a nonprofit microbiome research organization.

Until recently, OpenBiome operated a stool donation program, though it has since shifted its focus to research. Potential donors were screened for diseases and mental health conditions, pathogens, and antibiotic resistance. The pass rate was less than 3%.

“We take a very cautious approach because the association between diseases and the microbiome is still being understood,” Dr. Osman said.

FMT also carries risks – though so far, they seem mild. Side effects include mild diarrhea, nausea, belly pain, and fatigue. (The reason? Even the healthiest donor stool may not mix perfectly with your own.)

That’s where the idea of using your own stool comes in, said Yang-Yu Liu, PhD, a Harvard researcher who studies the microbiome and the lead author of the paper mentioned above. It’s not just more appealing but may also be a better “match” for your body.
 

Should you bank your stool?

While the researchers say we have reason to be optimistic about the future, it’s important to remember that many challenges remain. FMT is early in development, and there’s a lot about the microbiome we still don’t know.

There’s no guarantee, for example, that restoring a person’s microbiome to its formerly disease-free state will keep diseases at bay forever, said Dr. Weiss. If your genes raise your odds of having Crohn’s, for instance, it’s possible the disease could come back.

We also don’t know how long stool samples can be preserved, said Dr. Liu. Stool banks currently store fecal matter for 1 or 2 years, not decades. To protect the proteins and DNA structures for that long, samples would likely need to be stashed at the liquid nitrogen storage temperature of –196° C. (Currently, samples are stored at about –80° C.) Even then, testing would be needed to confirm if the fragile microorganisms in the stool can survive.

This raises another question: Who’s going to regulate all this?

The FDA regulates the use of FMT as a drug for the treatment of C. diff, but as Dr. Liu pointed out, many gastroenterologists consider the gut microbiota an organ. In that case, human fecal matter could be regulated the same way blood, bone, or even egg cells are.

Cord blood banking may be a helpful model, Dr. Liu said.

“We don’t have to start from scratch.”

Then there’s the question of cost. Cord blood banks could be a point of reference for that too, the researchers say. They charge about $1,500 to $2,820 for the first collection and processing, plus a yearly storage fee of $185 to $370.

Despite the unknowns, one thing is for sure: The interest in fecal banking is real – and growing. At least one microbiome firm, Cordlife Group Limited, based in Singapore, announced that it has started to allow people to bank their stool for future use.

“More people should talk about it and think about it,” said Dr. Liu.

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

Omega-3 supplements did not reduce fractures during a median 5.3-year follow-up in the more than 25,000 generally healthy men and women (≥ age 50 and ≥ age 55, respectively) in the Vitamin D and Omega-3 Trial (VITAL).

The large randomized controlled trial tested whether omega-3 fatty acid or vitamin D supplements prevented cardiovascular disease or cancer in a representative sample of midlife and older adults from 50 U.S. states – which they did not. In a further analysis of VITAL, vitamin D supplements (cholecalciferol, 2,000 IU/day) did not lower the risk of incident total, nonvertebral, and hip fractures, compared with placebo.

Dmitriy Danilchenko/Shutterstock

Now this new analysis shows that omega-3 fatty acid supplements (1 g/day of fish oil) did not reduce the risk of such fractures in the VITAL population either. Meryl S. LeBoff, MD, presented the latest findings during an oral session at the annual meeting of the American Society for Bone and Mineral Research.

“In this, the largest randomized controlled trial in the world, we did not find an effect of omega-3 fatty acid supplements on fractures,” Dr. LeBoff, from Brigham and Women’s Hospital and Harvard Medical School, both in Boston, told this news organization.

The current analysis did “unexpectedly” show that among participants who received the omega-3 fatty acid supplements, there was an increase in fractures in men, and fracture risk was higher in people with a normal or low body mass index and lower in people with higher BMI.

However, these subgroup findings need to be interpreted with caution and may be caused by chance, Dr. LeBoff warned. The researchers will be investigating these findings in further analyses.
 

Should patients take omega-3 supplements or not?

Asked whether, in the meantime, patients should start or keep taking fish oil supplements for possible health benefits, she noted that certain individuals might benefit.

For example, in VITAL, participants who ate less than 1.5 servings of fish per week and received omega-3 fatty acid supplements had a decrease in the combined cardiovascular endpoint, and Black participants who took fish oil supplements had a substantially reduced risk of the outcome, regardless of fish intake.

“I think everybody needs to review [the study findings] with clinicians and make a decision in terms of what would be best for them,” she said.

Session comoderator Bente Langdahl, MD, PhD, commented that “many people take omega-3 because they think it will help” knee, hip, or other joint pain.

Perhaps men are more prone to joint pain because of osteoarthritis and the supplements lessen the pain, so these men became more physically active and more prone to fractures, she speculated.

The current study shows that, “so far, we haven’t been able to demonstrate a reduced rate of fractures with fish oil supplements in clinical randomized trials” conducted in relatively healthy and not the oldest patients, she summarized. “We’re not talking about 80-year-olds.”

In this “well-conducted study, they were not able to see any difference” with omega-3 fatty acid supplements versus placebo, but apparently, there are no harms associated with taking these supplements, she said.

To patients who ask her about such supplements, Dr. Langdahl advised: “Try it out for 3 months. If it really helps you, if it takes away your joint pain or whatever, then that might work for you. But then remember to stop again because it might just be a temporary effect.”
 

Could fish oil supplements protect against fractures?

An estimated 22% of U.S. adults aged 60 and older take omega-3 fatty acid supplements, Dr. LeBoff noted.

Preclinical studies have shown that omega-3 fatty acids reduce bone resorption and have anti-inflammatory effects, but observational studies have reported conflicting findings.

The researchers conducted this ancillary study of VITAL to fill these knowledge gaps.

VITAL enrolled a national sample of 25,871 U.S. men and women, including 5,106 Black participants, with a mean age of 67 and a mean BMI of 28 kg/m2.

Importantly, participants were not recruited by low bone density, fractures, or vitamin D deficiency. Prior to entry, participants were required to stop taking omega-3 supplements and limit nonstudy vitamin D and calcium supplements.

The omega-3 fatty acid supplements used in the study contained eicosapentaenoic acid and docosahexaenoic acid in a 1.2:1 ratio.

VITAL had a 2x2 factorial design whereby 6,463 participants were randomized to receive the omega-3 fatty acid supplement and 6,474 were randomized to placebo. (Remaining participants were randomized to receive vitamin D or placebo.)

Participants in the omega-3 fatty acid and placebo groups had similar baseline characteristics. For example, about half (50.5%) were women, and on average, they ate 1.1 servings of dark-meat fish (such as salmon) per week.

Participants completed detailed questionnaires at baseline and each year.

Plasma omega-3 levels were measured at baseline and, in 1,583 participants, at 1 year of follow-up. The mean omega-3 index rose 54.7% in the omega-3 fatty acid group and changed less than 2% in the placebo group at 1 year.

Study pill adherence was 87.0% at 2 years and 85.7% at 5 years.

Fractures were self-reported on annual questionnaires and centrally adjudicated in medical record review.
 

No clinically meaningful effect of omega-3 fatty acids on fractures

During a median 5.3-year follow-up, researchers adjudicated 2,133 total fractures and confirmed 1,991 fractures (93%) in 1551 participants.

Incidences of total, nonvertebral, and hip fractures were similar in both groups.

Compared with placebo, omega-3 fatty acid supplements had no significant effect on risk of total fractures (hazard ratio, 1.02; 95% confidence interval, 0.92-1.13), nonvertebral fractures (HR, 1.01; 95% CI, 0.91-1.12), or hip fractures (HR, 0.89; 95% CI, 0.61-1.30), all adjusted for age, sex, and race.

The “confidence intervals were narrow, likely excluding a clinically meaningful effect,” Dr. LeBoff noted.

Among men, those who received fish oil supplements had a greater risk of fracture than those who received placebo (HR, 1.27; 95% CI, 1.07-1.51), but this result “was not corrected for multiple hypothesis testing,” Dr. LeBoff cautioned.

In the overall population, participants with a BMI less than 25 who received fish oil versus placebo had an increased risk of fracture, and those with a BMI of at least 30 who received fish oil versus placebo had a decreased risk of fracture, but the limits of the confidence intervals crossed 1.00.

After excluding digit, skull, and pathologic fractures, there was no significant reduction in total fractures (HR, 1.02; 95% CI, 0.92-1.14), nonvertebral fractures (HR, 1.02; 95% CI, 0.92-1.14), or hip fractures (HR, 0.90; 95% CI, 0.61-1.33), with omega-3 supplements versus placebo.

Similarly, there was no significant reduction in risk of major osteoporotic fractures (hip, wrist, humerus, and clinical spine fractures) or wrist fractures with omega-3 supplements versus placebo.

VITAL only studied one dose of omega-3 fatty acid supplements, and results may not be generalizable to younger adults, or older adults living in residential communities, Dr. LeBoff noted.

The study was supported by grants from the National Institute of Arthritis Musculoskeletal and Skin Diseases. VITAL was funded by the National Cancer Institute and the National Heart, Lung, and Blood Institute. Dr. LeBoff and Dr. Langdahl have reported no relevant financial relationships.

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

Omega-3 supplements did not reduce fractures during a median 5.3-year follow-up in the more than 25,000 generally healthy men and women (≥ age 50 and ≥ age 55, respectively) in the Vitamin D and Omega-3 Trial (VITAL).

The large randomized controlled trial tested whether omega-3 fatty acid or vitamin D supplements prevented cardiovascular disease or cancer in a representative sample of midlife and older adults from 50 U.S. states – which they did not. In a further analysis of VITAL, vitamin D supplements (cholecalciferol, 2,000 IU/day) did not lower the risk of incident total, nonvertebral, and hip fractures, compared with placebo.

Dmitriy Danilchenko/Shutterstock

Now this new analysis shows that omega-3 fatty acid supplements (1 g/day of fish oil) did not reduce the risk of such fractures in the VITAL population either. Meryl S. LeBoff, MD, presented the latest findings during an oral session at the annual meeting of the American Society for Bone and Mineral Research.

“In this, the largest randomized controlled trial in the world, we did not find an effect of omega-3 fatty acid supplements on fractures,” Dr. LeBoff, from Brigham and Women’s Hospital and Harvard Medical School, both in Boston, told this news organization.

The current analysis did “unexpectedly” show that among participants who received the omega-3 fatty acid supplements, there was an increase in fractures in men, and fracture risk was higher in people with a normal or low body mass index and lower in people with higher BMI.

However, these subgroup findings need to be interpreted with caution and may be caused by chance, Dr. LeBoff warned. The researchers will be investigating these findings in further analyses.
 

Should patients take omega-3 supplements or not?

Asked whether, in the meantime, patients should start or keep taking fish oil supplements for possible health benefits, she noted that certain individuals might benefit.

For example, in VITAL, participants who ate less than 1.5 servings of fish per week and received omega-3 fatty acid supplements had a decrease in the combined cardiovascular endpoint, and Black participants who took fish oil supplements had a substantially reduced risk of the outcome, regardless of fish intake.

“I think everybody needs to review [the study findings] with clinicians and make a decision in terms of what would be best for them,” she said.

Session comoderator Bente Langdahl, MD, PhD, commented that “many people take omega-3 because they think it will help” knee, hip, or other joint pain.

Perhaps men are more prone to joint pain because of osteoarthritis and the supplements lessen the pain, so these men became more physically active and more prone to fractures, she speculated.

The current study shows that, “so far, we haven’t been able to demonstrate a reduced rate of fractures with fish oil supplements in clinical randomized trials” conducted in relatively healthy and not the oldest patients, she summarized. “We’re not talking about 80-year-olds.”

In this “well-conducted study, they were not able to see any difference” with omega-3 fatty acid supplements versus placebo, but apparently, there are no harms associated with taking these supplements, she said.

To patients who ask her about such supplements, Dr. Langdahl advised: “Try it out for 3 months. If it really helps you, if it takes away your joint pain or whatever, then that might work for you. But then remember to stop again because it might just be a temporary effect.”
 

Could fish oil supplements protect against fractures?

An estimated 22% of U.S. adults aged 60 and older take omega-3 fatty acid supplements, Dr. LeBoff noted.

Preclinical studies have shown that omega-3 fatty acids reduce bone resorption and have anti-inflammatory effects, but observational studies have reported conflicting findings.

The researchers conducted this ancillary study of VITAL to fill these knowledge gaps.

VITAL enrolled a national sample of 25,871 U.S. men and women, including 5,106 Black participants, with a mean age of 67 and a mean BMI of 28 kg/m2.

Importantly, participants were not recruited by low bone density, fractures, or vitamin D deficiency. Prior to entry, participants were required to stop taking omega-3 supplements and limit nonstudy vitamin D and calcium supplements.

The omega-3 fatty acid supplements used in the study contained eicosapentaenoic acid and docosahexaenoic acid in a 1.2:1 ratio.

VITAL had a 2x2 factorial design whereby 6,463 participants were randomized to receive the omega-3 fatty acid supplement and 6,474 were randomized to placebo. (Remaining participants were randomized to receive vitamin D or placebo.)

Participants in the omega-3 fatty acid and placebo groups had similar baseline characteristics. For example, about half (50.5%) were women, and on average, they ate 1.1 servings of dark-meat fish (such as salmon) per week.

Participants completed detailed questionnaires at baseline and each year.

Plasma omega-3 levels were measured at baseline and, in 1,583 participants, at 1 year of follow-up. The mean omega-3 index rose 54.7% in the omega-3 fatty acid group and changed less than 2% in the placebo group at 1 year.

Study pill adherence was 87.0% at 2 years and 85.7% at 5 years.

Fractures were self-reported on annual questionnaires and centrally adjudicated in medical record review.
 

No clinically meaningful effect of omega-3 fatty acids on fractures

During a median 5.3-year follow-up, researchers adjudicated 2,133 total fractures and confirmed 1,991 fractures (93%) in 1551 participants.

Incidences of total, nonvertebral, and hip fractures were similar in both groups.

Compared with placebo, omega-3 fatty acid supplements had no significant effect on risk of total fractures (hazard ratio, 1.02; 95% confidence interval, 0.92-1.13), nonvertebral fractures (HR, 1.01; 95% CI, 0.91-1.12), or hip fractures (HR, 0.89; 95% CI, 0.61-1.30), all adjusted for age, sex, and race.

The “confidence intervals were narrow, likely excluding a clinically meaningful effect,” Dr. LeBoff noted.

Among men, those who received fish oil supplements had a greater risk of fracture than those who received placebo (HR, 1.27; 95% CI, 1.07-1.51), but this result “was not corrected for multiple hypothesis testing,” Dr. LeBoff cautioned.

In the overall population, participants with a BMI less than 25 who received fish oil versus placebo had an increased risk of fracture, and those with a BMI of at least 30 who received fish oil versus placebo had a decreased risk of fracture, but the limits of the confidence intervals crossed 1.00.

After excluding digit, skull, and pathologic fractures, there was no significant reduction in total fractures (HR, 1.02; 95% CI, 0.92-1.14), nonvertebral fractures (HR, 1.02; 95% CI, 0.92-1.14), or hip fractures (HR, 0.90; 95% CI, 0.61-1.33), with omega-3 supplements versus placebo.

Similarly, there was no significant reduction in risk of major osteoporotic fractures (hip, wrist, humerus, and clinical spine fractures) or wrist fractures with omega-3 supplements versus placebo.

VITAL only studied one dose of omega-3 fatty acid supplements, and results may not be generalizable to younger adults, or older adults living in residential communities, Dr. LeBoff noted.

The study was supported by grants from the National Institute of Arthritis Musculoskeletal and Skin Diseases. VITAL was funded by the National Cancer Institute and the National Heart, Lung, and Blood Institute. Dr. LeBoff and Dr. Langdahl have reported no relevant financial relationships.

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

Omega-3 supplements did not reduce fractures during a median 5.3-year follow-up in the more than 25,000 generally healthy men and women (≥ age 50 and ≥ age 55, respectively) in the Vitamin D and Omega-3 Trial (VITAL).

The large randomized controlled trial tested whether omega-3 fatty acid or vitamin D supplements prevented cardiovascular disease or cancer in a representative sample of midlife and older adults from 50 U.S. states – which they did not. In a further analysis of VITAL, vitamin D supplements (cholecalciferol, 2,000 IU/day) did not lower the risk of incident total, nonvertebral, and hip fractures, compared with placebo.

Dmitriy Danilchenko/Shutterstock

Now this new analysis shows that omega-3 fatty acid supplements (1 g/day of fish oil) did not reduce the risk of such fractures in the VITAL population either. Meryl S. LeBoff, MD, presented the latest findings during an oral session at the annual meeting of the American Society for Bone and Mineral Research.

“In this, the largest randomized controlled trial in the world, we did not find an effect of omega-3 fatty acid supplements on fractures,” Dr. LeBoff, from Brigham and Women’s Hospital and Harvard Medical School, both in Boston, told this news organization.

The current analysis did “unexpectedly” show that among participants who received the omega-3 fatty acid supplements, there was an increase in fractures in men, and fracture risk was higher in people with a normal or low body mass index and lower in people with higher BMI.

However, these subgroup findings need to be interpreted with caution and may be caused by chance, Dr. LeBoff warned. The researchers will be investigating these findings in further analyses.
 

Should patients take omega-3 supplements or not?

Asked whether, in the meantime, patients should start or keep taking fish oil supplements for possible health benefits, she noted that certain individuals might benefit.

For example, in VITAL, participants who ate less than 1.5 servings of fish per week and received omega-3 fatty acid supplements had a decrease in the combined cardiovascular endpoint, and Black participants who took fish oil supplements had a substantially reduced risk of the outcome, regardless of fish intake.

“I think everybody needs to review [the study findings] with clinicians and make a decision in terms of what would be best for them,” she said.

Session comoderator Bente Langdahl, MD, PhD, commented that “many people take omega-3 because they think it will help” knee, hip, or other joint pain.

Perhaps men are more prone to joint pain because of osteoarthritis and the supplements lessen the pain, so these men became more physically active and more prone to fractures, she speculated.

The current study shows that, “so far, we haven’t been able to demonstrate a reduced rate of fractures with fish oil supplements in clinical randomized trials” conducted in relatively healthy and not the oldest patients, she summarized. “We’re not talking about 80-year-olds.”

In this “well-conducted study, they were not able to see any difference” with omega-3 fatty acid supplements versus placebo, but apparently, there are no harms associated with taking these supplements, she said.

To patients who ask her about such supplements, Dr. Langdahl advised: “Try it out for 3 months. If it really helps you, if it takes away your joint pain or whatever, then that might work for you. But then remember to stop again because it might just be a temporary effect.”
 

Could fish oil supplements protect against fractures?

An estimated 22% of U.S. adults aged 60 and older take omega-3 fatty acid supplements, Dr. LeBoff noted.

Preclinical studies have shown that omega-3 fatty acids reduce bone resorption and have anti-inflammatory effects, but observational studies have reported conflicting findings.

The researchers conducted this ancillary study of VITAL to fill these knowledge gaps.

VITAL enrolled a national sample of 25,871 U.S. men and women, including 5,106 Black participants, with a mean age of 67 and a mean BMI of 28 kg/m2.

Importantly, participants were not recruited by low bone density, fractures, or vitamin D deficiency. Prior to entry, participants were required to stop taking omega-3 supplements and limit nonstudy vitamin D and calcium supplements.

The omega-3 fatty acid supplements used in the study contained eicosapentaenoic acid and docosahexaenoic acid in a 1.2:1 ratio.

VITAL had a 2x2 factorial design whereby 6,463 participants were randomized to receive the omega-3 fatty acid supplement and 6,474 were randomized to placebo. (Remaining participants were randomized to receive vitamin D or placebo.)

Participants in the omega-3 fatty acid and placebo groups had similar baseline characteristics. For example, about half (50.5%) were women, and on average, they ate 1.1 servings of dark-meat fish (such as salmon) per week.

Participants completed detailed questionnaires at baseline and each year.

Plasma omega-3 levels were measured at baseline and, in 1,583 participants, at 1 year of follow-up. The mean omega-3 index rose 54.7% in the omega-3 fatty acid group and changed less than 2% in the placebo group at 1 year.

Study pill adherence was 87.0% at 2 years and 85.7% at 5 years.

Fractures were self-reported on annual questionnaires and centrally adjudicated in medical record review.
 

No clinically meaningful effect of omega-3 fatty acids on fractures

During a median 5.3-year follow-up, researchers adjudicated 2,133 total fractures and confirmed 1,991 fractures (93%) in 1551 participants.

Incidences of total, nonvertebral, and hip fractures were similar in both groups.

Compared with placebo, omega-3 fatty acid supplements had no significant effect on risk of total fractures (hazard ratio, 1.02; 95% confidence interval, 0.92-1.13), nonvertebral fractures (HR, 1.01; 95% CI, 0.91-1.12), or hip fractures (HR, 0.89; 95% CI, 0.61-1.30), all adjusted for age, sex, and race.

The “confidence intervals were narrow, likely excluding a clinically meaningful effect,” Dr. LeBoff noted.

Among men, those who received fish oil supplements had a greater risk of fracture than those who received placebo (HR, 1.27; 95% CI, 1.07-1.51), but this result “was not corrected for multiple hypothesis testing,” Dr. LeBoff cautioned.

In the overall population, participants with a BMI less than 25 who received fish oil versus placebo had an increased risk of fracture, and those with a BMI of at least 30 who received fish oil versus placebo had a decreased risk of fracture, but the limits of the confidence intervals crossed 1.00.

After excluding digit, skull, and pathologic fractures, there was no significant reduction in total fractures (HR, 1.02; 95% CI, 0.92-1.14), nonvertebral fractures (HR, 1.02; 95% CI, 0.92-1.14), or hip fractures (HR, 0.90; 95% CI, 0.61-1.33), with omega-3 supplements versus placebo.

Similarly, there was no significant reduction in risk of major osteoporotic fractures (hip, wrist, humerus, and clinical spine fractures) or wrist fractures with omega-3 supplements versus placebo.

VITAL only studied one dose of omega-3 fatty acid supplements, and results may not be generalizable to younger adults, or older adults living in residential communities, Dr. LeBoff noted.

The study was supported by grants from the National Institute of Arthritis Musculoskeletal and Skin Diseases. VITAL was funded by the National Cancer Institute and the National Heart, Lung, and Blood Institute. Dr. LeBoff and Dr. Langdahl have reported no relevant financial relationships.

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