MDedge Rheumatology

“What do you think of all this election stuff?” I froze. Sitting on the exam table was a 50-something-year-old woman. Her hair was long, but not gray. She was wearing a mask without distinctive markings, such as Trump lips or #BLM to identify the political leanings of the owner. She had a subtle New York accent, perhaps dating back to the Giuliani years. It was hard to know her intention. “It’s a trap!” I could hear Admiral Ackbar’s voice in my head. “Don’t engage.” We all know nothing erodes trust faster than showing your blue or red colors before you know which your patient identifies.

Instead, I replied that indeed it has been a stressful year for us all. Then I paused. She shifted a bit and tugged at the gown sleeves and admitted this was the most stress she felt in years. She was seeing me for lichen sclerosus et atrophicus, a terribly itchy, sometimes-disfiguring eruption that can occur in the vulva. She was dealing with COVID-19, kids, divorce, a new partner, working from home, parents, and now the election drama. 

At this point in the visit, I knew I could help her. First, the treatment for lichen sclerosus is straightforward and mostly effective. Second, I knew I’d have 7 minutes to spare to just listen. It was a lucky break, as often no such gift of time presents itself while seeing patients in a busy clinic. We take vitals, history (typing), do an exam, make a diagnosis (more typing), and maybe a procedure (yet more typing). All of this is necessary, but sometimes not what our patient needs. Some really need just to connect and share their burden with someone who isn’t a friend or family. As physicians, we have a unique opportunity to see and hear people without judgment.

This reminds me of a recent episode from Sam Harris’s podcast, “Making Sense.” Mr. Harris, a philosopher (and “blue” all the way through) revealed his insight into Presidents Trump’s appeal. Leaving policy aside, Mr. Harris notes that people are drawn to the President because he never judges you. He is incapable of being sanctimonious, Mr. Harris argues, and therefore creates a safe space for people to continue their lives, however flawed, without expectation that they improve. 

I’m unsure just how much of this theory explains the devotion of his supporters, but it resonated with me. We doctors are sanctimonious by nature. The better part of my day is spent prodding people to be better: Wear more sunscreen, exercise more, stop believing in conspiracy theories, get your flu shot, and above all, stop scratching! In doing so, I’m in a way judging them. Finger wagging: You’re lazy or poor or dumb or stubborn. “You aren’t as good as me,” is what they might feel after 15 minutes of my pep talk.

But what if that’s wrong? What if they are just fine exactly the way they are? Perhaps what my lichen sclerosis patient needs more than anything is unconditional attention? She, like most of our patients, is well aware of how her shortcomings might contribute to her own anxiety or difficulties. And now she has this rash and that’s probably somehow her fault too, she thinks. 

How can I best help her? Betamethasone dipropionate b.i.d. for 2 weeks and spend the last 7 minutes just sitting and listening without judgment or advice. I don’t know who she wanted to win the election. It didn’t matter, she was exactly right to believe what she believed, either way.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

“What do you think of all this election stuff?” I froze. Sitting on the exam table was a 50-something-year-old woman. Her hair was long, but not gray. She was wearing a mask without distinctive markings, such as Trump lips or #BLM to identify the political leanings of the owner. She had a subtle New York accent, perhaps dating back to the Giuliani years. It was hard to know her intention. “It’s a trap!” I could hear Admiral Ackbar’s voice in my head. “Don’t engage.” We all know nothing erodes trust faster than showing your blue or red colors before you know which your patient identifies.

Instead, I replied that indeed it has been a stressful year for us all. Then I paused. She shifted a bit and tugged at the gown sleeves and admitted this was the most stress she felt in years. She was seeing me for lichen sclerosus et atrophicus, a terribly itchy, sometimes-disfiguring eruption that can occur in the vulva. She was dealing with COVID-19, kids, divorce, a new partner, working from home, parents, and now the election drama. 

At this point in the visit, I knew I could help her. First, the treatment for lichen sclerosus is straightforward and mostly effective. Second, I knew I’d have 7 minutes to spare to just listen. It was a lucky break, as often no such gift of time presents itself while seeing patients in a busy clinic. We take vitals, history (typing), do an exam, make a diagnosis (more typing), and maybe a procedure (yet more typing). All of this is necessary, but sometimes not what our patient needs. Some really need just to connect and share their burden with someone who isn’t a friend or family. As physicians, we have a unique opportunity to see and hear people without judgment.

This reminds me of a recent episode from Sam Harris’s podcast, “Making Sense.” Mr. Harris, a philosopher (and “blue” all the way through) revealed his insight into Presidents Trump’s appeal. Leaving policy aside, Mr. Harris notes that people are drawn to the President because he never judges you. He is incapable of being sanctimonious, Mr. Harris argues, and therefore creates a safe space for people to continue their lives, however flawed, without expectation that they improve. 

I’m unsure just how much of this theory explains the devotion of his supporters, but it resonated with me. We doctors are sanctimonious by nature. The better part of my day is spent prodding people to be better: Wear more sunscreen, exercise more, stop believing in conspiracy theories, get your flu shot, and above all, stop scratching! In doing so, I’m in a way judging them. Finger wagging: You’re lazy or poor or dumb or stubborn. “You aren’t as good as me,” is what they might feel after 15 minutes of my pep talk.

But what if that’s wrong? What if they are just fine exactly the way they are? Perhaps what my lichen sclerosis patient needs more than anything is unconditional attention? She, like most of our patients, is well aware of how her shortcomings might contribute to her own anxiety or difficulties. And now she has this rash and that’s probably somehow her fault too, she thinks. 

How can I best help her? Betamethasone dipropionate b.i.d. for 2 weeks and spend the last 7 minutes just sitting and listening without judgment or advice. I don’t know who she wanted to win the election. It didn’t matter, she was exactly right to believe what she believed, either way.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

“What do you think of all this election stuff?” I froze. Sitting on the exam table was a 50-something-year-old woman. Her hair was long, but not gray. She was wearing a mask without distinctive markings, such as Trump lips or #BLM to identify the political leanings of the owner. She had a subtle New York accent, perhaps dating back to the Giuliani years. It was hard to know her intention. “It’s a trap!” I could hear Admiral Ackbar’s voice in my head. “Don’t engage.” We all know nothing erodes trust faster than showing your blue or red colors before you know which your patient identifies.

Instead, I replied that indeed it has been a stressful year for us all. Then I paused. She shifted a bit and tugged at the gown sleeves and admitted this was the most stress she felt in years. She was seeing me for lichen sclerosus et atrophicus, a terribly itchy, sometimes-disfiguring eruption that can occur in the vulva. She was dealing with COVID-19, kids, divorce, a new partner, working from home, parents, and now the election drama. 

At this point in the visit, I knew I could help her. First, the treatment for lichen sclerosus is straightforward and mostly effective. Second, I knew I’d have 7 minutes to spare to just listen. It was a lucky break, as often no such gift of time presents itself while seeing patients in a busy clinic. We take vitals, history (typing), do an exam, make a diagnosis (more typing), and maybe a procedure (yet more typing). All of this is necessary, but sometimes not what our patient needs. Some really need just to connect and share their burden with someone who isn’t a friend or family. As physicians, we have a unique opportunity to see and hear people without judgment.

This reminds me of a recent episode from Sam Harris’s podcast, “Making Sense.” Mr. Harris, a philosopher (and “blue” all the way through) revealed his insight into Presidents Trump’s appeal. Leaving policy aside, Mr. Harris notes that people are drawn to the President because he never judges you. He is incapable of being sanctimonious, Mr. Harris argues, and therefore creates a safe space for people to continue their lives, however flawed, without expectation that they improve. 

I’m unsure just how much of this theory explains the devotion of his supporters, but it resonated with me. We doctors are sanctimonious by nature. The better part of my day is spent prodding people to be better: Wear more sunscreen, exercise more, stop believing in conspiracy theories, get your flu shot, and above all, stop scratching! In doing so, I’m in a way judging them. Finger wagging: You’re lazy or poor or dumb or stubborn. “You aren’t as good as me,” is what they might feel after 15 minutes of my pep talk.

But what if that’s wrong? What if they are just fine exactly the way they are? Perhaps what my lichen sclerosis patient needs more than anything is unconditional attention? She, like most of our patients, is well aware of how her shortcomings might contribute to her own anxiety or difficulties. And now she has this rash and that’s probably somehow her fault too, she thinks. 

How can I best help her? Betamethasone dipropionate b.i.d. for 2 weeks and spend the last 7 minutes just sitting and listening without judgment or advice. I don’t know who she wanted to win the election. It didn’t matter, she was exactly right to believe what she believed, either way.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

The Moderna mRNA-1273 vaccine, in development to prevent COVID-19, yielded 94.5% efficacy in early results and is generally well tolerated, the company announced early Monday. The product can be stored at refrigeration temperatures common to many physician offices, pharmacies, and hospitals.

The first interim results of the phase 3 COVE trial included 95 participants with confirmed COVID-19. An independent data safety monitoring board, which was appointed by the National Institutes of Health, informed Moderna that 90 of the patients who were positive for COVID-19 were in a placebo group and that 5 patients were in the mRNA-1273 vaccine group, resulting in a vaccine efficacy of 94.5% (P < .0001).

Interim data included 11 patients with severe COVID-19, all of whom were in the placebo group.

“This positive interim analysis from our phase 3 study has given us the first clinical validation that our vaccine can prevent COVID-19 disease, including severe disease,” said Stéphane Bancel, CEO of Moderna, said in a statement.

The vaccine met its primary study endpoint, which was based on adjudicated data that were collected starting 2 weeks after the second dose of mRNA-1273. The interim study population included people who could be at higher risk for COVID-19, including 15 adults aged 65 years and older and 20 participants from diverse communities.
 

Safety data

The DSMB also reviewed safety data for the COVE study interim results. The vaccine was generally safe and well tolerated, as determined on the basis of solicited adverse events. Most adverse events were mild to moderate and were generally short-lived, according to a company news release.

Injection-site pain was reported in 2.7% of participants after the first dose. After the second dose, 9.7% of participants reported fatigue, 8.9% reported myalgia, 5.2% reported arthralgia, 4.5% reported headache, 4.1% reported pain, and 2.0% reported erythema or redness at the injection site.

Moderna plans to request emergency-use authorization (EUA) from the Food and Drug Administration in the coming weeks. The company expects that the EUA will be based on more data from the COVE study, including a final analysis of 151 patients with a median follow-up of more than 2 months. Moderna also plans to seek authorizations from global regulatory agencies.

The company expects to have approximately 20 million doses of mRNA-1273 ready to ship in the United States by the end of the year. In addition, the company says it remains on track to manufacture between 500 million and 1 billion doses globally in 2021.

Moderna is developing distribution plans in conjunction with the Centers for Disease Control and Prevention, the federal government’s Operation Warp Speed, and McKesson, a COVID-19 vaccine distributor contracted by the U.S. government.
 

Refrigeration requirements

The mRNA-1273 vaccine can be shipped and stored for up to 6 months at –20° C (about –4° F), a temperature maintained in most home or medical freezers, according to Moderna. The company expects that, after the product thaws, it will remain stable at standard refrigerator temperatures of 2°-8° C (36°-46° F) for up to 30 days within the 6-month shelf life.

Because the mRNA-1273 vaccine is stable at these refrigerator temperatures, it can be stored at most physicians’ offices, pharmacies, and hospitals, the company noted. In contrast, the similar Pfizer BTN162b2 vaccine – early results for which showed a 90% efficacy rate – requires shipment and storage at “deep-freeze” conditions of –70° C or –80° C, which is more challenging from a logistic point of view.

Moderna’s mRNA-1273 can be kept at room temperature for up to 12 hours after removal from a refrigerator for patient administration. The vaccine will not require dilution prior to use.

More than 30,000 people aged older than 18 years in the United States are enrolled in the COVE study. The research is being conducted in collaboration with the National Institute of Allergy and Infectious Diseases and the Biomedical Advanced Research and Development Authority, part of the Office of the Assistant Secretary for Preparedness and Response at the Department of Health & Human Services.

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

The Moderna mRNA-1273 vaccine, in development to prevent COVID-19, yielded 94.5% efficacy in early results and is generally well tolerated, the company announced early Monday. The product can be stored at refrigeration temperatures common to many physician offices, pharmacies, and hospitals.

The first interim results of the phase 3 COVE trial included 95 participants with confirmed COVID-19. An independent data safety monitoring board, which was appointed by the National Institutes of Health, informed Moderna that 90 of the patients who were positive for COVID-19 were in a placebo group and that 5 patients were in the mRNA-1273 vaccine group, resulting in a vaccine efficacy of 94.5% (P < .0001).

Interim data included 11 patients with severe COVID-19, all of whom were in the placebo group.

“This positive interim analysis from our phase 3 study has given us the first clinical validation that our vaccine can prevent COVID-19 disease, including severe disease,” said Stéphane Bancel, CEO of Moderna, said in a statement.

The vaccine met its primary study endpoint, which was based on adjudicated data that were collected starting 2 weeks after the second dose of mRNA-1273. The interim study population included people who could be at higher risk for COVID-19, including 15 adults aged 65 years and older and 20 participants from diverse communities.
 

Safety data

The DSMB also reviewed safety data for the COVE study interim results. The vaccine was generally safe and well tolerated, as determined on the basis of solicited adverse events. Most adverse events were mild to moderate and were generally short-lived, according to a company news release.

Injection-site pain was reported in 2.7% of participants after the first dose. After the second dose, 9.7% of participants reported fatigue, 8.9% reported myalgia, 5.2% reported arthralgia, 4.5% reported headache, 4.1% reported pain, and 2.0% reported erythema or redness at the injection site.

Moderna plans to request emergency-use authorization (EUA) from the Food and Drug Administration in the coming weeks. The company expects that the EUA will be based on more data from the COVE study, including a final analysis of 151 patients with a median follow-up of more than 2 months. Moderna also plans to seek authorizations from global regulatory agencies.

The company expects to have approximately 20 million doses of mRNA-1273 ready to ship in the United States by the end of the year. In addition, the company says it remains on track to manufacture between 500 million and 1 billion doses globally in 2021.

Moderna is developing distribution plans in conjunction with the Centers for Disease Control and Prevention, the federal government’s Operation Warp Speed, and McKesson, a COVID-19 vaccine distributor contracted by the U.S. government.
 

Refrigeration requirements

The mRNA-1273 vaccine can be shipped and stored for up to 6 months at –20° C (about –4° F), a temperature maintained in most home or medical freezers, according to Moderna. The company expects that, after the product thaws, it will remain stable at standard refrigerator temperatures of 2°-8° C (36°-46° F) for up to 30 days within the 6-month shelf life.

Because the mRNA-1273 vaccine is stable at these refrigerator temperatures, it can be stored at most physicians’ offices, pharmacies, and hospitals, the company noted. In contrast, the similar Pfizer BTN162b2 vaccine – early results for which showed a 90% efficacy rate – requires shipment and storage at “deep-freeze” conditions of –70° C or –80° C, which is more challenging from a logistic point of view.

Moderna’s mRNA-1273 can be kept at room temperature for up to 12 hours after removal from a refrigerator for patient administration. The vaccine will not require dilution prior to use.

More than 30,000 people aged older than 18 years in the United States are enrolled in the COVE study. The research is being conducted in collaboration with the National Institute of Allergy and Infectious Diseases and the Biomedical Advanced Research and Development Authority, part of the Office of the Assistant Secretary for Preparedness and Response at the Department of Health & Human Services.

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

The Moderna mRNA-1273 vaccine, in development to prevent COVID-19, yielded 94.5% efficacy in early results and is generally well tolerated, the company announced early Monday. The product can be stored at refrigeration temperatures common to many physician offices, pharmacies, and hospitals.

The first interim results of the phase 3 COVE trial included 95 participants with confirmed COVID-19. An independent data safety monitoring board, which was appointed by the National Institutes of Health, informed Moderna that 90 of the patients who were positive for COVID-19 were in a placebo group and that 5 patients were in the mRNA-1273 vaccine group, resulting in a vaccine efficacy of 94.5% (P < .0001).

Interim data included 11 patients with severe COVID-19, all of whom were in the placebo group.

“This positive interim analysis from our phase 3 study has given us the first clinical validation that our vaccine can prevent COVID-19 disease, including severe disease,” said Stéphane Bancel, CEO of Moderna, said in a statement.

The vaccine met its primary study endpoint, which was based on adjudicated data that were collected starting 2 weeks after the second dose of mRNA-1273. The interim study population included people who could be at higher risk for COVID-19, including 15 adults aged 65 years and older and 20 participants from diverse communities.
 

Safety data

The DSMB also reviewed safety data for the COVE study interim results. The vaccine was generally safe and well tolerated, as determined on the basis of solicited adverse events. Most adverse events were mild to moderate and were generally short-lived, according to a company news release.

Injection-site pain was reported in 2.7% of participants after the first dose. After the second dose, 9.7% of participants reported fatigue, 8.9% reported myalgia, 5.2% reported arthralgia, 4.5% reported headache, 4.1% reported pain, and 2.0% reported erythema or redness at the injection site.

Moderna plans to request emergency-use authorization (EUA) from the Food and Drug Administration in the coming weeks. The company expects that the EUA will be based on more data from the COVE study, including a final analysis of 151 patients with a median follow-up of more than 2 months. Moderna also plans to seek authorizations from global regulatory agencies.

The company expects to have approximately 20 million doses of mRNA-1273 ready to ship in the United States by the end of the year. In addition, the company says it remains on track to manufacture between 500 million and 1 billion doses globally in 2021.

Moderna is developing distribution plans in conjunction with the Centers for Disease Control and Prevention, the federal government’s Operation Warp Speed, and McKesson, a COVID-19 vaccine distributor contracted by the U.S. government.
 

Refrigeration requirements

The mRNA-1273 vaccine can be shipped and stored for up to 6 months at –20° C (about –4° F), a temperature maintained in most home or medical freezers, according to Moderna. The company expects that, after the product thaws, it will remain stable at standard refrigerator temperatures of 2°-8° C (36°-46° F) for up to 30 days within the 6-month shelf life.

Because the mRNA-1273 vaccine is stable at these refrigerator temperatures, it can be stored at most physicians’ offices, pharmacies, and hospitals, the company noted. In contrast, the similar Pfizer BTN162b2 vaccine – early results for which showed a 90% efficacy rate – requires shipment and storage at “deep-freeze” conditions of –70° C or –80° C, which is more challenging from a logistic point of view.

Moderna’s mRNA-1273 can be kept at room temperature for up to 12 hours after removal from a refrigerator for patient administration. The vaccine will not require dilution prior to use.

More than 30,000 people aged older than 18 years in the United States are enrolled in the COVE study. The research is being conducted in collaboration with the National Institute of Allergy and Infectious Diseases and the Biomedical Advanced Research and Development Authority, part of the Office of the Assistant Secretary for Preparedness and Response at the Department of Health & Human Services.

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

Not all chronic systemic inflammatory diseases are equal enhancers of atherosclerotic cardiovascular disease risk, according to a large case-control study.  

Current AHA/American College of Cardiology guidelines cite three chronic inflammatory diseases as atherosclerotic cardiovascular disease risk enhancers: rheumatoid arthritis, psoriasis, and HIV infection. But this study of those three diseases, along with three others marked by elevated high sensitivity C-reactive protein (systemic sclerosis, inflammatory bowel disease, and systemic lupus erythematosus [SLE]), showed that chronic inflammatory diseases are not monolithic in terms of their associated risk of incident coronary heart disease (CHD).

Indeed, two of the six inflammatory diseases – psoriasis and inflammatory bowel disease – turned out to be not at all associated with increased cardiovascular risk in the 37,117-patient study. The highest-risk disease was SLE, not specifically mentioned in the guidelines, Arjun Sinha, MD, a cardiology fellow at Northwestern University, Chicago, noted in his presentation at the virtual American Heart Association scientific sessions. 

The study included 18,129 patients with one of the six chronic inflammatory diseases and 18,988 matched controls, none with CHD at baseline. All regularly received outpatient care at Northwestern during 2000-2019. There were 1,011 incident CHD events during a median of 3.5 years of follow-up. 

In a Cox proportional hazards analysis adjusted for demographics, insurance status, hypertension, diabetes, current smoking, total cholesterol, and estimated glomerular filtration rate, here’s how the chronic inflammatory diseases stacked up in terms of incident CHD and MI risks: 

• SLE: hazard ratio for CHD, 2.85; for MI, 4.76.
• Systemic sclerosis: HR for CHD, 2.14; for MI, 3.19.
• HIV: HR for CHD, 1.38; for MI, 1.69.
• Rheumatoid arthritis: HR for CHD, 1.22; for MI, 1.45.
• Psoriasis: no significant increase.
• Inflammatory bowel disease: no significant increase.

In an exploratory analysis, Dr. Sinha and coinvestigators evaluated the risk of incident CHD stratified by disease severity. For lack of standardized disease severity scales, the investigators relied upon tertiles of CD4 T cell count in the HIV group and CRP in the others. The HR for new-onset CHD in the more than 5,000 patients with psoriasis didn’t vary by CRP tertile. However, there was a nonsignificant trend for greater disease severity, as reflected by CRP tertile, to be associated with increased incident CHD risk in the HIV and inflammatory bowel disease groups. 

In contrast, patients with rheumatoid arthritis or systemic sclerosis who were in the top CRP tertile had a significantly greater risk of developing CHD than that of controls, with HRs of 2.11 in the rheumatoid arthritis group and 4.59 with systemic sclerosis, although patients in the other two tertiles weren’t at significantly increased risk. But all three tertiles of CRP in patients with SLE were associated with significantly increased CHD risk: 3.17-fold in the lowest tertile of lupus severity, 5.38-fold in the middle tertile, and 4.04-fold in the top tertile for inflammation. 

These findings could be used in clinical practice to fine-tune atherosclerotic cardiovascular disease risk assessment based upon chronic inflammatory disease type and severity. That’s information which in turn can help guide the timing and intensity of preventive therapy for patients with each disease type. 

But studying the association between chronic systemic inflammatory diseases and CHD risk can be useful in additional ways, according to Dr. Sinha. These inflammatory diseases can serve as models of atherosclerosis that shed light on the non–lipid-related mechanisms involved in cardiovascular disease. 

“The gradient in risk may be hypothesis-generating with respect to which specific inflammatory pathways may contribute to CHD,” he explained. 

Each of these six chronic inflammatory diseases is characterized by a different form of major immune dysfunction, Dr. Sinha continued. A case in point is SLE, the inflammatory disease associated with the highest risk of CHD and MI. Lupus is characterized by a form of neutrophil dysfunction marked by increased formation and reduced degradation of neutrophil extracellular traps, or NETs, as well as by an increase in autoreactive B cells and dysfunctional CD4+ T helper cells. The increase in NETs of of particular interest because NETs have also been shown to contribute to the development of atherosclerosis, endothelial dysfunction, plaque erosion, and thrombosis. 

In another exploratory analysis, Dr. Sinha and coworkers found that SLE patients with a neutrophil count above the median level were twice as likely to develop CHD than were those with a neutrophil count below the median. 

A better understanding of the upstream pathways linking NET formation in SLE and atherosclerosis could lead to development of new or repurposed medications that target immune dysfunction in order to curb atherosclerosis, said Dr. Sinha, whose study won the AHA’s Samuel A. Levine Early Career Clinical Investigator Award. 

He reported having no financial conflicts regarding his study. 

[email protected] 

Not all chronic systemic inflammatory diseases are equal enhancers of atherosclerotic cardiovascular disease risk, according to a large case-control study.  

Current AHA/American College of Cardiology guidelines cite three chronic inflammatory diseases as atherosclerotic cardiovascular disease risk enhancers: rheumatoid arthritis, psoriasis, and HIV infection. But this study of those three diseases, along with three others marked by elevated high sensitivity C-reactive protein (systemic sclerosis, inflammatory bowel disease, and systemic lupus erythematosus [SLE]), showed that chronic inflammatory diseases are not monolithic in terms of their associated risk of incident coronary heart disease (CHD).

Indeed, two of the six inflammatory diseases – psoriasis and inflammatory bowel disease – turned out to be not at all associated with increased cardiovascular risk in the 37,117-patient study. The highest-risk disease was SLE, not specifically mentioned in the guidelines, Arjun Sinha, MD, a cardiology fellow at Northwestern University, Chicago, noted in his presentation at the virtual American Heart Association scientific sessions. 

The study included 18,129 patients with one of the six chronic inflammatory diseases and 18,988 matched controls, none with CHD at baseline. All regularly received outpatient care at Northwestern during 2000-2019. There were 1,011 incident CHD events during a median of 3.5 years of follow-up. 

In a Cox proportional hazards analysis adjusted for demographics, insurance status, hypertension, diabetes, current smoking, total cholesterol, and estimated glomerular filtration rate, here’s how the chronic inflammatory diseases stacked up in terms of incident CHD and MI risks: 

• SLE: hazard ratio for CHD, 2.85; for MI, 4.76.
• Systemic sclerosis: HR for CHD, 2.14; for MI, 3.19.
• HIV: HR for CHD, 1.38; for MI, 1.69.
• Rheumatoid arthritis: HR for CHD, 1.22; for MI, 1.45.
• Psoriasis: no significant increase.
• Inflammatory bowel disease: no significant increase.

In an exploratory analysis, Dr. Sinha and coinvestigators evaluated the risk of incident CHD stratified by disease severity. For lack of standardized disease severity scales, the investigators relied upon tertiles of CD4 T cell count in the HIV group and CRP in the others. The HR for new-onset CHD in the more than 5,000 patients with psoriasis didn’t vary by CRP tertile. However, there was a nonsignificant trend for greater disease severity, as reflected by CRP tertile, to be associated with increased incident CHD risk in the HIV and inflammatory bowel disease groups. 

In contrast, patients with rheumatoid arthritis or systemic sclerosis who were in the top CRP tertile had a significantly greater risk of developing CHD than that of controls, with HRs of 2.11 in the rheumatoid arthritis group and 4.59 with systemic sclerosis, although patients in the other two tertiles weren’t at significantly increased risk. But all three tertiles of CRP in patients with SLE were associated with significantly increased CHD risk: 3.17-fold in the lowest tertile of lupus severity, 5.38-fold in the middle tertile, and 4.04-fold in the top tertile for inflammation. 

These findings could be used in clinical practice to fine-tune atherosclerotic cardiovascular disease risk assessment based upon chronic inflammatory disease type and severity. That’s information which in turn can help guide the timing and intensity of preventive therapy for patients with each disease type. 

But studying the association between chronic systemic inflammatory diseases and CHD risk can be useful in additional ways, according to Dr. Sinha. These inflammatory diseases can serve as models of atherosclerosis that shed light on the non–lipid-related mechanisms involved in cardiovascular disease. 

“The gradient in risk may be hypothesis-generating with respect to which specific inflammatory pathways may contribute to CHD,” he explained. 

Each of these six chronic inflammatory diseases is characterized by a different form of major immune dysfunction, Dr. Sinha continued. A case in point is SLE, the inflammatory disease associated with the highest risk of CHD and MI. Lupus is characterized by a form of neutrophil dysfunction marked by increased formation and reduced degradation of neutrophil extracellular traps, or NETs, as well as by an increase in autoreactive B cells and dysfunctional CD4+ T helper cells. The increase in NETs of of particular interest because NETs have also been shown to contribute to the development of atherosclerosis, endothelial dysfunction, plaque erosion, and thrombosis. 

In another exploratory analysis, Dr. Sinha and coworkers found that SLE patients with a neutrophil count above the median level were twice as likely to develop CHD than were those with a neutrophil count below the median. 

A better understanding of the upstream pathways linking NET formation in SLE and atherosclerosis could lead to development of new or repurposed medications that target immune dysfunction in order to curb atherosclerosis, said Dr. Sinha, whose study won the AHA’s Samuel A. Levine Early Career Clinical Investigator Award. 

He reported having no financial conflicts regarding his study. 

[email protected] 

Not all chronic systemic inflammatory diseases are equal enhancers of atherosclerotic cardiovascular disease risk, according to a large case-control study.  

Current AHA/American College of Cardiology guidelines cite three chronic inflammatory diseases as atherosclerotic cardiovascular disease risk enhancers: rheumatoid arthritis, psoriasis, and HIV infection. But this study of those three diseases, along with three others marked by elevated high sensitivity C-reactive protein (systemic sclerosis, inflammatory bowel disease, and systemic lupus erythematosus [SLE]), showed that chronic inflammatory diseases are not monolithic in terms of their associated risk of incident coronary heart disease (CHD).

Indeed, two of the six inflammatory diseases – psoriasis and inflammatory bowel disease – turned out to be not at all associated with increased cardiovascular risk in the 37,117-patient study. The highest-risk disease was SLE, not specifically mentioned in the guidelines, Arjun Sinha, MD, a cardiology fellow at Northwestern University, Chicago, noted in his presentation at the virtual American Heart Association scientific sessions. 

The study included 18,129 patients with one of the six chronic inflammatory diseases and 18,988 matched controls, none with CHD at baseline. All regularly received outpatient care at Northwestern during 2000-2019. There were 1,011 incident CHD events during a median of 3.5 years of follow-up. 

In a Cox proportional hazards analysis adjusted for demographics, insurance status, hypertension, diabetes, current smoking, total cholesterol, and estimated glomerular filtration rate, here’s how the chronic inflammatory diseases stacked up in terms of incident CHD and MI risks: 

• SLE: hazard ratio for CHD, 2.85; for MI, 4.76.
• Systemic sclerosis: HR for CHD, 2.14; for MI, 3.19.
• HIV: HR for CHD, 1.38; for MI, 1.69.
• Rheumatoid arthritis: HR for CHD, 1.22; for MI, 1.45.
• Psoriasis: no significant increase.
• Inflammatory bowel disease: no significant increase.

In an exploratory analysis, Dr. Sinha and coinvestigators evaluated the risk of incident CHD stratified by disease severity. For lack of standardized disease severity scales, the investigators relied upon tertiles of CD4 T cell count in the HIV group and CRP in the others. The HR for new-onset CHD in the more than 5,000 patients with psoriasis didn’t vary by CRP tertile. However, there was a nonsignificant trend for greater disease severity, as reflected by CRP tertile, to be associated with increased incident CHD risk in the HIV and inflammatory bowel disease groups. 

In contrast, patients with rheumatoid arthritis or systemic sclerosis who were in the top CRP tertile had a significantly greater risk of developing CHD than that of controls, with HRs of 2.11 in the rheumatoid arthritis group and 4.59 with systemic sclerosis, although patients in the other two tertiles weren’t at significantly increased risk. But all three tertiles of CRP in patients with SLE were associated with significantly increased CHD risk: 3.17-fold in the lowest tertile of lupus severity, 5.38-fold in the middle tertile, and 4.04-fold in the top tertile for inflammation. 

These findings could be used in clinical practice to fine-tune atherosclerotic cardiovascular disease risk assessment based upon chronic inflammatory disease type and severity. That’s information which in turn can help guide the timing and intensity of preventive therapy for patients with each disease type. 

But studying the association between chronic systemic inflammatory diseases and CHD risk can be useful in additional ways, according to Dr. Sinha. These inflammatory diseases can serve as models of atherosclerosis that shed light on the non–lipid-related mechanisms involved in cardiovascular disease. 

“The gradient in risk may be hypothesis-generating with respect to which specific inflammatory pathways may contribute to CHD,” he explained. 

Each of these six chronic inflammatory diseases is characterized by a different form of major immune dysfunction, Dr. Sinha continued. A case in point is SLE, the inflammatory disease associated with the highest risk of CHD and MI. Lupus is characterized by a form of neutrophil dysfunction marked by increased formation and reduced degradation of neutrophil extracellular traps, or NETs, as well as by an increase in autoreactive B cells and dysfunctional CD4+ T helper cells. The increase in NETs of of particular interest because NETs have also been shown to contribute to the development of atherosclerosis, endothelial dysfunction, plaque erosion, and thrombosis. 

In another exploratory analysis, Dr. Sinha and coworkers found that SLE patients with a neutrophil count above the median level were twice as likely to develop CHD than were those with a neutrophil count below the median. 

A better understanding of the upstream pathways linking NET formation in SLE and atherosclerosis could lead to development of new or repurposed medications that target immune dysfunction in order to curb atherosclerosis, said Dr. Sinha, whose study won the AHA’s Samuel A. Levine Early Career Clinical Investigator Award. 

He reported having no financial conflicts regarding his study. 

[email protected] 

"The writing is on the wall” that virtual care is not meeting the needs of people with HIV who struggled with viral suppression even before the COVID-19 pandemic, said Jason Farley, PhD, ANP-BC, AACRN, associate professor of nursing at Johns Hopkins University, Baltimore. So it’s time for HIV care teams, especially clinics in the Ryan White HIV/AIDS Program, to get creative in bringing wraparound services to patients.

That may mean reallocating the workforce so that one person serves as a community health worker. Or it could mean increasing texts and video calls; helping patients find online support groups to address problems with alcohol or drug use; and conducting an overall assessment of patients’ needs as the pandemic continues.

“The virtual patient-centered medical home may be the new normal after COVID-19, and we have to be thinking about how we use this model with patients for whom it works, but supplement this model in patients that it does not,” Farley said at the virtual Association of Nurses in AIDS Care (ANAC) 2020 Annual Meeting. That work “is essential to our being able to facilitate the best patient outcomes possible.”
 

Early data, tiered interventions

Farley referred to an article published in September in the Journal AIDS that confirmed unpublished data mentioned at the International AIDS Conference 2020. The article reported that viral suppression rates among people with HIV who attended San Francisco’s Ward 86 HIV clinic dropped by 31% from pre-COVID levels.

Of the 1766 people who attended the clinic, about 1 in 5 had detectable HIV viral loads at any point in 2019. But that rate was 31% higher after shelter-in-place orders were issued. And although patients participated in telemedicine visits at more or less the same rate before and after the pandemic (31% vs. 30% no-shows), viral suppression rates dropped. The impact was especially acute for homeless individuals.

“This destabilization occurred despite our population attending telemedicine visits at a higher rate than expected, given the 60% drop in ambulatory care visit volume nationwide,” the authors stated in their article. “Telehealth visits, while offering greater patient convenience, may lead to less access to clinic-based social support services essential to achieving viral suppression among vulnerable groups.”

That’s the challenge HIV clinics now face, Farley said at the ANAC meeting.

He suggested a differentiated care approach in which there are four tiers of care, starting with the standard level of outreach, which may include email, electronic health record blasts, and robo-calls to remind people of their appointments and to refill their medications. Those with sustained viral suppression may only need 90-day automatic refills of their medications. Those who are vulnerable to nonadherence may need to be contacted weekly or more often by the clinic. Such contact could be made by a social worker, a community health worker, or through some form of virtual support.

Patients at tier 4, who have labile viral suppression, need far more than that. These are the 15% of patients with HIV who struggled with viral suppression before the pandemic. They are the patients that Farley’s team focuses on at Baltimore’s John G. Bartlett Specialty Clinic for Infectious Disease.

“We’ve completely deconstructed the patient-centered medical home,” he said of the early move to virtual care. He suggested that clinicians assess their services and ask themselves some questions:

• Has someone on the team reached out to every patient and checked in to see what their biggest needs are, medical or not, during the pandemic? Have they assessed the patient’s ability to receive video calls or text messages?
• How have group-support programs that address stigma or the social determinants of health fared in the transition to virtual medicine?
• Are patients who are in recovery being supported in order that they may engage with recovery programs online?
• How well have counseling services done in engaging people in virtual care? Currently, given the overall increase in mental health challenges during the pandemic, one would expect that the use of mental health counseling is increasing. “If they’re stagnant or going down, someone needs to be reflecting on that issue internally in the clinic,” he said.
• Are patients being contacted regarding the effects that isolation is having on their lives? “The things that would normally allow us to self-mitigate and self-manage these conditions, like going to the gym, meeting with friends, religious services – all of those are being cut,” he said.
• Is there an early alert from an in-person pharmacy to trigger outreach via a community health worker for patients who haven’t picked up their medications in a week or more?

Farley pointed to a 2015 model for an enhanced e-health approach to chronic care management that called for e-support from the community and that was enhanced through virtual communities.

These are some of the approaches Farley has taken at his clinic. He leads a team that focuses specifically on patients who struggled with engagement before the pandemic. Through a grant from the US Department of Health & Human Services’ Health Resources and Services Administration – even before the pandemic – that team has been funding community health workers who have multiple contacts with patients online and virtually and are able to offer what he calls “unapologetically enabling” support for patients so that they are able to focus on their health.

He gave the following example. Before the pandemic, a community health worker on the team had been working with a patient who showed up at every scheduled visit and swore that she was taking her medications, although clearly she was not. A community health worker, who was made available through the grant, was able to recognize that the patient’s biggest challenge in her life was providing childcare for her special-needs child. The community health worker worked with the patient for months to find stable childcare for the child, paid 2 months of rent for the patient so that she would not become homeless, and helped her find transitional housing. When the pandemic hit, the community health worker was already texting and conducting video calls with the patient regularly.

For the past 9 months, that patient has had an undetectable viral load, Farley said.

“Nine months during a pandemic,” Farley reiterated, “and the community health worker keeps working with her, keeps meeting with her.”
 

Stigma on stigma

The need for this level of support from the clinic may be even more important for people with HIV who acquire COVID-19, said Orlando Harris, PhD, assistant professor of community health systems at the University of California, San Francisco, (UCSF) School of Nursing. HIV-related stigma is a well-known deterrent to care for people living with the virus. During the presentation, Harris asked Farley about the impact of COVID-19 stigma on people with both HIV and COVID-19.

Farley said that patients at his clinic have told him that they have “ostracized” friends who have tested positive for COVID-19. Harris remembered a person with HIV who participated in one of his trials telling the researchers that despite all his precautions – wearing a mask, staying socially distant – he still acquired COVID-19. There was nothing he could have done, Harris said, other than just not go to the grocery store.

The fear of contracting another disease that is associated with stigma, as well as the need to disclose it, can inflame memories of the trauma of being diagnosed with HIV, Harris said. And with patient-centered medical homes struggling to reconstitute their wraparound services via telehealth, he said he wonders whether clinicians should be doing more.

“I worry about people who have survived being diagnosed with HIV in the ‘80s and the ‘90s before antiretroviral therapy showed up on the scene,” he told Medscape Medical News. “I worry that the folks that survived one pandemic [may] be feeling fearful or living in that fear that this new pandemic might take them out. That’s why I’m stressing the need for us to really consider, as clinicians and also as researchers the support systems, the coping mechanisms, the counseling, or what have you to support those living with HIV and vulnerable to COVID-19.”

During telehealth visits, that can be achieved simply by asking people how they are really doing and what their coping mechanisms are.

For their part, the clinicians at San Francisco’s Ward 86 are not trying to provide that support through telehealth on the same level as they were at the beginning of the pandemic, said Matthew Spinelli, MD, assistant professor of medicine, and Monica Gandhi, MD, associate chief of the Division of HIV, Infectious Diseases and Global Medicine, who are both at UCSF and are coauthors of the study.

They still offer telemedicine appointments to patients who request them, said Spinelli. He said about one-third of his patients still prefer to receive their care virtually. The rest have gone back to face-to-face support.

“The analysis led us to promptly open up care as much as possible to our patients, with the idea that telehealth is not cutting it for vulnerable patients with HIV,” Gandhi told Medscape Medical News via email. “We don’t think it’s right for a population who relies on social support from the clinic.”
 

This article first appeared on Medscape.com.

"The writing is on the wall” that virtual care is not meeting the needs of people with HIV who struggled with viral suppression even before the COVID-19 pandemic, said Jason Farley, PhD, ANP-BC, AACRN, associate professor of nursing at Johns Hopkins University, Baltimore. So it’s time for HIV care teams, especially clinics in the Ryan White HIV/AIDS Program, to get creative in bringing wraparound services to patients.

That may mean reallocating the workforce so that one person serves as a community health worker. Or it could mean increasing texts and video calls; helping patients find online support groups to address problems with alcohol or drug use; and conducting an overall assessment of patients’ needs as the pandemic continues.

“The virtual patient-centered medical home may be the new normal after COVID-19, and we have to be thinking about how we use this model with patients for whom it works, but supplement this model in patients that it does not,” Farley said at the virtual Association of Nurses in AIDS Care (ANAC) 2020 Annual Meeting. That work “is essential to our being able to facilitate the best patient outcomes possible.”
 

Early data, tiered interventions

Farley referred to an article published in September in the Journal AIDS that confirmed unpublished data mentioned at the International AIDS Conference 2020. The article reported that viral suppression rates among people with HIV who attended San Francisco’s Ward 86 HIV clinic dropped by 31% from pre-COVID levels.

Of the 1766 people who attended the clinic, about 1 in 5 had detectable HIV viral loads at any point in 2019. But that rate was 31% higher after shelter-in-place orders were issued. And although patients participated in telemedicine visits at more or less the same rate before and after the pandemic (31% vs. 30% no-shows), viral suppression rates dropped. The impact was especially acute for homeless individuals.

“This destabilization occurred despite our population attending telemedicine visits at a higher rate than expected, given the 60% drop in ambulatory care visit volume nationwide,” the authors stated in their article. “Telehealth visits, while offering greater patient convenience, may lead to less access to clinic-based social support services essential to achieving viral suppression among vulnerable groups.”

That’s the challenge HIV clinics now face, Farley said at the ANAC meeting.

He suggested a differentiated care approach in which there are four tiers of care, starting with the standard level of outreach, which may include email, electronic health record blasts, and robo-calls to remind people of their appointments and to refill their medications. Those with sustained viral suppression may only need 90-day automatic refills of their medications. Those who are vulnerable to nonadherence may need to be contacted weekly or more often by the clinic. Such contact could be made by a social worker, a community health worker, or through some form of virtual support.

Patients at tier 4, who have labile viral suppression, need far more than that. These are the 15% of patients with HIV who struggled with viral suppression before the pandemic. They are the patients that Farley’s team focuses on at Baltimore’s John G. Bartlett Specialty Clinic for Infectious Disease.

“We’ve completely deconstructed the patient-centered medical home,” he said of the early move to virtual care. He suggested that clinicians assess their services and ask themselves some questions:

• Has someone on the team reached out to every patient and checked in to see what their biggest needs are, medical or not, during the pandemic? Have they assessed the patient’s ability to receive video calls or text messages?
• How have group-support programs that address stigma or the social determinants of health fared in the transition to virtual medicine?
• Are patients who are in recovery being supported in order that they may engage with recovery programs online?
• How well have counseling services done in engaging people in virtual care? Currently, given the overall increase in mental health challenges during the pandemic, one would expect that the use of mental health counseling is increasing. “If they’re stagnant or going down, someone needs to be reflecting on that issue internally in the clinic,” he said.
• Are patients being contacted regarding the effects that isolation is having on their lives? “The things that would normally allow us to self-mitigate and self-manage these conditions, like going to the gym, meeting with friends, religious services – all of those are being cut,” he said.
• Is there an early alert from an in-person pharmacy to trigger outreach via a community health worker for patients who haven’t picked up their medications in a week or more?

Farley pointed to a 2015 model for an enhanced e-health approach to chronic care management that called for e-support from the community and that was enhanced through virtual communities.

These are some of the approaches Farley has taken at his clinic. He leads a team that focuses specifically on patients who struggled with engagement before the pandemic. Through a grant from the US Department of Health & Human Services’ Health Resources and Services Administration – even before the pandemic – that team has been funding community health workers who have multiple contacts with patients online and virtually and are able to offer what he calls “unapologetically enabling” support for patients so that they are able to focus on their health.

He gave the following example. Before the pandemic, a community health worker on the team had been working with a patient who showed up at every scheduled visit and swore that she was taking her medications, although clearly she was not. A community health worker, who was made available through the grant, was able to recognize that the patient’s biggest challenge in her life was providing childcare for her special-needs child. The community health worker worked with the patient for months to find stable childcare for the child, paid 2 months of rent for the patient so that she would not become homeless, and helped her find transitional housing. When the pandemic hit, the community health worker was already texting and conducting video calls with the patient regularly.

For the past 9 months, that patient has had an undetectable viral load, Farley said.

“Nine months during a pandemic,” Farley reiterated, “and the community health worker keeps working with her, keeps meeting with her.”
 

Stigma on stigma

The need for this level of support from the clinic may be even more important for people with HIV who acquire COVID-19, said Orlando Harris, PhD, assistant professor of community health systems at the University of California, San Francisco, (UCSF) School of Nursing. HIV-related stigma is a well-known deterrent to care for people living with the virus. During the presentation, Harris asked Farley about the impact of COVID-19 stigma on people with both HIV and COVID-19.

Farley said that patients at his clinic have told him that they have “ostracized” friends who have tested positive for COVID-19. Harris remembered a person with HIV who participated in one of his trials telling the researchers that despite all his precautions – wearing a mask, staying socially distant – he still acquired COVID-19. There was nothing he could have done, Harris said, other than just not go to the grocery store.

The fear of contracting another disease that is associated with stigma, as well as the need to disclose it, can inflame memories of the trauma of being diagnosed with HIV, Harris said. And with patient-centered medical homes struggling to reconstitute their wraparound services via telehealth, he said he wonders whether clinicians should be doing more.

“I worry about people who have survived being diagnosed with HIV in the ‘80s and the ‘90s before antiretroviral therapy showed up on the scene,” he told Medscape Medical News. “I worry that the folks that survived one pandemic [may] be feeling fearful or living in that fear that this new pandemic might take them out. That’s why I’m stressing the need for us to really consider, as clinicians and also as researchers the support systems, the coping mechanisms, the counseling, or what have you to support those living with HIV and vulnerable to COVID-19.”

During telehealth visits, that can be achieved simply by asking people how they are really doing and what their coping mechanisms are.

For their part, the clinicians at San Francisco’s Ward 86 are not trying to provide that support through telehealth on the same level as they were at the beginning of the pandemic, said Matthew Spinelli, MD, assistant professor of medicine, and Monica Gandhi, MD, associate chief of the Division of HIV, Infectious Diseases and Global Medicine, who are both at UCSF and are coauthors of the study.

They still offer telemedicine appointments to patients who request them, said Spinelli. He said about one-third of his patients still prefer to receive their care virtually. The rest have gone back to face-to-face support.

“The analysis led us to promptly open up care as much as possible to our patients, with the idea that telehealth is not cutting it for vulnerable patients with HIV,” Gandhi told Medscape Medical News via email. “We don’t think it’s right for a population who relies on social support from the clinic.”
 

This article first appeared on Medscape.com.

"The writing is on the wall” that virtual care is not meeting the needs of people with HIV who struggled with viral suppression even before the COVID-19 pandemic, said Jason Farley, PhD, ANP-BC, AACRN, associate professor of nursing at Johns Hopkins University, Baltimore. So it’s time for HIV care teams, especially clinics in the Ryan White HIV/AIDS Program, to get creative in bringing wraparound services to patients.

That may mean reallocating the workforce so that one person serves as a community health worker. Or it could mean increasing texts and video calls; helping patients find online support groups to address problems with alcohol or drug use; and conducting an overall assessment of patients’ needs as the pandemic continues.

“The virtual patient-centered medical home may be the new normal after COVID-19, and we have to be thinking about how we use this model with patients for whom it works, but supplement this model in patients that it does not,” Farley said at the virtual Association of Nurses in AIDS Care (ANAC) 2020 Annual Meeting. That work “is essential to our being able to facilitate the best patient outcomes possible.”
 

Early data, tiered interventions

Farley referred to an article published in September in the Journal AIDS that confirmed unpublished data mentioned at the International AIDS Conference 2020. The article reported that viral suppression rates among people with HIV who attended San Francisco’s Ward 86 HIV clinic dropped by 31% from pre-COVID levels.

Of the 1766 people who attended the clinic, about 1 in 5 had detectable HIV viral loads at any point in 2019. But that rate was 31% higher after shelter-in-place orders were issued. And although patients participated in telemedicine visits at more or less the same rate before and after the pandemic (31% vs. 30% no-shows), viral suppression rates dropped. The impact was especially acute for homeless individuals.

“This destabilization occurred despite our population attending telemedicine visits at a higher rate than expected, given the 60% drop in ambulatory care visit volume nationwide,” the authors stated in their article. “Telehealth visits, while offering greater patient convenience, may lead to less access to clinic-based social support services essential to achieving viral suppression among vulnerable groups.”

That’s the challenge HIV clinics now face, Farley said at the ANAC meeting.

He suggested a differentiated care approach in which there are four tiers of care, starting with the standard level of outreach, which may include email, electronic health record blasts, and robo-calls to remind people of their appointments and to refill their medications. Those with sustained viral suppression may only need 90-day automatic refills of their medications. Those who are vulnerable to nonadherence may need to be contacted weekly or more often by the clinic. Such contact could be made by a social worker, a community health worker, or through some form of virtual support.

Patients at tier 4, who have labile viral suppression, need far more than that. These are the 15% of patients with HIV who struggled with viral suppression before the pandemic. They are the patients that Farley’s team focuses on at Baltimore’s John G. Bartlett Specialty Clinic for Infectious Disease.

“We’ve completely deconstructed the patient-centered medical home,” he said of the early move to virtual care. He suggested that clinicians assess their services and ask themselves some questions:

• Has someone on the team reached out to every patient and checked in to see what their biggest needs are, medical or not, during the pandemic? Have they assessed the patient’s ability to receive video calls or text messages?
• How have group-support programs that address stigma or the social determinants of health fared in the transition to virtual medicine?
• Are patients who are in recovery being supported in order that they may engage with recovery programs online?
• How well have counseling services done in engaging people in virtual care? Currently, given the overall increase in mental health challenges during the pandemic, one would expect that the use of mental health counseling is increasing. “If they’re stagnant or going down, someone needs to be reflecting on that issue internally in the clinic,” he said.
• Are patients being contacted regarding the effects that isolation is having on their lives? “The things that would normally allow us to self-mitigate and self-manage these conditions, like going to the gym, meeting with friends, religious services – all of those are being cut,” he said.
• Is there an early alert from an in-person pharmacy to trigger outreach via a community health worker for patients who haven’t picked up their medications in a week or more?

Farley pointed to a 2015 model for an enhanced e-health approach to chronic care management that called for e-support from the community and that was enhanced through virtual communities.

These are some of the approaches Farley has taken at his clinic. He leads a team that focuses specifically on patients who struggled with engagement before the pandemic. Through a grant from the US Department of Health & Human Services’ Health Resources and Services Administration – even before the pandemic – that team has been funding community health workers who have multiple contacts with patients online and virtually and are able to offer what he calls “unapologetically enabling” support for patients so that they are able to focus on their health.

He gave the following example. Before the pandemic, a community health worker on the team had been working with a patient who showed up at every scheduled visit and swore that she was taking her medications, although clearly she was not. A community health worker, who was made available through the grant, was able to recognize that the patient’s biggest challenge in her life was providing childcare for her special-needs child. The community health worker worked with the patient for months to find stable childcare for the child, paid 2 months of rent for the patient so that she would not become homeless, and helped her find transitional housing. When the pandemic hit, the community health worker was already texting and conducting video calls with the patient regularly.

For the past 9 months, that patient has had an undetectable viral load, Farley said.

“Nine months during a pandemic,” Farley reiterated, “and the community health worker keeps working with her, keeps meeting with her.”
 

Stigma on stigma

The need for this level of support from the clinic may be even more important for people with HIV who acquire COVID-19, said Orlando Harris, PhD, assistant professor of community health systems at the University of California, San Francisco, (UCSF) School of Nursing. HIV-related stigma is a well-known deterrent to care for people living with the virus. During the presentation, Harris asked Farley about the impact of COVID-19 stigma on people with both HIV and COVID-19.

Farley said that patients at his clinic have told him that they have “ostracized” friends who have tested positive for COVID-19. Harris remembered a person with HIV who participated in one of his trials telling the researchers that despite all his precautions – wearing a mask, staying socially distant – he still acquired COVID-19. There was nothing he could have done, Harris said, other than just not go to the grocery store.

The fear of contracting another disease that is associated with stigma, as well as the need to disclose it, can inflame memories of the trauma of being diagnosed with HIV, Harris said. And with patient-centered medical homes struggling to reconstitute their wraparound services via telehealth, he said he wonders whether clinicians should be doing more.

“I worry about people who have survived being diagnosed with HIV in the ‘80s and the ‘90s before antiretroviral therapy showed up on the scene,” he told Medscape Medical News. “I worry that the folks that survived one pandemic [may] be feeling fearful or living in that fear that this new pandemic might take them out. That’s why I’m stressing the need for us to really consider, as clinicians and also as researchers the support systems, the coping mechanisms, the counseling, or what have you to support those living with HIV and vulnerable to COVID-19.”

During telehealth visits, that can be achieved simply by asking people how they are really doing and what their coping mechanisms are.

For their part, the clinicians at San Francisco’s Ward 86 are not trying to provide that support through telehealth on the same level as they were at the beginning of the pandemic, said Matthew Spinelli, MD, assistant professor of medicine, and Monica Gandhi, MD, associate chief of the Division of HIV, Infectious Diseases and Global Medicine, who are both at UCSF and are coauthors of the study.

They still offer telemedicine appointments to patients who request them, said Spinelli. He said about one-third of his patients still prefer to receive their care virtually. The rest have gone back to face-to-face support.

“The analysis led us to promptly open up care as much as possible to our patients, with the idea that telehealth is not cutting it for vulnerable patients with HIV,” Gandhi told Medscape Medical News via email. “We don’t think it’s right for a population who relies on social support from the clinic.”
 

This article first appeared on Medscape.com.

Coronavirus infections are expected to continue to climb in the upper Midwest and intermountain West of the United States, which will strain an already-maxed-out system as increased hospitalizations and deaths follow, say infectious diseases specialists.

“I think the situation in 2 to 4 weeks is going to be grim,” said Andrew Pavia, MD, chief of the division of pediatric infectious diseases at the University of Utah School of Medicine in Salt Lake City, on a call yesterday with reporters, sponsored by the Infectious Diseases Society of America (IDSA).

Cases began rising in Utah in mid-September and have gone up steeply since, increasing from 450 cases per day to 2,650 reported on Nov. 8, according to the Johns Hopkins Coronavirus Resource Center. The New York Times reports that the 7-day rolling average for hospitalizations have gone up 34% and deaths have risen 93%, with 11 deaths this past Tuesday.

Other states in the west – Montana, Idaho, and Wyoming, which reported 1,232 cases on Tuesday and have been averaging 660 cases a day in the last week, according to the Times – are being equally hard hit. The same is true for states in the upper Midwest, including North Dakota, South Dakota, Minnesota, Wisconsin, and Iowa.

Most of the states being hit now have large swaths of rural countryside, which means health resources are limited and spread out, said Pavia.

“The situation really has to be described as dire,” said Pavia, noting that intensive care units in Utah are full, including contingency units that were purpose-built for the pandemic. Physicians and nurses are burned out and in short supply, he said. Instead of a 1:1 or 1:2 nurse-to-ICU patient ratio, the ratio is now 1:4, said Pavia. “Throughout the region, people are facing a crisis in staffing.”

The University of Utah hospital normally takes referrals from Idaho, Wyoming, and northern Arizona, but is prioritizing Utah residents for ICU admission, said Pavia.

Both Pavia and Daniel P. McQuillen, MD, president-elect of IDSA, also noted the shortage of infectious diseases specialists, which began at least a decade ago. McQuillen, senior infectious diseases physician at Beth Israel Lahey Health in Boston, said he and colleagues had done some research earlier this year anticipating the pandemic’s spread, and found that some 80% of counties – including the rural counties in the states now being hit – have one or zero infectious disease specialists.

Those specialists can help improve patient outcomes, explained McQuillen.
 

Colleges likely driving spike

Pavia said the reasons for sharp increases in the region vary, but there are several areas of commonality. Most of the states didn’t have many cases early in the pandemic, “so perhaps there was less fear of the virus.” There were fewer actions by government officials, driven perhaps by the reluctance to take on individuals who are distrustful of government, he said.

Cases started going up after some events – such as the August motorcycle rally in Sturgis, South Dakota – but the acceleration in September was likely driven by the reopening of colleges across the region, said Pavia.

“Most of the states have kept in-person schooling, and probably more importantly, they’ve kept extracurricular activities in sports,” he said, adding that in many of the areas the weather has turned cooler, driving people indoors.

McQuillen said it has been shown that a significant amount of transmission occurs within homes – and college students may be bringing the virus home and fueling spread, in addition to people not wearing masks while at small family gatherings.

Both he and Pavia said more emphasis needs to be placed on mitigation measures such as mask-wearing as well as on testing. IDSA is starting #MaskUpAmerica, a public service campaign aimed at getting people to wear masks in all community settings, including at work, in churches, at social gatherings, in gyms, and on public transportation.

Pavia said in some places people are refusing to be tested because they don’t want to be quarantined.

Utah Gov. Gary Herbert (R) issued a statewide mask mandate this past weekend and announced some other restrictions, including a 2-week pause on most, but not all, athletic events, according to CBS News. But local pushback could weaken those measures, said Pavia.

Many people are looking to vaccines to usher in a return to normal. But, said Pavia, “vaccines aren’t going to help us out much this winter,” noting that initial doses will be given mostly to first responders and healthcare workers.

“The only way we’re going to get out of this this winter is by doing the things that we’ve been talking about for months – wearing a mask, watching your social distance, and avoiding large gatherings,” he said.

There is an end in sight, said Pavia, but it won’t be in early 2021. “That end is next summer or fall,” he said. “And that’s a hard message to give but it’s really critical.”

McQuillen agreed: “Wearing masks and distancing are exactly all we have probably until middle of next year.”
 

This article first appeared on Medscape.com.

Coronavirus infections are expected to continue to climb in the upper Midwest and intermountain West of the United States, which will strain an already-maxed-out system as increased hospitalizations and deaths follow, say infectious diseases specialists.

“I think the situation in 2 to 4 weeks is going to be grim,” said Andrew Pavia, MD, chief of the division of pediatric infectious diseases at the University of Utah School of Medicine in Salt Lake City, on a call yesterday with reporters, sponsored by the Infectious Diseases Society of America (IDSA).

Cases began rising in Utah in mid-September and have gone up steeply since, increasing from 450 cases per day to 2,650 reported on Nov. 8, according to the Johns Hopkins Coronavirus Resource Center. The New York Times reports that the 7-day rolling average for hospitalizations have gone up 34% and deaths have risen 93%, with 11 deaths this past Tuesday.

Other states in the west – Montana, Idaho, and Wyoming, which reported 1,232 cases on Tuesday and have been averaging 660 cases a day in the last week, according to the Times – are being equally hard hit. The same is true for states in the upper Midwest, including North Dakota, South Dakota, Minnesota, Wisconsin, and Iowa.

Most of the states being hit now have large swaths of rural countryside, which means health resources are limited and spread out, said Pavia.

“The situation really has to be described as dire,” said Pavia, noting that intensive care units in Utah are full, including contingency units that were purpose-built for the pandemic. Physicians and nurses are burned out and in short supply, he said. Instead of a 1:1 or 1:2 nurse-to-ICU patient ratio, the ratio is now 1:4, said Pavia. “Throughout the region, people are facing a crisis in staffing.”

The University of Utah hospital normally takes referrals from Idaho, Wyoming, and northern Arizona, but is prioritizing Utah residents for ICU admission, said Pavia.

Both Pavia and Daniel P. McQuillen, MD, president-elect of IDSA, also noted the shortage of infectious diseases specialists, which began at least a decade ago. McQuillen, senior infectious diseases physician at Beth Israel Lahey Health in Boston, said he and colleagues had done some research earlier this year anticipating the pandemic’s spread, and found that some 80% of counties – including the rural counties in the states now being hit – have one or zero infectious disease specialists.

Those specialists can help improve patient outcomes, explained McQuillen.
 

Colleges likely driving spike

Pavia said the reasons for sharp increases in the region vary, but there are several areas of commonality. Most of the states didn’t have many cases early in the pandemic, “so perhaps there was less fear of the virus.” There were fewer actions by government officials, driven perhaps by the reluctance to take on individuals who are distrustful of government, he said.

Cases started going up after some events – such as the August motorcycle rally in Sturgis, South Dakota – but the acceleration in September was likely driven by the reopening of colleges across the region, said Pavia.

“Most of the states have kept in-person schooling, and probably more importantly, they’ve kept extracurricular activities in sports,” he said, adding that in many of the areas the weather has turned cooler, driving people indoors.

McQuillen said it has been shown that a significant amount of transmission occurs within homes – and college students may be bringing the virus home and fueling spread, in addition to people not wearing masks while at small family gatherings.

Both he and Pavia said more emphasis needs to be placed on mitigation measures such as mask-wearing as well as on testing. IDSA is starting #MaskUpAmerica, a public service campaign aimed at getting people to wear masks in all community settings, including at work, in churches, at social gatherings, in gyms, and on public transportation.

Pavia said in some places people are refusing to be tested because they don’t want to be quarantined.

Utah Gov. Gary Herbert (R) issued a statewide mask mandate this past weekend and announced some other restrictions, including a 2-week pause on most, but not all, athletic events, according to CBS News. But local pushback could weaken those measures, said Pavia.

Many people are looking to vaccines to usher in a return to normal. But, said Pavia, “vaccines aren’t going to help us out much this winter,” noting that initial doses will be given mostly to first responders and healthcare workers.

“The only way we’re going to get out of this this winter is by doing the things that we’ve been talking about for months – wearing a mask, watching your social distance, and avoiding large gatherings,” he said.

There is an end in sight, said Pavia, but it won’t be in early 2021. “That end is next summer or fall,” he said. “And that’s a hard message to give but it’s really critical.”

McQuillen agreed: “Wearing masks and distancing are exactly all we have probably until middle of next year.”
 

This article first appeared on Medscape.com.

Coronavirus infections are expected to continue to climb in the upper Midwest and intermountain West of the United States, which will strain an already-maxed-out system as increased hospitalizations and deaths follow, say infectious diseases specialists.

“I think the situation in 2 to 4 weeks is going to be grim,” said Andrew Pavia, MD, chief of the division of pediatric infectious diseases at the University of Utah School of Medicine in Salt Lake City, on a call yesterday with reporters, sponsored by the Infectious Diseases Society of America (IDSA).

Cases began rising in Utah in mid-September and have gone up steeply since, increasing from 450 cases per day to 2,650 reported on Nov. 8, according to the Johns Hopkins Coronavirus Resource Center. The New York Times reports that the 7-day rolling average for hospitalizations have gone up 34% and deaths have risen 93%, with 11 deaths this past Tuesday.

Other states in the west – Montana, Idaho, and Wyoming, which reported 1,232 cases on Tuesday and have been averaging 660 cases a day in the last week, according to the Times – are being equally hard hit. The same is true for states in the upper Midwest, including North Dakota, South Dakota, Minnesota, Wisconsin, and Iowa.

Most of the states being hit now have large swaths of rural countryside, which means health resources are limited and spread out, said Pavia.

“The situation really has to be described as dire,” said Pavia, noting that intensive care units in Utah are full, including contingency units that were purpose-built for the pandemic. Physicians and nurses are burned out and in short supply, he said. Instead of a 1:1 or 1:2 nurse-to-ICU patient ratio, the ratio is now 1:4, said Pavia. “Throughout the region, people are facing a crisis in staffing.”

The University of Utah hospital normally takes referrals from Idaho, Wyoming, and northern Arizona, but is prioritizing Utah residents for ICU admission, said Pavia.

Both Pavia and Daniel P. McQuillen, MD, president-elect of IDSA, also noted the shortage of infectious diseases specialists, which began at least a decade ago. McQuillen, senior infectious diseases physician at Beth Israel Lahey Health in Boston, said he and colleagues had done some research earlier this year anticipating the pandemic’s spread, and found that some 80% of counties – including the rural counties in the states now being hit – have one or zero infectious disease specialists.

Those specialists can help improve patient outcomes, explained McQuillen.
 

Colleges likely driving spike

Pavia said the reasons for sharp increases in the region vary, but there are several areas of commonality. Most of the states didn’t have many cases early in the pandemic, “so perhaps there was less fear of the virus.” There were fewer actions by government officials, driven perhaps by the reluctance to take on individuals who are distrustful of government, he said.

Cases started going up after some events – such as the August motorcycle rally in Sturgis, South Dakota – but the acceleration in September was likely driven by the reopening of colleges across the region, said Pavia.

“Most of the states have kept in-person schooling, and probably more importantly, they’ve kept extracurricular activities in sports,” he said, adding that in many of the areas the weather has turned cooler, driving people indoors.

McQuillen said it has been shown that a significant amount of transmission occurs within homes – and college students may be bringing the virus home and fueling spread, in addition to people not wearing masks while at small family gatherings.

Both he and Pavia said more emphasis needs to be placed on mitigation measures such as mask-wearing as well as on testing. IDSA is starting #MaskUpAmerica, a public service campaign aimed at getting people to wear masks in all community settings, including at work, in churches, at social gatherings, in gyms, and on public transportation.

Pavia said in some places people are refusing to be tested because they don’t want to be quarantined.

Utah Gov. Gary Herbert (R) issued a statewide mask mandate this past weekend and announced some other restrictions, including a 2-week pause on most, but not all, athletic events, according to CBS News. But local pushback could weaken those measures, said Pavia.

Many people are looking to vaccines to usher in a return to normal. But, said Pavia, “vaccines aren’t going to help us out much this winter,” noting that initial doses will be given mostly to first responders and healthcare workers.

“The only way we’re going to get out of this this winter is by doing the things that we’ve been talking about for months – wearing a mask, watching your social distance, and avoiding large gatherings,” he said.

There is an end in sight, said Pavia, but it won’t be in early 2021. “That end is next summer or fall,” he said. “And that’s a hard message to give but it’s really critical.”

McQuillen agreed: “Wearing masks and distancing are exactly all we have probably until middle of next year.”
 

This article first appeared on Medscape.com.

One in five COVID-19 patients are diagnosed with a psychiatric disorder such as anxiety or depression within 3 months of testing positive for the virus, new research suggests.

“People have been worried that COVID-19 survivors will be at greater risk of psychiatric disorders, and our findings in a large and detailed study show this to be true,” principal investigator Paul Harrison, BM, DM, professor of psychiatry, University of Oxford, Oxford, United Kingdom, said in a statement.

Health services “need to be ready to provide care, especially since our results are likely to be underestimates of the actual number of cases,” said Harrison.

The study also showed that having a psychiatric disorder independently increases the risk of getting COVID-19 – a finding that’s in line with research published earlier this month.

“Having a psychiatric illness should be added to the list of risk factors for COVID-19,” study coauthor Maxime Taquet, PhD, University of Oxford, said in the release.

The study was published online Nov. 9 in The Lancet Psychiatry.
 

Double the risk

The investigators took advantage of the TriNetX analytics network, which captured deidentified data from electronic health records of a total of 69.8 million patients from 54 healthcare organizations in the United States.

Of those patients, 62,354 adults were diagnosed with COVID-19 between Jan. 20 and Aug. 1, 2020.

To assess the psychiatric sequelae of COVID-19, the investigators created propensity score–matched cohorts of patients who had received a diagnosis of other conditions that represented a range of common acute presentations.

In 14 to 90 days after being diagnosed with COVID-19, 5.8% of patients received a first recorded diagnosis of psychiatric illness. Among patients with health problems other than COVID, 2.5% to 3.4% of patients received a psychiatric diagnosis, the authors report. The risk was greatest for anxiety disorders, depression, and insomnia.

Older COVID-19 patients had a two- to threefold increased risk for a first dementia diagnosis, a finding that supports an earlier UK study.

Some of this excess risk could reflect misdiagnosed cases of delirium or transient cognitive impairment due to reversible cerebral events, the authors noted.

The study also revealed a bidirectional relationship between mental illness and COVID-19. Individuals with a psychiatric diagnosis were about 65% more likely to be diagnosed with COVID-19 in comparison with their counterparts who did not have mental illness, independently of known physical health risk factors for COVID-19.

“We did not anticipate that psychiatric history would be an independent risk factor for COVID-19. This finding appears robust, being observed in all age strata and in both sexes, and was substantial,” the authors write.

At present, “we don’t understand what the explanation is for the associations between COVID and mental illness. We are looking into this in more detail to try and understand better what subgroups are particularly vulnerable in this regard,” Harrison told Medscape Medical News.
 

“Ambitious” research

Commenting on the findings for Medscape Medical News, Roy H. Perlis, MD, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, said this is “an ambitious effort to understand the short-term consequences of COVID in terms of brain diseases.”

Perlis said he’s not particularly surprised by the increase in psychiatric diagnoses among COVID-19 patients.

“After COVID infection, people are more likely to get close medical follow-up than usual. They’re more likely to be accessing the healthcare system; after all, they’ve already had COVID, so they’re probably less fearful of seeing their doctor. But, that probably also means they’re more likely to get a new diagnosis of something like depression,” he said.

Dementia may be the clearest illustration of this, Perlis said. “It seems less likely that dementia develops a month after COVID; more likely, something that happens during the illness leads someone to be more likely to diagnose dementia later on,” he noted.

Perlis cautioned against being “unnecessarily alarmed” by the findings in this study.

“We know that rates of depression in the UK and the US, as in much of the world, are substantially elevated right now. Much of this is likely a consequence of the stress and disruption that accompanies the pandemic,” said Perlis.

The study was funded by the National Institute for Health Research. Harrison has disclosed no relevant financial relationships. One author is an employee of TriNetX. Perlis has received consulting fees for service on scientific advisory boards of Belle Artificial Intelligence, Burrage Capital, Genomind, Psy Therapeutics, Outermost Therapeutics, RID Ventures, and Takeda. He holds equity in Psy Therapeutics and Outermost Therapeutics.
 

This article first appeared on Medscape.com.

One in five COVID-19 patients are diagnosed with a psychiatric disorder such as anxiety or depression within 3 months of testing positive for the virus, new research suggests.

“People have been worried that COVID-19 survivors will be at greater risk of psychiatric disorders, and our findings in a large and detailed study show this to be true,” principal investigator Paul Harrison, BM, DM, professor of psychiatry, University of Oxford, Oxford, United Kingdom, said in a statement.

Health services “need to be ready to provide care, especially since our results are likely to be underestimates of the actual number of cases,” said Harrison.

The study also showed that having a psychiatric disorder independently increases the risk of getting COVID-19 – a finding that’s in line with research published earlier this month.

“Having a psychiatric illness should be added to the list of risk factors for COVID-19,” study coauthor Maxime Taquet, PhD, University of Oxford, said in the release.

The study was published online Nov. 9 in The Lancet Psychiatry.
 

Double the risk

The investigators took advantage of the TriNetX analytics network, which captured deidentified data from electronic health records of a total of 69.8 million patients from 54 healthcare organizations in the United States.

Of those patients, 62,354 adults were diagnosed with COVID-19 between Jan. 20 and Aug. 1, 2020.

To assess the psychiatric sequelae of COVID-19, the investigators created propensity score–matched cohorts of patients who had received a diagnosis of other conditions that represented a range of common acute presentations.

In 14 to 90 days after being diagnosed with COVID-19, 5.8% of patients received a first recorded diagnosis of psychiatric illness. Among patients with health problems other than COVID, 2.5% to 3.4% of patients received a psychiatric diagnosis, the authors report. The risk was greatest for anxiety disorders, depression, and insomnia.

Older COVID-19 patients had a two- to threefold increased risk for a first dementia diagnosis, a finding that supports an earlier UK study.

Some of this excess risk could reflect misdiagnosed cases of delirium or transient cognitive impairment due to reversible cerebral events, the authors noted.

The study also revealed a bidirectional relationship between mental illness and COVID-19. Individuals with a psychiatric diagnosis were about 65% more likely to be diagnosed with COVID-19 in comparison with their counterparts who did not have mental illness, independently of known physical health risk factors for COVID-19.

“We did not anticipate that psychiatric history would be an independent risk factor for COVID-19. This finding appears robust, being observed in all age strata and in both sexes, and was substantial,” the authors write.

At present, “we don’t understand what the explanation is for the associations between COVID and mental illness. We are looking into this in more detail to try and understand better what subgroups are particularly vulnerable in this regard,” Harrison told Medscape Medical News.
 

“Ambitious” research

Commenting on the findings for Medscape Medical News, Roy H. Perlis, MD, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, said this is “an ambitious effort to understand the short-term consequences of COVID in terms of brain diseases.”

Perlis said he’s not particularly surprised by the increase in psychiatric diagnoses among COVID-19 patients.

“After COVID infection, people are more likely to get close medical follow-up than usual. They’re more likely to be accessing the healthcare system; after all, they’ve already had COVID, so they’re probably less fearful of seeing their doctor. But, that probably also means they’re more likely to get a new diagnosis of something like depression,” he said.

Dementia may be the clearest illustration of this, Perlis said. “It seems less likely that dementia develops a month after COVID; more likely, something that happens during the illness leads someone to be more likely to diagnose dementia later on,” he noted.

Perlis cautioned against being “unnecessarily alarmed” by the findings in this study.

“We know that rates of depression in the UK and the US, as in much of the world, are substantially elevated right now. Much of this is likely a consequence of the stress and disruption that accompanies the pandemic,” said Perlis.

The study was funded by the National Institute for Health Research. Harrison has disclosed no relevant financial relationships. One author is an employee of TriNetX. Perlis has received consulting fees for service on scientific advisory boards of Belle Artificial Intelligence, Burrage Capital, Genomind, Psy Therapeutics, Outermost Therapeutics, RID Ventures, and Takeda. He holds equity in Psy Therapeutics and Outermost Therapeutics.
 

This article first appeared on Medscape.com.

One in five COVID-19 patients are diagnosed with a psychiatric disorder such as anxiety or depression within 3 months of testing positive for the virus, new research suggests.

“People have been worried that COVID-19 survivors will be at greater risk of psychiatric disorders, and our findings in a large and detailed study show this to be true,” principal investigator Paul Harrison, BM, DM, professor of psychiatry, University of Oxford, Oxford, United Kingdom, said in a statement.

Health services “need to be ready to provide care, especially since our results are likely to be underestimates of the actual number of cases,” said Harrison.

The study also showed that having a psychiatric disorder independently increases the risk of getting COVID-19 – a finding that’s in line with research published earlier this month.

“Having a psychiatric illness should be added to the list of risk factors for COVID-19,” study coauthor Maxime Taquet, PhD, University of Oxford, said in the release.

The study was published online Nov. 9 in The Lancet Psychiatry.
 

Double the risk

The investigators took advantage of the TriNetX analytics network, which captured deidentified data from electronic health records of a total of 69.8 million patients from 54 healthcare organizations in the United States.

Of those patients, 62,354 adults were diagnosed with COVID-19 between Jan. 20 and Aug. 1, 2020.

To assess the psychiatric sequelae of COVID-19, the investigators created propensity score–matched cohorts of patients who had received a diagnosis of other conditions that represented a range of common acute presentations.

In 14 to 90 days after being diagnosed with COVID-19, 5.8% of patients received a first recorded diagnosis of psychiatric illness. Among patients with health problems other than COVID, 2.5% to 3.4% of patients received a psychiatric diagnosis, the authors report. The risk was greatest for anxiety disorders, depression, and insomnia.

Older COVID-19 patients had a two- to threefold increased risk for a first dementia diagnosis, a finding that supports an earlier UK study.

Some of this excess risk could reflect misdiagnosed cases of delirium or transient cognitive impairment due to reversible cerebral events, the authors noted.

The study also revealed a bidirectional relationship between mental illness and COVID-19. Individuals with a psychiatric diagnosis were about 65% more likely to be diagnosed with COVID-19 in comparison with their counterparts who did not have mental illness, independently of known physical health risk factors for COVID-19.

“We did not anticipate that psychiatric history would be an independent risk factor for COVID-19. This finding appears robust, being observed in all age strata and in both sexes, and was substantial,” the authors write.

At present, “we don’t understand what the explanation is for the associations between COVID and mental illness. We are looking into this in more detail to try and understand better what subgroups are particularly vulnerable in this regard,” Harrison told Medscape Medical News.
 

“Ambitious” research

Commenting on the findings for Medscape Medical News, Roy H. Perlis, MD, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, said this is “an ambitious effort to understand the short-term consequences of COVID in terms of brain diseases.”

Perlis said he’s not particularly surprised by the increase in psychiatric diagnoses among COVID-19 patients.

“After COVID infection, people are more likely to get close medical follow-up than usual. They’re more likely to be accessing the healthcare system; after all, they’ve already had COVID, so they’re probably less fearful of seeing their doctor. But, that probably also means they’re more likely to get a new diagnosis of something like depression,” he said.

Dementia may be the clearest illustration of this, Perlis said. “It seems less likely that dementia develops a month after COVID; more likely, something that happens during the illness leads someone to be more likely to diagnose dementia later on,” he noted.

Perlis cautioned against being “unnecessarily alarmed” by the findings in this study.

“We know that rates of depression in the UK and the US, as in much of the world, are substantially elevated right now. Much of this is likely a consequence of the stress and disruption that accompanies the pandemic,” said Perlis.

The study was funded by the National Institute for Health Research. Harrison has disclosed no relevant financial relationships. One author is an employee of TriNetX. Perlis has received consulting fees for service on scientific advisory boards of Belle Artificial Intelligence, Burrage Capital, Genomind, Psy Therapeutics, Outermost Therapeutics, RID Ventures, and Takeda. He holds equity in Psy Therapeutics and Outermost Therapeutics.
 

This article first appeared on Medscape.com.

Increasingly, clinicians are being called upon to advise athletes who have recovered from COVID-19 on when it is safe for them to return to play.

Now, they have two reports that offer more insights into the cardiotoxic effects of COVID-19 on the athletic heart.

In the first report, researchers report a high prevalence of pericardial involvement in college-student athletes who have recovered from COVID-19 and give their practical advice on how to let these athletes return to play safely.

In the second report, an expert panel of sports cardiologists provides a comprehensive guide to the appropriate imaging of athletes who may have cardiovascular complications from COVID-19.

Both are published in JACC: Cardiovascular Imaging.

“We were asked by the editors of JACC to submit this paper, and the impetus for it was the fact that there are so many athletes returning after being infected with COVID-19, we need to try and give guidance to cardiologists as to how best to evaluate these athletes,” Dermot Phelan, MD, PhD, Sanger Heart and Vascular Institute, Atrium Health, Charlotte, N.C., and lead author of the consensus statement, said in an interview.

The consensus statement acknowledges that information about the cardiovascular complications of COVID-19 continues to evolve. Meanwhile, pathologies such as myocarditis, pericarditis, and right ventricular dysfunction, in the absence of significant clinical symptoms, in athletes who have been affected by COVID-19 remain of considerable concern.

It also emphasizes the unique challenges the average cardiologist faces in distinguishing between what is normal for an athlete’s heart and what is true pathology after COVID-19 infection; details how different imaging modalities can help in screening, evaluating, and monitoring athletes with suspected cardiovascular complications of COVID-19 infection; and discusses the strengths and limitations of these modalities.

Finally, the consensus statement provides some well-needed guidance on return-to-play decision-making, for both the athlete and the clinician.
 

Athletic remodeling or covid-19 damage?

Athletes can develop certain cardiovascular characteristics because of their athletic activity, and sometimes, this can cloud the diagnostic picture.

“Is this change due to the effects of COVID-19, or is it just because this is an athlete’s heart? This was an international expert consensus, made up of sports cardiologists from all over the world who have a lot of experience in dealing with athletes,” Dr. Phelan said. “We were trying to relay the important information to the cardiologist who is not used to dealing with athletes on a day-to-day basis, as to what they might expect to find in that athlete, and what is not an expected finding and should be tested further.”

Phelan, a sports cardiologist, is familiar with what is normal for an athlete’s heart and what is pathology.

“We know that athletes, particularly long-term endurance athletes, develop changes in the heart that can affect not only the electrics but the structure of the heart, and sometimes, that overlaps with abnormalities with pathology. This can be a challenge for the nonsports cardiologist to differentiate,” he said.

Phelan and his group have written two other consensus documents on the management of cardiovascular problems that develop in some athletes who have been infected with COVID-19.

The first was published in May in JAMA Cardiology, and the second, which revised some of the original recommendations made in the first document, was published online Oct. 26 in JAMA Cardiology.

The first set of recommendations called for imaging studies to be done in all athletes, but the second set states that athletes who recover and are asymptomatic do not need extensive (and expensive) imaging tests.

“These two papers work hand in hand,” Dr. Phelan said. “In May, we had very little experience with COVID, and there was a lot of concern about hospitalized patients having a very high incidence of heart disease. We published those recommendations, but we recognized at the time that we had very little data and that we would reconsider once we had more experience with data.

“This current set of recommendations that we have put forth here are for those athletes who do need to get further testing, so it’s a step beyond,” Dr. Phelan added. “So the second iteration states that young athletes who had mild or no symptoms didn’t need to go through all of that cardiac testing, but others do need it.”

To do widespread cardiovascular imaging for many individuals would be very costly. Realistically, there are not that many centers in the United States that have all the sophisticated equipment required to do such testing, Dr. Phelan noted.

“One of our major points is difficulty obtaining the test, but also the cost; these are very expensive tests. There are limitations. They are useful when used in the correct context,” he said.
 

To play or not to play, that is the question

Partho P. Sengupta, MD, DM, had to answer that question for more than 50 young athletes who were returning to college at West Virginia University, anxious to be back with their teams and on the playing field. They had been infected with COVID-19 and needed to know when they could return to play.

Dr. Sengupta, who is also an author for the Phelan et al consensus statement on imaging, said there was a lot of pressure – from all the various stakeholders, and from anxious parents, worried college athletes, their teammates, and the university – to determine if the youngsters could return to play.

The fear was that COVID-19 infection left the young athlete’s heart vulnerable to myocarditis and, thus, sudden death on the playing field after strenuous activity.

“At the time we were doing this imaging, there was a lot of concern in the media, and papers were coming out reporting a lot of cardiac involvement or myocarditis associated with COVID-19. Nobody really knew what to do,” he explained.

“There were all kinds of questions, concerns. The parents were putting pressure on us, the athletes wanted to know, the teams, the university. So we put together a team and completed all of the examinations, including testing of blood markers, within a 2-week period. These young athletes, they’re scared, they’re worried and anxious, they don’t know what’s going to happen with their scholarship, so there was some urgency to this work,” Dr. Sengupta said.

“We had to screen all comers within a very short period. We had 54 consecutive patients, gave them full screening, full battery of tests, blood tests, all in a 2-week period,” he said.

Speed was of the essence, and Dr. Sengupta and his team rolled up their sleeves and got to work “We had to know who was safe to clear to return to play and who might need extra follow-up.”
 

Screening echocardiograms

They performed screening echocardiograms on 54 consecutive college athletes who had tested positive for COVID-19 on reverse transcription polymerase chain reaction nasal swab testing or who showed that they had IgG antibodies against COVID-19. The screening echocardiograms were done after the athletes had quarantined for at least 14 days and were no longer infectious.

Most (85%) were male, and the mean age was 19 years. A total of 16 (30%) athletes were asymptomatic, 36 (66%) reported mild COVID-19 related symptoms, and two (4%) reported moderate symptoms.

Of the 54 athletes who were initially screened with echocardiography, 48 (11 asymptomatic, 37 symptomatic), went on to have cardiac magnetic resonance imaging.

Results showed that more than half the athletes (27; 56.3%), showed some cardiac abnormality. The most common was pericardial late enhancement with associated pericardial effusion, affecting 19 (39.5%) athletes.

Of these, six (12.5%) had reduced global longitudinal strain (GLS) or an increased native T1.

One patient showed myocardial enhancement.

Additionally, seven athletes (14.6%) had reduced left ventricular ejection fraction or reduced GLS with or without increased native T1. Native T2 levels were normal in all subjects and no specific imaging features of myocardial inflammation were identified.

Participants were brought back to receive the results of their tests and to get an individualized plan about their safe return to play 3 to 5 weeks after they had ceased to be infectious with COVID-19.

“We saw pericardial inflammation that was resolving. We did not see any blood biomarkers to suggest that there was active inflammation going on,” he said. “We also did not see any muscle inflammation, but we did see pockets of fluid in over a third of our athletes.”

Fortunately, most were deemed able to get back to playing safely, despite having evidence of pericardial inflammation.

This was on strict condition that they be monitored very closely for any adverse events that might occur as they began to exercise again.

“Once they go back to the field to start exercising and practicing, it is under great supervision. We instructed all of our sports physicians and other team managers that these people need to be observed very carefully. So as long as they were asymptomatic, even though the signs of pericardial inflammation were there, if there were no signs of inflammation in the blood, we let them go back to play, closely monitored,” Dr. Sengupta said.

A small number remained very symptomatic at the end of the 5 weeks and were referred to cardiac rehabilitation, Dr. Sengupta said. “They were tired, fatigued, short of breath, even 5 weeks after they got over COVID, so we sent them for cardiac rehab to help them get conditioned again.”

The researchers plan to reevaluate and reimage all of the athletes in another 3 months to monitor their cardiac health.

Dr. Sengupta acknowledged the limitations of this single-center, nonrandomized, controlled report, but insists reports such as this add a bit more to what we are learning about COVID-19 every day.

“These kids were coming to us and asking questions. You have to use the best science you have available to you at that point in time. Some people ask why we did not have a control group, but how do you design a control population in the midst of a pandemic? The science may or may not be perfect, I agree, but the information we obtained is important,” he said.

“Right now, I don’t think we have enough science, and we are still learning. It is very difficult to predict who will develop the heart muscle disease or the pericardial disease,” Dr. Sengupta said. “We had to do our work quickly to give answers to the young athletes, their parents, their teammates, their university, as soon as possible, and we were doing this under pandemic conditions.”

The work was supported by the National Science Foundation National Institute of General Medical Sciences of the National Institutes of Health. Dr. Phelan reported no relevant financial relationships. Dr. Sengupta reported that he is a consultant for HeartSciences, Kencor Health, and Ultromics.

This article first appeared on Medscape.com.

Increasingly, clinicians are being called upon to advise athletes who have recovered from COVID-19 on when it is safe for them to return to play.

Now, they have two reports that offer more insights into the cardiotoxic effects of COVID-19 on the athletic heart.

In the first report, researchers report a high prevalence of pericardial involvement in college-student athletes who have recovered from COVID-19 and give their practical advice on how to let these athletes return to play safely.

In the second report, an expert panel of sports cardiologists provides a comprehensive guide to the appropriate imaging of athletes who may have cardiovascular complications from COVID-19.

Both are published in JACC: Cardiovascular Imaging.

“We were asked by the editors of JACC to submit this paper, and the impetus for it was the fact that there are so many athletes returning after being infected with COVID-19, we need to try and give guidance to cardiologists as to how best to evaluate these athletes,” Dermot Phelan, MD, PhD, Sanger Heart and Vascular Institute, Atrium Health, Charlotte, N.C., and lead author of the consensus statement, said in an interview.

The consensus statement acknowledges that information about the cardiovascular complications of COVID-19 continues to evolve. Meanwhile, pathologies such as myocarditis, pericarditis, and right ventricular dysfunction, in the absence of significant clinical symptoms, in athletes who have been affected by COVID-19 remain of considerable concern.

It also emphasizes the unique challenges the average cardiologist faces in distinguishing between what is normal for an athlete’s heart and what is true pathology after COVID-19 infection; details how different imaging modalities can help in screening, evaluating, and monitoring athletes with suspected cardiovascular complications of COVID-19 infection; and discusses the strengths and limitations of these modalities.

Finally, the consensus statement provides some well-needed guidance on return-to-play decision-making, for both the athlete and the clinician.
 

Athletic remodeling or covid-19 damage?

Athletes can develop certain cardiovascular characteristics because of their athletic activity, and sometimes, this can cloud the diagnostic picture.

“Is this change due to the effects of COVID-19, or is it just because this is an athlete’s heart? This was an international expert consensus, made up of sports cardiologists from all over the world who have a lot of experience in dealing with athletes,” Dr. Phelan said. “We were trying to relay the important information to the cardiologist who is not used to dealing with athletes on a day-to-day basis, as to what they might expect to find in that athlete, and what is not an expected finding and should be tested further.”

Phelan, a sports cardiologist, is familiar with what is normal for an athlete’s heart and what is pathology.

“We know that athletes, particularly long-term endurance athletes, develop changes in the heart that can affect not only the electrics but the structure of the heart, and sometimes, that overlaps with abnormalities with pathology. This can be a challenge for the nonsports cardiologist to differentiate,” he said.

Phelan and his group have written two other consensus documents on the management of cardiovascular problems that develop in some athletes who have been infected with COVID-19.

The first was published in May in JAMA Cardiology, and the second, which revised some of the original recommendations made in the first document, was published online Oct. 26 in JAMA Cardiology.

The first set of recommendations called for imaging studies to be done in all athletes, but the second set states that athletes who recover and are asymptomatic do not need extensive (and expensive) imaging tests.

“These two papers work hand in hand,” Dr. Phelan said. “In May, we had very little experience with COVID, and there was a lot of concern about hospitalized patients having a very high incidence of heart disease. We published those recommendations, but we recognized at the time that we had very little data and that we would reconsider once we had more experience with data.

“This current set of recommendations that we have put forth here are for those athletes who do need to get further testing, so it’s a step beyond,” Dr. Phelan added. “So the second iteration states that young athletes who had mild or no symptoms didn’t need to go through all of that cardiac testing, but others do need it.”

To do widespread cardiovascular imaging for many individuals would be very costly. Realistically, there are not that many centers in the United States that have all the sophisticated equipment required to do such testing, Dr. Phelan noted.

“One of our major points is difficulty obtaining the test, but also the cost; these are very expensive tests. There are limitations. They are useful when used in the correct context,” he said.
 

To play or not to play, that is the question

Partho P. Sengupta, MD, DM, had to answer that question for more than 50 young athletes who were returning to college at West Virginia University, anxious to be back with their teams and on the playing field. They had been infected with COVID-19 and needed to know when they could return to play.

Dr. Sengupta, who is also an author for the Phelan et al consensus statement on imaging, said there was a lot of pressure – from all the various stakeholders, and from anxious parents, worried college athletes, their teammates, and the university – to determine if the youngsters could return to play.

The fear was that COVID-19 infection left the young athlete’s heart vulnerable to myocarditis and, thus, sudden death on the playing field after strenuous activity.

“At the time we were doing this imaging, there was a lot of concern in the media, and papers were coming out reporting a lot of cardiac involvement or myocarditis associated with COVID-19. Nobody really knew what to do,” he explained.

“There were all kinds of questions, concerns. The parents were putting pressure on us, the athletes wanted to know, the teams, the university. So we put together a team and completed all of the examinations, including testing of blood markers, within a 2-week period. These young athletes, they’re scared, they’re worried and anxious, they don’t know what’s going to happen with their scholarship, so there was some urgency to this work,” Dr. Sengupta said.

“We had to screen all comers within a very short period. We had 54 consecutive patients, gave them full screening, full battery of tests, blood tests, all in a 2-week period,” he said.

Speed was of the essence, and Dr. Sengupta and his team rolled up their sleeves and got to work “We had to know who was safe to clear to return to play and who might need extra follow-up.”
 

Screening echocardiograms

They performed screening echocardiograms on 54 consecutive college athletes who had tested positive for COVID-19 on reverse transcription polymerase chain reaction nasal swab testing or who showed that they had IgG antibodies against COVID-19. The screening echocardiograms were done after the athletes had quarantined for at least 14 days and were no longer infectious.

Most (85%) were male, and the mean age was 19 years. A total of 16 (30%) athletes were asymptomatic, 36 (66%) reported mild COVID-19 related symptoms, and two (4%) reported moderate symptoms.

Of the 54 athletes who were initially screened with echocardiography, 48 (11 asymptomatic, 37 symptomatic), went on to have cardiac magnetic resonance imaging.

Results showed that more than half the athletes (27; 56.3%), showed some cardiac abnormality. The most common was pericardial late enhancement with associated pericardial effusion, affecting 19 (39.5%) athletes.

Of these, six (12.5%) had reduced global longitudinal strain (GLS) or an increased native T1.

One patient showed myocardial enhancement.

Additionally, seven athletes (14.6%) had reduced left ventricular ejection fraction or reduced GLS with or without increased native T1. Native T2 levels were normal in all subjects and no specific imaging features of myocardial inflammation were identified.

Participants were brought back to receive the results of their tests and to get an individualized plan about their safe return to play 3 to 5 weeks after they had ceased to be infectious with COVID-19.

“We saw pericardial inflammation that was resolving. We did not see any blood biomarkers to suggest that there was active inflammation going on,” he said. “We also did not see any muscle inflammation, but we did see pockets of fluid in over a third of our athletes.”

Fortunately, most were deemed able to get back to playing safely, despite having evidence of pericardial inflammation.

This was on strict condition that they be monitored very closely for any adverse events that might occur as they began to exercise again.

“Once they go back to the field to start exercising and practicing, it is under great supervision. We instructed all of our sports physicians and other team managers that these people need to be observed very carefully. So as long as they were asymptomatic, even though the signs of pericardial inflammation were there, if there were no signs of inflammation in the blood, we let them go back to play, closely monitored,” Dr. Sengupta said.

A small number remained very symptomatic at the end of the 5 weeks and were referred to cardiac rehabilitation, Dr. Sengupta said. “They were tired, fatigued, short of breath, even 5 weeks after they got over COVID, so we sent them for cardiac rehab to help them get conditioned again.”

The researchers plan to reevaluate and reimage all of the athletes in another 3 months to monitor their cardiac health.

Dr. Sengupta acknowledged the limitations of this single-center, nonrandomized, controlled report, but insists reports such as this add a bit more to what we are learning about COVID-19 every day.

“These kids were coming to us and asking questions. You have to use the best science you have available to you at that point in time. Some people ask why we did not have a control group, but how do you design a control population in the midst of a pandemic? The science may or may not be perfect, I agree, but the information we obtained is important,” he said.

“Right now, I don’t think we have enough science, and we are still learning. It is very difficult to predict who will develop the heart muscle disease or the pericardial disease,” Dr. Sengupta said. “We had to do our work quickly to give answers to the young athletes, their parents, their teammates, their university, as soon as possible, and we were doing this under pandemic conditions.”

The work was supported by the National Science Foundation National Institute of General Medical Sciences of the National Institutes of Health. Dr. Phelan reported no relevant financial relationships. Dr. Sengupta reported that he is a consultant for HeartSciences, Kencor Health, and Ultromics.

This article first appeared on Medscape.com.

Increasingly, clinicians are being called upon to advise athletes who have recovered from COVID-19 on when it is safe for them to return to play.

Now, they have two reports that offer more insights into the cardiotoxic effects of COVID-19 on the athletic heart.

In the first report, researchers report a high prevalence of pericardial involvement in college-student athletes who have recovered from COVID-19 and give their practical advice on how to let these athletes return to play safely.

In the second report, an expert panel of sports cardiologists provides a comprehensive guide to the appropriate imaging of athletes who may have cardiovascular complications from COVID-19.

Both are published in JACC: Cardiovascular Imaging.

“We were asked by the editors of JACC to submit this paper, and the impetus for it was the fact that there are so many athletes returning after being infected with COVID-19, we need to try and give guidance to cardiologists as to how best to evaluate these athletes,” Dermot Phelan, MD, PhD, Sanger Heart and Vascular Institute, Atrium Health, Charlotte, N.C., and lead author of the consensus statement, said in an interview.

The consensus statement acknowledges that information about the cardiovascular complications of COVID-19 continues to evolve. Meanwhile, pathologies such as myocarditis, pericarditis, and right ventricular dysfunction, in the absence of significant clinical symptoms, in athletes who have been affected by COVID-19 remain of considerable concern.

It also emphasizes the unique challenges the average cardiologist faces in distinguishing between what is normal for an athlete’s heart and what is true pathology after COVID-19 infection; details how different imaging modalities can help in screening, evaluating, and monitoring athletes with suspected cardiovascular complications of COVID-19 infection; and discusses the strengths and limitations of these modalities.

Finally, the consensus statement provides some well-needed guidance on return-to-play decision-making, for both the athlete and the clinician.
 

Athletic remodeling or covid-19 damage?

Athletes can develop certain cardiovascular characteristics because of their athletic activity, and sometimes, this can cloud the diagnostic picture.

“Is this change due to the effects of COVID-19, or is it just because this is an athlete’s heart? This was an international expert consensus, made up of sports cardiologists from all over the world who have a lot of experience in dealing with athletes,” Dr. Phelan said. “We were trying to relay the important information to the cardiologist who is not used to dealing with athletes on a day-to-day basis, as to what they might expect to find in that athlete, and what is not an expected finding and should be tested further.”

Phelan, a sports cardiologist, is familiar with what is normal for an athlete’s heart and what is pathology.

“We know that athletes, particularly long-term endurance athletes, develop changes in the heart that can affect not only the electrics but the structure of the heart, and sometimes, that overlaps with abnormalities with pathology. This can be a challenge for the nonsports cardiologist to differentiate,” he said.

Phelan and his group have written two other consensus documents on the management of cardiovascular problems that develop in some athletes who have been infected with COVID-19.

The first was published in May in JAMA Cardiology, and the second, which revised some of the original recommendations made in the first document, was published online Oct. 26 in JAMA Cardiology.

The first set of recommendations called for imaging studies to be done in all athletes, but the second set states that athletes who recover and are asymptomatic do not need extensive (and expensive) imaging tests.

“These two papers work hand in hand,” Dr. Phelan said. “In May, we had very little experience with COVID, and there was a lot of concern about hospitalized patients having a very high incidence of heart disease. We published those recommendations, but we recognized at the time that we had very little data and that we would reconsider once we had more experience with data.

“This current set of recommendations that we have put forth here are for those athletes who do need to get further testing, so it’s a step beyond,” Dr. Phelan added. “So the second iteration states that young athletes who had mild or no symptoms didn’t need to go through all of that cardiac testing, but others do need it.”

To do widespread cardiovascular imaging for many individuals would be very costly. Realistically, there are not that many centers in the United States that have all the sophisticated equipment required to do such testing, Dr. Phelan noted.

“One of our major points is difficulty obtaining the test, but also the cost; these are very expensive tests. There are limitations. They are useful when used in the correct context,” he said.
 

To play or not to play, that is the question

Partho P. Sengupta, MD, DM, had to answer that question for more than 50 young athletes who were returning to college at West Virginia University, anxious to be back with their teams and on the playing field. They had been infected with COVID-19 and needed to know when they could return to play.

Dr. Sengupta, who is also an author for the Phelan et al consensus statement on imaging, said there was a lot of pressure – from all the various stakeholders, and from anxious parents, worried college athletes, their teammates, and the university – to determine if the youngsters could return to play.

The fear was that COVID-19 infection left the young athlete’s heart vulnerable to myocarditis and, thus, sudden death on the playing field after strenuous activity.

“At the time we were doing this imaging, there was a lot of concern in the media, and papers were coming out reporting a lot of cardiac involvement or myocarditis associated with COVID-19. Nobody really knew what to do,” he explained.

“There were all kinds of questions, concerns. The parents were putting pressure on us, the athletes wanted to know, the teams, the university. So we put together a team and completed all of the examinations, including testing of blood markers, within a 2-week period. These young athletes, they’re scared, they’re worried and anxious, they don’t know what’s going to happen with their scholarship, so there was some urgency to this work,” Dr. Sengupta said.

“We had to screen all comers within a very short period. We had 54 consecutive patients, gave them full screening, full battery of tests, blood tests, all in a 2-week period,” he said.

Speed was of the essence, and Dr. Sengupta and his team rolled up their sleeves and got to work “We had to know who was safe to clear to return to play and who might need extra follow-up.”
 

Screening echocardiograms

They performed screening echocardiograms on 54 consecutive college athletes who had tested positive for COVID-19 on reverse transcription polymerase chain reaction nasal swab testing or who showed that they had IgG antibodies against COVID-19. The screening echocardiograms were done after the athletes had quarantined for at least 14 days and were no longer infectious.

Most (85%) were male, and the mean age was 19 years. A total of 16 (30%) athletes were asymptomatic, 36 (66%) reported mild COVID-19 related symptoms, and two (4%) reported moderate symptoms.

Of the 54 athletes who were initially screened with echocardiography, 48 (11 asymptomatic, 37 symptomatic), went on to have cardiac magnetic resonance imaging.

Results showed that more than half the athletes (27; 56.3%), showed some cardiac abnormality. The most common was pericardial late enhancement with associated pericardial effusion, affecting 19 (39.5%) athletes.

Of these, six (12.5%) had reduced global longitudinal strain (GLS) or an increased native T1.

One patient showed myocardial enhancement.

Additionally, seven athletes (14.6%) had reduced left ventricular ejection fraction or reduced GLS with or without increased native T1. Native T2 levels were normal in all subjects and no specific imaging features of myocardial inflammation were identified.

Participants were brought back to receive the results of their tests and to get an individualized plan about their safe return to play 3 to 5 weeks after they had ceased to be infectious with COVID-19.

“We saw pericardial inflammation that was resolving. We did not see any blood biomarkers to suggest that there was active inflammation going on,” he said. “We also did not see any muscle inflammation, but we did see pockets of fluid in over a third of our athletes.”

Fortunately, most were deemed able to get back to playing safely, despite having evidence of pericardial inflammation.

This was on strict condition that they be monitored very closely for any adverse events that might occur as they began to exercise again.

“Once they go back to the field to start exercising and practicing, it is under great supervision. We instructed all of our sports physicians and other team managers that these people need to be observed very carefully. So as long as they were asymptomatic, even though the signs of pericardial inflammation were there, if there were no signs of inflammation in the blood, we let them go back to play, closely monitored,” Dr. Sengupta said.

A small number remained very symptomatic at the end of the 5 weeks and were referred to cardiac rehabilitation, Dr. Sengupta said. “They were tired, fatigued, short of breath, even 5 weeks after they got over COVID, so we sent them for cardiac rehab to help them get conditioned again.”

The researchers plan to reevaluate and reimage all of the athletes in another 3 months to monitor their cardiac health.

Dr. Sengupta acknowledged the limitations of this single-center, nonrandomized, controlled report, but insists reports such as this add a bit more to what we are learning about COVID-19 every day.

“These kids were coming to us and asking questions. You have to use the best science you have available to you at that point in time. Some people ask why we did not have a control group, but how do you design a control population in the midst of a pandemic? The science may or may not be perfect, I agree, but the information we obtained is important,” he said.

“Right now, I don’t think we have enough science, and we are still learning. It is very difficult to predict who will develop the heart muscle disease or the pericardial disease,” Dr. Sengupta said. “We had to do our work quickly to give answers to the young athletes, their parents, their teammates, their university, as soon as possible, and we were doing this under pandemic conditions.”

The work was supported by the National Science Foundation National Institute of General Medical Sciences of the National Institutes of Health. Dr. Phelan reported no relevant financial relationships. Dr. Sengupta reported that he is a consultant for HeartSciences, Kencor Health, and Ultromics.

This article first appeared on Medscape.com.

The largest U.S. physician organization on Tuesday took a step to prepare for future payments for administration of two leading COVID-19 vaccine candidates, publishing new billing codes tailored to track each use of these medications.

The American Medical Association updated its CPT code set to reflect the expected future availability of COVID-19 vaccines. The new codes apply to the experimental vaccine being developed by Pfizer, in collaboration with a smaller German firm BioNTech, and to the similar product expected from Moderna, according to an AMA press release.

Positive news has emerged this week about both of these vaccines, which were developed using a newer – and as yet unproven – approach. They seek to use messenger RNA to instruct cells to produce a target protein for SARS-CoV-2.

New York–based Pfizer on Monday announced interim phase 3 data that was widely viewed as promising. Pfizer said the vaccine appeared to be 90% effective in preventing COVID-19 in trial volunteers who were without evidence of prior infection of the virus.

In a press release, Pfizer said it plans to ask the Food and Drug Administration to consider a special clearance, known as an emergency-use authorization, “soon after” a safety milestone is achieved in its vaccine trial. That milestone could be reached this month.

Moderna said it was on track to report early data from a late-stage trial of its experimental coronavirus vaccine later this month, and could file with the FDA for an emergency-use authorization in early December, according to a Reuters report.

The severity of the global pandemic has put the FDA under pressure to move quickly on approval of COVID-19 vaccines, based on limited data, while also working to make sure these products are safe. The creation of CPT codes for each of two coronavirus vaccines, as well as accompanying administration codes, will set up a way to keep tabs on each dose of each of these shots, the AMA said.

American Medical Association

“Correlating each coronavirus vaccine with its own unique CPT code provides analytical advantages to help track, allocate and optimize resources as an immunization program ramps up in the United States,” AMA President Susan R. Bailey, MD, said in the release.

AMA plans to introduce more vaccine-specific CPT codes as more vaccine candidates approach FDA review. These vaccine-specific CPT codes can go into effect only after the FDA grants a clearance.

The newly created Category I CPT codes and long descriptors for the vaccine products are:
 

• 91300; severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 30 mcg/0.3mL dosage, diluent reconstituted, for intramuscular use (Pfizer/BioNTech)
• 91301; severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 100 mcg/0.5mL dosage, for intramuscular use (Moderna)

These two administrative codes would apply to the Pfizer-BioNTech shot:

• 0001A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 30 mcg/0.3 mL dosage, diluent reconstituted; first dose.
• 0002A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 30 mcg/0.3 mL dosage, diluent reconstituted; second dose.

And these two administrative codes would apply to the Moderna shot:

• 0011A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 100 mcg/0.5 mL dosage; first dose.
• 0012A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 100 mcg/0.5 mL dosage; second dose.

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

The largest U.S. physician organization on Tuesday took a step to prepare for future payments for administration of two leading COVID-19 vaccine candidates, publishing new billing codes tailored to track each use of these medications.

The American Medical Association updated its CPT code set to reflect the expected future availability of COVID-19 vaccines. The new codes apply to the experimental vaccine being developed by Pfizer, in collaboration with a smaller German firm BioNTech, and to the similar product expected from Moderna, according to an AMA press release.

Positive news has emerged this week about both of these vaccines, which were developed using a newer – and as yet unproven – approach. They seek to use messenger RNA to instruct cells to produce a target protein for SARS-CoV-2.

New York–based Pfizer on Monday announced interim phase 3 data that was widely viewed as promising. Pfizer said the vaccine appeared to be 90% effective in preventing COVID-19 in trial volunteers who were without evidence of prior infection of the virus.

In a press release, Pfizer said it plans to ask the Food and Drug Administration to consider a special clearance, known as an emergency-use authorization, “soon after” a safety milestone is achieved in its vaccine trial. That milestone could be reached this month.

Moderna said it was on track to report early data from a late-stage trial of its experimental coronavirus vaccine later this month, and could file with the FDA for an emergency-use authorization in early December, according to a Reuters report.

The severity of the global pandemic has put the FDA under pressure to move quickly on approval of COVID-19 vaccines, based on limited data, while also working to make sure these products are safe. The creation of CPT codes for each of two coronavirus vaccines, as well as accompanying administration codes, will set up a way to keep tabs on each dose of each of these shots, the AMA said.

American Medical Association

“Correlating each coronavirus vaccine with its own unique CPT code provides analytical advantages to help track, allocate and optimize resources as an immunization program ramps up in the United States,” AMA President Susan R. Bailey, MD, said in the release.

AMA plans to introduce more vaccine-specific CPT codes as more vaccine candidates approach FDA review. These vaccine-specific CPT codes can go into effect only after the FDA grants a clearance.

The newly created Category I CPT codes and long descriptors for the vaccine products are:
 

• 91300; severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 30 mcg/0.3mL dosage, diluent reconstituted, for intramuscular use (Pfizer/BioNTech)
• 91301; severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 100 mcg/0.5mL dosage, for intramuscular use (Moderna)

These two administrative codes would apply to the Pfizer-BioNTech shot:

• 0001A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 30 mcg/0.3 mL dosage, diluent reconstituted; first dose.
• 0002A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 30 mcg/0.3 mL dosage, diluent reconstituted; second dose.

And these two administrative codes would apply to the Moderna shot:

• 0011A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 100 mcg/0.5 mL dosage; first dose.
• 0012A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 100 mcg/0.5 mL dosage; second dose.

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

The largest U.S. physician organization on Tuesday took a step to prepare for future payments for administration of two leading COVID-19 vaccine candidates, publishing new billing codes tailored to track each use of these medications.

The American Medical Association updated its CPT code set to reflect the expected future availability of COVID-19 vaccines. The new codes apply to the experimental vaccine being developed by Pfizer, in collaboration with a smaller German firm BioNTech, and to the similar product expected from Moderna, according to an AMA press release.

Positive news has emerged this week about both of these vaccines, which were developed using a newer – and as yet unproven – approach. They seek to use messenger RNA to instruct cells to produce a target protein for SARS-CoV-2.

New York–based Pfizer on Monday announced interim phase 3 data that was widely viewed as promising. Pfizer said the vaccine appeared to be 90% effective in preventing COVID-19 in trial volunteers who were without evidence of prior infection of the virus.

In a press release, Pfizer said it plans to ask the Food and Drug Administration to consider a special clearance, known as an emergency-use authorization, “soon after” a safety milestone is achieved in its vaccine trial. That milestone could be reached this month.

Moderna said it was on track to report early data from a late-stage trial of its experimental coronavirus vaccine later this month, and could file with the FDA for an emergency-use authorization in early December, according to a Reuters report.

The severity of the global pandemic has put the FDA under pressure to move quickly on approval of COVID-19 vaccines, based on limited data, while also working to make sure these products are safe. The creation of CPT codes for each of two coronavirus vaccines, as well as accompanying administration codes, will set up a way to keep tabs on each dose of each of these shots, the AMA said.

American Medical Association

“Correlating each coronavirus vaccine with its own unique CPT code provides analytical advantages to help track, allocate and optimize resources as an immunization program ramps up in the United States,” AMA President Susan R. Bailey, MD, said in the release.

AMA plans to introduce more vaccine-specific CPT codes as more vaccine candidates approach FDA review. These vaccine-specific CPT codes can go into effect only after the FDA grants a clearance.

The newly created Category I CPT codes and long descriptors for the vaccine products are:
 

• 91300; severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 30 mcg/0.3mL dosage, diluent reconstituted, for intramuscular use (Pfizer/BioNTech)
• 91301; severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 100 mcg/0.5mL dosage, for intramuscular use (Moderna)

These two administrative codes would apply to the Pfizer-BioNTech shot:

• 0001A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 30 mcg/0.3 mL dosage, diluent reconstituted; first dose.
• 0002A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 30 mcg/0.3 mL dosage, diluent reconstituted; second dose.

And these two administrative codes would apply to the Moderna shot:

• 0011A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 100 mcg/0.5 mL dosage; first dose.
• 0012A; Immunization administration by intramuscular injection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease [COVID-19]) vaccine, mRNA-LNP, spike protein, preservative free, 100 mcg/0.5 mL dosage; second dose.

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

Patients with Sjögren’s syndrome can be categorized into four distinct symptom clusters – independent of age, sex, and some disease manifestations – that may both improve symptom relief and aid in the development of targeted therapies, investigators reported.

Analysis of data from a survey conducted by the Sjögren’s Foundation identified four symptom clusters based on the grouping of five common characteristics: anxiety, depression, pain, fatigue, and dryness, Sara S. McCoy, MD, of the University of Wisconsin–Madison, and colleagues reported.

“Verification of features unique to each Sjögren’s cluster might provide guidance for future cluster-targeted therapy,” Dr. McCoy said in an oral abstract presentation during the virtual annual meeting of the American College of Rheumatology.

The dearth of Food and Drug Administration–approved disease-modifying therapies for Sjögren’s syndrome can be attributed in part to the small number of patients with extraglandular disease manifestations, the heterogeneity of disease, and the failure of available therapy to improve common symptoms such as fatigue, dryness, quality-of-life decrements, anxiety and depression, she said.
 

Symptom clusters verify smaller study’s findings

Dr. McCoy and colleagues explored whether symptom clusters identified in a 2019 study from the United Kingdom would apply to a larger U.S. population.

In the U.K. study, Jessica R. Tarn, PhD, and colleagues performed a hierarchical cluster analysis to identify subgroups among 608 patients in the U.K. Primary Sjögren’s Syndrome Registry and in 396 patients in two independent validation cohorts from Norway and France.

They identified four subgroups they categorized as low symptom burden, high symptom burden, dryness dominant with fatigue, and pain dominant with fatigue, and reported that the groups showed significant difference in serum and transcriptomic markers.

In the U.S. study, McCoy et al. sought to verify the symptom-based cluster and report on differences in key measures between the groups. They used data from a survey by the Sjögren’s Foundation of 2,961 adults with self-reported Sjögren’s syndrome. The investigators then used an unsupervised hierarchical clustering method to identify the optimal phenotypically similar clusters based on patient-reported severity of anxiety (from never to daily), depression (never to daily), pain on a visual analog scale (0 to 10), fatigue on a VAS, and dryness on a VAS. They collected data on demographics, medications, quality of life, and Sjögren’s-specific symptom frequency and systemic manifestations within each cluster, and identified cluster differences controlled for age, sex, race, and Social Security disability.

They identified four symptom-based clusters from 2,806 participants for whom complete data on the five key symptoms were available:

• Cluster 1 patients (prevalence, 30%) had high symptom burden in all categories.
• Cluster 2 patients (22%) had high anxiety and depression (22%), with some fatigue.
• Cluster 3 patients (34%) had predominant high dryness and fatigue.
• Cluster 4 patients (14%) had low symptom burden.

“We found that clusters differed in Sjögren’s-specific symptoms,” Dr. McCoy said.

For example, patients in the high-symptom-burden cluster had, as the name implies, an overall higher burden of symptoms among all major ocular, oral, and other dryness symptoms, as well as systemic organ system symptoms, whereas patients in the low-symptom-burden group consistently had the lowest levels of symptoms across the spectrum.

“We also noticed significant differences in systemic medication use. High symptom burden and high dryness and fatigue had higher use of systemic therapies targeting dryness, as might be expected,” she said.

The highest corticosteroid use was in the high-symptom-burden group, while hydroxychloroquine use was highest in the high-anxiety/depression group. Antidepressant use was also high in these two groups.

In addition, 35% of patients in the high-symptom-burden group used prescription opioid analgesics, compared with just 7% in the low-symptom-burden group.

The categories from low to high symptom burden also significantly correlated with quality-of-life measures, including Social Security Disability enrollment, emotional burden of disease, effects of disease on independence, and effects of Sjögren’s on relationships with family and friends (P < .001 for all).

Systemic manifestations of disease differed significantly among the groups for inflammatory arthritis, interstitial lung disease, and neuropathy, but there were no significant differences in the incidence of leukopenia or lymphoma.

The investigators plan to perform symptom-based cluster analysis with validated Sjögren’s syndrome populations, and propose studies to define phenotypic features of distinct clusters “to better define subsets of this heterogeneous disease, and ultimately inform targeted therapy,” Dr. McCoy concluded.
 

Opportunity to tailor practice and research

During the question-and-answer period following the presentation, Gabriela Hernandez-Molina, MD, of the Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán in Mexico City, commented that “fatigue and pain might be also attributed to other comorbidities in these patients such as fibromyalgia,” and asked Dr. McCoy to comment on that.

“That’s exactly what we’re driving at,” Dr. McCoy replied. “Fatigue and pain frequently affect how patients experience their disease, and it would be beneficial to take this into account when we evaluate patients, and also for the studies that we’re performing, as well as future ‘-omic’ studies – transcriptomics and what-not – there’s potential here to take that type of patient we frequently see and try to tailor our clinical practice and our research to clearly what we’re seeing in practice, which is these other comorbidities.”

Dana DiRenzo, MD, from Johns Hopkins University, Baltimore, who moderated the session, asked how the information is changing the management of patients with Sjögren’s syndrome in clinic.

Dr. McCoy said that the study was based on self-reported data that can introduce bias, and that she and colleagues plan to validate the results before applying them to clinical care.

The study was supported by grants from the National Institutes of Health and the University of Wisconsin. Dr. McCoy disclosed consulting fees from Novartis and Bristol-Myers Squibb. Dr. Hernandez-Molina and Dr. DiRenzo reported no relevant disclosures.

SOURCE: McCoy SS et al. Arthritis Rheumatol. 2020;72(suppl 10), Abstract 1504.

Patients with Sjögren’s syndrome can be categorized into four distinct symptom clusters – independent of age, sex, and some disease manifestations – that may both improve symptom relief and aid in the development of targeted therapies, investigators reported.

Analysis of data from a survey conducted by the Sjögren’s Foundation identified four symptom clusters based on the grouping of five common characteristics: anxiety, depression, pain, fatigue, and dryness, Sara S. McCoy, MD, of the University of Wisconsin–Madison, and colleagues reported.

“Verification of features unique to each Sjögren’s cluster might provide guidance for future cluster-targeted therapy,” Dr. McCoy said in an oral abstract presentation during the virtual annual meeting of the American College of Rheumatology.

The dearth of Food and Drug Administration–approved disease-modifying therapies for Sjögren’s syndrome can be attributed in part to the small number of patients with extraglandular disease manifestations, the heterogeneity of disease, and the failure of available therapy to improve common symptoms such as fatigue, dryness, quality-of-life decrements, anxiety and depression, she said.
 

Symptom clusters verify smaller study’s findings

Dr. McCoy and colleagues explored whether symptom clusters identified in a 2019 study from the United Kingdom would apply to a larger U.S. population.

In the U.K. study, Jessica R. Tarn, PhD, and colleagues performed a hierarchical cluster analysis to identify subgroups among 608 patients in the U.K. Primary Sjögren’s Syndrome Registry and in 396 patients in two independent validation cohorts from Norway and France.

They identified four subgroups they categorized as low symptom burden, high symptom burden, dryness dominant with fatigue, and pain dominant with fatigue, and reported that the groups showed significant difference in serum and transcriptomic markers.

In the U.S. study, McCoy et al. sought to verify the symptom-based cluster and report on differences in key measures between the groups. They used data from a survey by the Sjögren’s Foundation of 2,961 adults with self-reported Sjögren’s syndrome. The investigators then used an unsupervised hierarchical clustering method to identify the optimal phenotypically similar clusters based on patient-reported severity of anxiety (from never to daily), depression (never to daily), pain on a visual analog scale (0 to 10), fatigue on a VAS, and dryness on a VAS. They collected data on demographics, medications, quality of life, and Sjögren’s-specific symptom frequency and systemic manifestations within each cluster, and identified cluster differences controlled for age, sex, race, and Social Security disability.

They identified four symptom-based clusters from 2,806 participants for whom complete data on the five key symptoms were available:

• Cluster 1 patients (prevalence, 30%) had high symptom burden in all categories.
• Cluster 2 patients (22%) had high anxiety and depression (22%), with some fatigue.
• Cluster 3 patients (34%) had predominant high dryness and fatigue.
• Cluster 4 patients (14%) had low symptom burden.

“We found that clusters differed in Sjögren’s-specific symptoms,” Dr. McCoy said.

For example, patients in the high-symptom-burden cluster had, as the name implies, an overall higher burden of symptoms among all major ocular, oral, and other dryness symptoms, as well as systemic organ system symptoms, whereas patients in the low-symptom-burden group consistently had the lowest levels of symptoms across the spectrum.

“We also noticed significant differences in systemic medication use. High symptom burden and high dryness and fatigue had higher use of systemic therapies targeting dryness, as might be expected,” she said.

The highest corticosteroid use was in the high-symptom-burden group, while hydroxychloroquine use was highest in the high-anxiety/depression group. Antidepressant use was also high in these two groups.

In addition, 35% of patients in the high-symptom-burden group used prescription opioid analgesics, compared with just 7% in the low-symptom-burden group.

The categories from low to high symptom burden also significantly correlated with quality-of-life measures, including Social Security Disability enrollment, emotional burden of disease, effects of disease on independence, and effects of Sjögren’s on relationships with family and friends (P < .001 for all).

Systemic manifestations of disease differed significantly among the groups for inflammatory arthritis, interstitial lung disease, and neuropathy, but there were no significant differences in the incidence of leukopenia or lymphoma.

The investigators plan to perform symptom-based cluster analysis with validated Sjögren’s syndrome populations, and propose studies to define phenotypic features of distinct clusters “to better define subsets of this heterogeneous disease, and ultimately inform targeted therapy,” Dr. McCoy concluded.
 

Opportunity to tailor practice and research

During the question-and-answer period following the presentation, Gabriela Hernandez-Molina, MD, of the Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán in Mexico City, commented that “fatigue and pain might be also attributed to other comorbidities in these patients such as fibromyalgia,” and asked Dr. McCoy to comment on that.

“That’s exactly what we’re driving at,” Dr. McCoy replied. “Fatigue and pain frequently affect how patients experience their disease, and it would be beneficial to take this into account when we evaluate patients, and also for the studies that we’re performing, as well as future ‘-omic’ studies – transcriptomics and what-not – there’s potential here to take that type of patient we frequently see and try to tailor our clinical practice and our research to clearly what we’re seeing in practice, which is these other comorbidities.”

Dana DiRenzo, MD, from Johns Hopkins University, Baltimore, who moderated the session, asked how the information is changing the management of patients with Sjögren’s syndrome in clinic.

Dr. McCoy said that the study was based on self-reported data that can introduce bias, and that she and colleagues plan to validate the results before applying them to clinical care.

The study was supported by grants from the National Institutes of Health and the University of Wisconsin. Dr. McCoy disclosed consulting fees from Novartis and Bristol-Myers Squibb. Dr. Hernandez-Molina and Dr. DiRenzo reported no relevant disclosures.

SOURCE: McCoy SS et al. Arthritis Rheumatol. 2020;72(suppl 10), Abstract 1504.

Patients with Sjögren’s syndrome can be categorized into four distinct symptom clusters – independent of age, sex, and some disease manifestations – that may both improve symptom relief and aid in the development of targeted therapies, investigators reported.

Analysis of data from a survey conducted by the Sjögren’s Foundation identified four symptom clusters based on the grouping of five common characteristics: anxiety, depression, pain, fatigue, and dryness, Sara S. McCoy, MD, of the University of Wisconsin–Madison, and colleagues reported.

“Verification of features unique to each Sjögren’s cluster might provide guidance for future cluster-targeted therapy,” Dr. McCoy said in an oral abstract presentation during the virtual annual meeting of the American College of Rheumatology.

The dearth of Food and Drug Administration–approved disease-modifying therapies for Sjögren’s syndrome can be attributed in part to the small number of patients with extraglandular disease manifestations, the heterogeneity of disease, and the failure of available therapy to improve common symptoms such as fatigue, dryness, quality-of-life decrements, anxiety and depression, she said.
 

Symptom clusters verify smaller study’s findings

Dr. McCoy and colleagues explored whether symptom clusters identified in a 2019 study from the United Kingdom would apply to a larger U.S. population.

In the U.K. study, Jessica R. Tarn, PhD, and colleagues performed a hierarchical cluster analysis to identify subgroups among 608 patients in the U.K. Primary Sjögren’s Syndrome Registry and in 396 patients in two independent validation cohorts from Norway and France.

They identified four subgroups they categorized as low symptom burden, high symptom burden, dryness dominant with fatigue, and pain dominant with fatigue, and reported that the groups showed significant difference in serum and transcriptomic markers.

In the U.S. study, McCoy et al. sought to verify the symptom-based cluster and report on differences in key measures between the groups. They used data from a survey by the Sjögren’s Foundation of 2,961 adults with self-reported Sjögren’s syndrome. The investigators then used an unsupervised hierarchical clustering method to identify the optimal phenotypically similar clusters based on patient-reported severity of anxiety (from never to daily), depression (never to daily), pain on a visual analog scale (0 to 10), fatigue on a VAS, and dryness on a VAS. They collected data on demographics, medications, quality of life, and Sjögren’s-specific symptom frequency and systemic manifestations within each cluster, and identified cluster differences controlled for age, sex, race, and Social Security disability.

They identified four symptom-based clusters from 2,806 participants for whom complete data on the five key symptoms were available:

• Cluster 1 patients (prevalence, 30%) had high symptom burden in all categories.
• Cluster 2 patients (22%) had high anxiety and depression (22%), with some fatigue.
• Cluster 3 patients (34%) had predominant high dryness and fatigue.
• Cluster 4 patients (14%) had low symptom burden.

“We found that clusters differed in Sjögren’s-specific symptoms,” Dr. McCoy said.

For example, patients in the high-symptom-burden cluster had, as the name implies, an overall higher burden of symptoms among all major ocular, oral, and other dryness symptoms, as well as systemic organ system symptoms, whereas patients in the low-symptom-burden group consistently had the lowest levels of symptoms across the spectrum.

“We also noticed significant differences in systemic medication use. High symptom burden and high dryness and fatigue had higher use of systemic therapies targeting dryness, as might be expected,” she said.

The highest corticosteroid use was in the high-symptom-burden group, while hydroxychloroquine use was highest in the high-anxiety/depression group. Antidepressant use was also high in these two groups.

In addition, 35% of patients in the high-symptom-burden group used prescription opioid analgesics, compared with just 7% in the low-symptom-burden group.

The categories from low to high symptom burden also significantly correlated with quality-of-life measures, including Social Security Disability enrollment, emotional burden of disease, effects of disease on independence, and effects of Sjögren’s on relationships with family and friends (P < .001 for all).

Systemic manifestations of disease differed significantly among the groups for inflammatory arthritis, interstitial lung disease, and neuropathy, but there were no significant differences in the incidence of leukopenia or lymphoma.

The investigators plan to perform symptom-based cluster analysis with validated Sjögren’s syndrome populations, and propose studies to define phenotypic features of distinct clusters “to better define subsets of this heterogeneous disease, and ultimately inform targeted therapy,” Dr. McCoy concluded.
 

Opportunity to tailor practice and research

During the question-and-answer period following the presentation, Gabriela Hernandez-Molina, MD, of the Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán in Mexico City, commented that “fatigue and pain might be also attributed to other comorbidities in these patients such as fibromyalgia,” and asked Dr. McCoy to comment on that.

“That’s exactly what we’re driving at,” Dr. McCoy replied. “Fatigue and pain frequently affect how patients experience their disease, and it would be beneficial to take this into account when we evaluate patients, and also for the studies that we’re performing, as well as future ‘-omic’ studies – transcriptomics and what-not – there’s potential here to take that type of patient we frequently see and try to tailor our clinical practice and our research to clearly what we’re seeing in practice, which is these other comorbidities.”

Dana DiRenzo, MD, from Johns Hopkins University, Baltimore, who moderated the session, asked how the information is changing the management of patients with Sjögren’s syndrome in clinic.

Dr. McCoy said that the study was based on self-reported data that can introduce bias, and that she and colleagues plan to validate the results before applying them to clinical care.

The study was supported by grants from the National Institutes of Health and the University of Wisconsin. Dr. McCoy disclosed consulting fees from Novartis and Bristol-Myers Squibb. Dr. Hernandez-Molina and Dr. DiRenzo reported no relevant disclosures.

SOURCE: McCoy SS et al. Arthritis Rheumatol. 2020;72(suppl 10), Abstract 1504.

No significant differences in major adverse cardiovascular events (MACE) emerged between methotrexate and hydroxychloroquine (HCQ) treatment in a comparison of adults 65 years or older with rheumatoid arthritis. However, researchers reported some elevation in risk for stroke in the methotrexate group and for myocardial infarction and heart failure in the HCQ group.

The primary outcome, a composite of MI, stroke, or cardiovascular death, had an incidence of 23.39 per 1,000 person-years in the methotrexate group versus 24.33 in the HCQ group in this observational study of nearly 60,000 people.

“These results suggest an importance of looking at different individual events of cardiovascular disease rather than the whole ‘CV’ disease only,” Seoyoung Kim, MD, said in an interview. “The other important thing is that the mortality was not significantly different between the two groups.”

For example, the researchers reported 256 cardiovascular-related deaths in the methotrexate group and 263 such deaths in the HCQ cohort.
 

Addressing a recognized risk

“It is well known that patients with rheumatoid arthritis have excessive morbidity and mortality,” Dr. Kim, of the division of rheumatology at Brigham and Women’s Hospital and associate professor of medicine at Harvard Medical School in Boston, said at the virtual annual meeting of the American College of Rheumatology.

Among prior studies in this area, the Cardiovascular Inflammation Reduction Trial (CIRT) found no significant reduction in cardiovascular events among people taking methotrexate versus placebo. However, the study of 4,786 people was not specific to RA, Dr. Kim said. The lack of efficacy on this endpoint prompted researchers to stop CIRT early.

“So what does the conclusion of the CIRT trial mean for rheumatoid arthritis patients?” Dr. Kim asked.

To find out, she and colleagues compared risk of MACE among participants newly starting either methotrexate or HCQ. The study included 59,329 people aged 65 and older who were identified through Medicare claims data from 2008 to 2016. Mean age was 74 years, and 80% were women.

The investigators used propensity score matching to control for multiple covariates for demographics, other medications, and comorbidities. Use of other medications was similar between groups, including glucocorticoids, NSAIDs, and statins. Baseline cardiovascular morbidities likewise were well balanced, Dr. Kim said.

The hazard ratio for the primary MACE outcome was 0.96 (95% confidence interval, 0.86-1.08).

Secondary outcomes

MI was less common in the methotrexate group, for example, with an incidence of 8.49 per 1,000 person-years versus 10.68 per 1,000 person-years in the HCQ cohort. This finding was statically significant, Dr. Kim said, with a hazard ratio of 0.80 favoring methotrexate.

Heart failure also occurred less often in the methotrexate cohort, with an incidence rate of 8.57 per 1,000 person-years versus a rate of 14.24 in the HCQ group. The hazard ratio again favored methotrexate at 0.60.

In contrast, strokes were more common with methotrexate than with (incidence of 7.94 vs. 6.01 per 1,000 person-years).

Another secondary outcome, all-cause mortality, was not significantly different between groups. There were 821 deaths in the methotrexate group (28.65 per 1,000 person-years) and 796 deaths in the HCQ group (31.33 per 1,000 person-years).
 

Studying causality next?

Session moderator Maya Buch, MD, PhD, professor of rheumatology at the University of Manchester (England), asked Dr. Kim why she found significant differences in some secondary outcomes but not the primary composite endpoint.

“When we think of cardiovascular diseases, we tend to think of them all developing through the same mechanism. But perhaps the exact mechanism might not be identical,” Dr. Kim replied. The findings do not suggest causality because the study was observational, she added, “but maybe this will lead to a randomized, controlled trial.”

When asked for comment, Dr. Buch said that the study was “interesting” and “suggestive of differences in type of MACE between the two drugs evaluated,” but that there should be caution in interpreting the findings because of the lack of detailed information on RA disease and activity in claims databases, in addition to other factors, even though the investigators made adjustments for known differences through propensity score matching.

The division of pharmacoepidemiology and pharmacoeconomics at Brigham and Women’s Hospital supported the study. Dr. Kim has received support for Brigham and Women’s Hospital for unrelated research from Pfizer, AbbVie, Roche, and Bristol-Myers Squibb. Several other coauthors reported having financial relationships with pharmaceutical companies that make drugs for RA. Dr. Buch had no relevant disclosures.

SOURCE: He M et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 1993.

No significant differences in major adverse cardiovascular events (MACE) emerged between methotrexate and hydroxychloroquine (HCQ) treatment in a comparison of adults 65 years or older with rheumatoid arthritis. However, researchers reported some elevation in risk for stroke in the methotrexate group and for myocardial infarction and heart failure in the HCQ group.

The primary outcome, a composite of MI, stroke, or cardiovascular death, had an incidence of 23.39 per 1,000 person-years in the methotrexate group versus 24.33 in the HCQ group in this observational study of nearly 60,000 people.

“These results suggest an importance of looking at different individual events of cardiovascular disease rather than the whole ‘CV’ disease only,” Seoyoung Kim, MD, said in an interview. “The other important thing is that the mortality was not significantly different between the two groups.”

For example, the researchers reported 256 cardiovascular-related deaths in the methotrexate group and 263 such deaths in the HCQ cohort.
 

Addressing a recognized risk

“It is well known that patients with rheumatoid arthritis have excessive morbidity and mortality,” Dr. Kim, of the division of rheumatology at Brigham and Women’s Hospital and associate professor of medicine at Harvard Medical School in Boston, said at the virtual annual meeting of the American College of Rheumatology.

Among prior studies in this area, the Cardiovascular Inflammation Reduction Trial (CIRT) found no significant reduction in cardiovascular events among people taking methotrexate versus placebo. However, the study of 4,786 people was not specific to RA, Dr. Kim said. The lack of efficacy on this endpoint prompted researchers to stop CIRT early.

“So what does the conclusion of the CIRT trial mean for rheumatoid arthritis patients?” Dr. Kim asked.

To find out, she and colleagues compared risk of MACE among participants newly starting either methotrexate or HCQ. The study included 59,329 people aged 65 and older who were identified through Medicare claims data from 2008 to 2016. Mean age was 74 years, and 80% were women.

The investigators used propensity score matching to control for multiple covariates for demographics, other medications, and comorbidities. Use of other medications was similar between groups, including glucocorticoids, NSAIDs, and statins. Baseline cardiovascular morbidities likewise were well balanced, Dr. Kim said.

The hazard ratio for the primary MACE outcome was 0.96 (95% confidence interval, 0.86-1.08).

Secondary outcomes

MI was less common in the methotrexate group, for example, with an incidence of 8.49 per 1,000 person-years versus 10.68 per 1,000 person-years in the HCQ cohort. This finding was statically significant, Dr. Kim said, with a hazard ratio of 0.80 favoring methotrexate.

Heart failure also occurred less often in the methotrexate cohort, with an incidence rate of 8.57 per 1,000 person-years versus a rate of 14.24 in the HCQ group. The hazard ratio again favored methotrexate at 0.60.

In contrast, strokes were more common with methotrexate than with (incidence of 7.94 vs. 6.01 per 1,000 person-years).

Another secondary outcome, all-cause mortality, was not significantly different between groups. There were 821 deaths in the methotrexate group (28.65 per 1,000 person-years) and 796 deaths in the HCQ group (31.33 per 1,000 person-years).
 

Studying causality next?

Session moderator Maya Buch, MD, PhD, professor of rheumatology at the University of Manchester (England), asked Dr. Kim why she found significant differences in some secondary outcomes but not the primary composite endpoint.

“When we think of cardiovascular diseases, we tend to think of them all developing through the same mechanism. But perhaps the exact mechanism might not be identical,” Dr. Kim replied. The findings do not suggest causality because the study was observational, she added, “but maybe this will lead to a randomized, controlled trial.”

When asked for comment, Dr. Buch said that the study was “interesting” and “suggestive of differences in type of MACE between the two drugs evaluated,” but that there should be caution in interpreting the findings because of the lack of detailed information on RA disease and activity in claims databases, in addition to other factors, even though the investigators made adjustments for known differences through propensity score matching.

The division of pharmacoepidemiology and pharmacoeconomics at Brigham and Women’s Hospital supported the study. Dr. Kim has received support for Brigham and Women’s Hospital for unrelated research from Pfizer, AbbVie, Roche, and Bristol-Myers Squibb. Several other coauthors reported having financial relationships with pharmaceutical companies that make drugs for RA. Dr. Buch had no relevant disclosures.

SOURCE: He M et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 1993.

No significant differences in major adverse cardiovascular events (MACE) emerged between methotrexate and hydroxychloroquine (HCQ) treatment in a comparison of adults 65 years or older with rheumatoid arthritis. However, researchers reported some elevation in risk for stroke in the methotrexate group and for myocardial infarction and heart failure in the HCQ group.

The primary outcome, a composite of MI, stroke, or cardiovascular death, had an incidence of 23.39 per 1,000 person-years in the methotrexate group versus 24.33 in the HCQ group in this observational study of nearly 60,000 people.

“These results suggest an importance of looking at different individual events of cardiovascular disease rather than the whole ‘CV’ disease only,” Seoyoung Kim, MD, said in an interview. “The other important thing is that the mortality was not significantly different between the two groups.”

For example, the researchers reported 256 cardiovascular-related deaths in the methotrexate group and 263 such deaths in the HCQ cohort.
 

Addressing a recognized risk

“It is well known that patients with rheumatoid arthritis have excessive morbidity and mortality,” Dr. Kim, of the division of rheumatology at Brigham and Women’s Hospital and associate professor of medicine at Harvard Medical School in Boston, said at the virtual annual meeting of the American College of Rheumatology.

Among prior studies in this area, the Cardiovascular Inflammation Reduction Trial (CIRT) found no significant reduction in cardiovascular events among people taking methotrexate versus placebo. However, the study of 4,786 people was not specific to RA, Dr. Kim said. The lack of efficacy on this endpoint prompted researchers to stop CIRT early.

“So what does the conclusion of the CIRT trial mean for rheumatoid arthritis patients?” Dr. Kim asked.

To find out, she and colleagues compared risk of MACE among participants newly starting either methotrexate or HCQ. The study included 59,329 people aged 65 and older who were identified through Medicare claims data from 2008 to 2016. Mean age was 74 years, and 80% were women.

The investigators used propensity score matching to control for multiple covariates for demographics, other medications, and comorbidities. Use of other medications was similar between groups, including glucocorticoids, NSAIDs, and statins. Baseline cardiovascular morbidities likewise were well balanced, Dr. Kim said.

The hazard ratio for the primary MACE outcome was 0.96 (95% confidence interval, 0.86-1.08).

Secondary outcomes

MI was less common in the methotrexate group, for example, with an incidence of 8.49 per 1,000 person-years versus 10.68 per 1,000 person-years in the HCQ cohort. This finding was statically significant, Dr. Kim said, with a hazard ratio of 0.80 favoring methotrexate.

Heart failure also occurred less often in the methotrexate cohort, with an incidence rate of 8.57 per 1,000 person-years versus a rate of 14.24 in the HCQ group. The hazard ratio again favored methotrexate at 0.60.

In contrast, strokes were more common with methotrexate than with (incidence of 7.94 vs. 6.01 per 1,000 person-years).

Another secondary outcome, all-cause mortality, was not significantly different between groups. There were 821 deaths in the methotrexate group (28.65 per 1,000 person-years) and 796 deaths in the HCQ group (31.33 per 1,000 person-years).
 

Studying causality next?

Session moderator Maya Buch, MD, PhD, professor of rheumatology at the University of Manchester (England), asked Dr. Kim why she found significant differences in some secondary outcomes but not the primary composite endpoint.

“When we think of cardiovascular diseases, we tend to think of them all developing through the same mechanism. But perhaps the exact mechanism might not be identical,” Dr. Kim replied. The findings do not suggest causality because the study was observational, she added, “but maybe this will lead to a randomized, controlled trial.”

When asked for comment, Dr. Buch said that the study was “interesting” and “suggestive of differences in type of MACE between the two drugs evaluated,” but that there should be caution in interpreting the findings because of the lack of detailed information on RA disease and activity in claims databases, in addition to other factors, even though the investigators made adjustments for known differences through propensity score matching.

The division of pharmacoepidemiology and pharmacoeconomics at Brigham and Women’s Hospital supported the study. Dr. Kim has received support for Brigham and Women’s Hospital for unrelated research from Pfizer, AbbVie, Roche, and Bristol-Myers Squibb. Several other coauthors reported having financial relationships with pharmaceutical companies that make drugs for RA. Dr. Buch had no relevant disclosures.

SOURCE: He M et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 1993.