MDedge Rheumatology

The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.

“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.

The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.

Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”

Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.

Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.

“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.

The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.

“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”

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

The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.

“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.

The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.

Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”

Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.

Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.

“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.

The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.

“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”

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

The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.

“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.

The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.

Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”

Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.

Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.

“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.

The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.

“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”

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

More people with fever and body aches are turning to NSAIDs to ease symptoms, but the drugs have come under new scrutiny as investigators work to determine whether they are a safe way to relieve the pain of COVID-19 vaccination or symptoms of the disease.

Early on in the pandemic, French health officials warned that NSAIDs, such as ibuprofen, could worsen coronavirus disease, and they recommended switching to acetaminophen instead.

The National Health Service in the United Kingdom followed with a similar recommendation for acetaminophen.

But the European Medicines Agency took a different approach, reporting “no scientific evidence” that NSAIDs could worsen COVID-19. The U.S. Food and Drug Administration also opted not to take a stance.

The debate prompted discussion on social media, with various reactions from around the world. It also inspired Craig Wilen, MD, PhD, from Yale University, New Haven, Conn., and associates to examine the effect of NSAIDs on COVID-19 infection and immune response. Their findings were published online Jan.20 in the Journal of Virology.

“It really bothered me that non–evidence-based decisions were driving the conversation,” Dr. Wilen said. “Millions of people are taking NSAIDs every day and clinical decisions about their care shouldn’t be made on a hypothesis.”

One theory is that NSAIDs alter susceptibility to infection by modifying ACE2. The drugs might also change the cell entry receptor for SARS-CoV-2, alter virus replication, or even modify the immune response.

British researchers, also questioning the safety of NSAIDs in patients with COVID-19, delved into National Health Service records to study two large groups of patients, some of whom were taking the pain relievers.

“We were watching the controversy and the lack of evidence and wanted to contribute,” lead investigator Angel Wong, PhD, from the London School of Hygiene and Tropical Medicine, said in an interview.

And with nearly 11 million NSAID prescriptions dispensed in primary care in England alone in the past 12 months, the inconsistency was concerning.

The team compared COVID-19–related deaths in two groups: one group of more than 700,000 people taking NSAIDs, including patients with rheumatoid arthritis and osteoarthritis; and another of almost 3.5 million people not on the medication.

NSAIDs work by inhibiting cyclooxygenase-1 and COX-2 enzymes in the body, which are crucial for the generation of prostaglandins. These lipid molecules play a role in inflammation and are blocked by NSAIDs.

The investigators found no evidence of a harmful effect of NSAIDs on COVID-19-related deaths; their results were published online Jan. 21 in the Annals of the Rheumatic Diseases.

The results, they pointed out, are in line with a Danish study that also showed no evidence of a higher risk for severe COVID-19 outcomes with NSAID use.

“It’s reassuring,” Dr. Wong said, “that patients can safely continue treatment.”
 

More new evidence

Dr. Wilen’s team found that SARS-CoV-2 infection stimulated COX-2 expression in human and mice cells. However, suppression of COX-2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry, or viral replication.

In their mouse model of SARS-CoV-2 infection, the investigators saw that NSAIDs impaired the production of proinflammatory cytokines and neutralizing antibodies. The findings suggest that NSAIDs influence COVID-19 outcomes by dampening the inflammatory response and production of protective antibodies, rather than modifying susceptibility to infection or viral replication.

Understanding the effect of NSAIDs on cytokine production is critical, Dr. Wilen pointed out, because they might be protective early in COVID-19 but pathologic at later stages.

Timing is crucial in the case of other immunomodulatory drugs. For example, dexamethasone lowers mortality in COVID-19 patients on respiratory support but is potentially harmful for those with milder disease.

There still is a lot to learn, Dr. Wilen acknowledged. “We may be seeing something similar going on with NSAIDs, where the timing of treatment is important.”

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

More people with fever and body aches are turning to NSAIDs to ease symptoms, but the drugs have come under new scrutiny as investigators work to determine whether they are a safe way to relieve the pain of COVID-19 vaccination or symptoms of the disease.

Early on in the pandemic, French health officials warned that NSAIDs, such as ibuprofen, could worsen coronavirus disease, and they recommended switching to acetaminophen instead.

The National Health Service in the United Kingdom followed with a similar recommendation for acetaminophen.

But the European Medicines Agency took a different approach, reporting “no scientific evidence” that NSAIDs could worsen COVID-19. The U.S. Food and Drug Administration also opted not to take a stance.

The debate prompted discussion on social media, with various reactions from around the world. It also inspired Craig Wilen, MD, PhD, from Yale University, New Haven, Conn., and associates to examine the effect of NSAIDs on COVID-19 infection and immune response. Their findings were published online Jan.20 in the Journal of Virology.

“It really bothered me that non–evidence-based decisions were driving the conversation,” Dr. Wilen said. “Millions of people are taking NSAIDs every day and clinical decisions about their care shouldn’t be made on a hypothesis.”

One theory is that NSAIDs alter susceptibility to infection by modifying ACE2. The drugs might also change the cell entry receptor for SARS-CoV-2, alter virus replication, or even modify the immune response.

British researchers, also questioning the safety of NSAIDs in patients with COVID-19, delved into National Health Service records to study two large groups of patients, some of whom were taking the pain relievers.

“We were watching the controversy and the lack of evidence and wanted to contribute,” lead investigator Angel Wong, PhD, from the London School of Hygiene and Tropical Medicine, said in an interview.

And with nearly 11 million NSAID prescriptions dispensed in primary care in England alone in the past 12 months, the inconsistency was concerning.

The team compared COVID-19–related deaths in two groups: one group of more than 700,000 people taking NSAIDs, including patients with rheumatoid arthritis and osteoarthritis; and another of almost 3.5 million people not on the medication.

NSAIDs work by inhibiting cyclooxygenase-1 and COX-2 enzymes in the body, which are crucial for the generation of prostaglandins. These lipid molecules play a role in inflammation and are blocked by NSAIDs.

The investigators found no evidence of a harmful effect of NSAIDs on COVID-19-related deaths; their results were published online Jan. 21 in the Annals of the Rheumatic Diseases.

The results, they pointed out, are in line with a Danish study that also showed no evidence of a higher risk for severe COVID-19 outcomes with NSAID use.

“It’s reassuring,” Dr. Wong said, “that patients can safely continue treatment.”
 

More new evidence

Dr. Wilen’s team found that SARS-CoV-2 infection stimulated COX-2 expression in human and mice cells. However, suppression of COX-2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry, or viral replication.

In their mouse model of SARS-CoV-2 infection, the investigators saw that NSAIDs impaired the production of proinflammatory cytokines and neutralizing antibodies. The findings suggest that NSAIDs influence COVID-19 outcomes by dampening the inflammatory response and production of protective antibodies, rather than modifying susceptibility to infection or viral replication.

Understanding the effect of NSAIDs on cytokine production is critical, Dr. Wilen pointed out, because they might be protective early in COVID-19 but pathologic at later stages.

Timing is crucial in the case of other immunomodulatory drugs. For example, dexamethasone lowers mortality in COVID-19 patients on respiratory support but is potentially harmful for those with milder disease.

There still is a lot to learn, Dr. Wilen acknowledged. “We may be seeing something similar going on with NSAIDs, where the timing of treatment is important.”

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

More people with fever and body aches are turning to NSAIDs to ease symptoms, but the drugs have come under new scrutiny as investigators work to determine whether they are a safe way to relieve the pain of COVID-19 vaccination or symptoms of the disease.

Early on in the pandemic, French health officials warned that NSAIDs, such as ibuprofen, could worsen coronavirus disease, and they recommended switching to acetaminophen instead.

The National Health Service in the United Kingdom followed with a similar recommendation for acetaminophen.

But the European Medicines Agency took a different approach, reporting “no scientific evidence” that NSAIDs could worsen COVID-19. The U.S. Food and Drug Administration also opted not to take a stance.

The debate prompted discussion on social media, with various reactions from around the world. It also inspired Craig Wilen, MD, PhD, from Yale University, New Haven, Conn., and associates to examine the effect of NSAIDs on COVID-19 infection and immune response. Their findings were published online Jan.20 in the Journal of Virology.

“It really bothered me that non–evidence-based decisions were driving the conversation,” Dr. Wilen said. “Millions of people are taking NSAIDs every day and clinical decisions about their care shouldn’t be made on a hypothesis.”

One theory is that NSAIDs alter susceptibility to infection by modifying ACE2. The drugs might also change the cell entry receptor for SARS-CoV-2, alter virus replication, or even modify the immune response.

British researchers, also questioning the safety of NSAIDs in patients with COVID-19, delved into National Health Service records to study two large groups of patients, some of whom were taking the pain relievers.

“We were watching the controversy and the lack of evidence and wanted to contribute,” lead investigator Angel Wong, PhD, from the London School of Hygiene and Tropical Medicine, said in an interview.

And with nearly 11 million NSAID prescriptions dispensed in primary care in England alone in the past 12 months, the inconsistency was concerning.

The team compared COVID-19–related deaths in two groups: one group of more than 700,000 people taking NSAIDs, including patients with rheumatoid arthritis and osteoarthritis; and another of almost 3.5 million people not on the medication.

NSAIDs work by inhibiting cyclooxygenase-1 and COX-2 enzymes in the body, which are crucial for the generation of prostaglandins. These lipid molecules play a role in inflammation and are blocked by NSAIDs.

The investigators found no evidence of a harmful effect of NSAIDs on COVID-19-related deaths; their results were published online Jan. 21 in the Annals of the Rheumatic Diseases.

The results, they pointed out, are in line with a Danish study that also showed no evidence of a higher risk for severe COVID-19 outcomes with NSAID use.

“It’s reassuring,” Dr. Wong said, “that patients can safely continue treatment.”
 

More new evidence

Dr. Wilen’s team found that SARS-CoV-2 infection stimulated COX-2 expression in human and mice cells. However, suppression of COX-2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry, or viral replication.

In their mouse model of SARS-CoV-2 infection, the investigators saw that NSAIDs impaired the production of proinflammatory cytokines and neutralizing antibodies. The findings suggest that NSAIDs influence COVID-19 outcomes by dampening the inflammatory response and production of protective antibodies, rather than modifying susceptibility to infection or viral replication.

Understanding the effect of NSAIDs on cytokine production is critical, Dr. Wilen pointed out, because they might be protective early in COVID-19 but pathologic at later stages.

Timing is crucial in the case of other immunomodulatory drugs. For example, dexamethasone lowers mortality in COVID-19 patients on respiratory support but is potentially harmful for those with milder disease.

There still is a lot to learn, Dr. Wilen acknowledged. “We may be seeing something similar going on with NSAIDs, where the timing of treatment is important.”

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

Li et al looked at risk of thromboembolic disease in patients with RA within the first 5 years of diagnosis compared to those without RA. Using a population database in British Columbia, Canada, 39,142 RA patients were matched to 78,078 non-RA patients and those with prior venous thromboembolism (VTE) were excluded. Incidence rates of VTE, pulmonary embolism (PE), and deep venous thrombosis (DVT) were higher among the RA cohort than the non-RA cohort; this observation held true after adjusting for age, sex, glucocorticoid, and contraceptive use. It would be interesting to know if the increased risk holds true after control of inflammation (i.e. in patients with established RA in low vs. high disease activity states). In the absence of information about BMI and tobacco use, more studies are necessary to provide further support for this finding.

As noted above, RA is associated with cardiovascular disease (CVD), along with risk of death from cardiovascular complications. Because CVD is itself a risk factor for dementia, Sattui et al examined the potential for systemic inflammation and CVD to increase risk of developing dementia in RA patients. Using CMS claims data from 2006 to 2014, they studied 56,000 RA patients age 65 or older and looked at risk of dementia according to CVD status (no CVD or risk factors, CVD risk factors without disease, and CVD). Incidence rates for dementia were higher among RA patients with CVD risk factors than those without, and highest among RA patients with CVD. This effect was age-dependent, with a more significant risk among RA patients age 65-74, perhaps because of a general increase in dementia in older adults. As RA disease activity was not obtainable in this study, the effects of systemic inflammation are difficult to attribute. In addition, there may be some misclassification of data regarding coding of dementia subtypes (i.e. vascular and Alzheimer dementia). However, as there are limited studies in this area, this study provides credible evidence for an increase in dementia in RA patients with CVD, which should be further investigated.

Finally, hydroxychloroquine (HCQ) has come under increased scrutiny in the past year in terms of its potential use outside of treatment of lupus and RA as well as potential side effects. Cardiac toxicity related to HCQ is thought to be rare; Sorour et al looked at the association between chronic HCQ use in patients with RA and the development of heart failure (HF) using a retrospective study comparing patients who developed HF after RA diagnosis to those who did not develop HF. HCQ use was similar in both groups and a higher cumulative HCQ dose was not associated with increased risk of HF. As it is small and retrospective, larger prospective studies would be helpful, but this remains reassuring as to the safety of HCQ in RA patients.

Li et al looked at risk of thromboembolic disease in patients with RA within the first 5 years of diagnosis compared to those without RA. Using a population database in British Columbia, Canada, 39,142 RA patients were matched to 78,078 non-RA patients and those with prior venous thromboembolism (VTE) were excluded. Incidence rates of VTE, pulmonary embolism (PE), and deep venous thrombosis (DVT) were higher among the RA cohort than the non-RA cohort; this observation held true after adjusting for age, sex, glucocorticoid, and contraceptive use. It would be interesting to know if the increased risk holds true after control of inflammation (i.e. in patients with established RA in low vs. high disease activity states). In the absence of information about BMI and tobacco use, more studies are necessary to provide further support for this finding.

As noted above, RA is associated with cardiovascular disease (CVD), along with risk of death from cardiovascular complications. Because CVD is itself a risk factor for dementia, Sattui et al examined the potential for systemic inflammation and CVD to increase risk of developing dementia in RA patients. Using CMS claims data from 2006 to 2014, they studied 56,000 RA patients age 65 or older and looked at risk of dementia according to CVD status (no CVD or risk factors, CVD risk factors without disease, and CVD). Incidence rates for dementia were higher among RA patients with CVD risk factors than those without, and highest among RA patients with CVD. This effect was age-dependent, with a more significant risk among RA patients age 65-74, perhaps because of a general increase in dementia in older adults. As RA disease activity was not obtainable in this study, the effects of systemic inflammation are difficult to attribute. In addition, there may be some misclassification of data regarding coding of dementia subtypes (i.e. vascular and Alzheimer dementia). However, as there are limited studies in this area, this study provides credible evidence for an increase in dementia in RA patients with CVD, which should be further investigated.

Finally, hydroxychloroquine (HCQ) has come under increased scrutiny in the past year in terms of its potential use outside of treatment of lupus and RA as well as potential side effects. Cardiac toxicity related to HCQ is thought to be rare; Sorour et al looked at the association between chronic HCQ use in patients with RA and the development of heart failure (HF) using a retrospective study comparing patients who developed HF after RA diagnosis to those who did not develop HF. HCQ use was similar in both groups and a higher cumulative HCQ dose was not associated with increased risk of HF. As it is small and retrospective, larger prospective studies would be helpful, but this remains reassuring as to the safety of HCQ in RA patients.

Li et al looked at risk of thromboembolic disease in patients with RA within the first 5 years of diagnosis compared to those without RA. Using a population database in British Columbia, Canada, 39,142 RA patients were matched to 78,078 non-RA patients and those with prior venous thromboembolism (VTE) were excluded. Incidence rates of VTE, pulmonary embolism (PE), and deep venous thrombosis (DVT) were higher among the RA cohort than the non-RA cohort; this observation held true after adjusting for age, sex, glucocorticoid, and contraceptive use. It would be interesting to know if the increased risk holds true after control of inflammation (i.e. in patients with established RA in low vs. high disease activity states). In the absence of information about BMI and tobacco use, more studies are necessary to provide further support for this finding.

As noted above, RA is associated with cardiovascular disease (CVD), along with risk of death from cardiovascular complications. Because CVD is itself a risk factor for dementia, Sattui et al examined the potential for systemic inflammation and CVD to increase risk of developing dementia in RA patients. Using CMS claims data from 2006 to 2014, they studied 56,000 RA patients age 65 or older and looked at risk of dementia according to CVD status (no CVD or risk factors, CVD risk factors without disease, and CVD). Incidence rates for dementia were higher among RA patients with CVD risk factors than those without, and highest among RA patients with CVD. This effect was age-dependent, with a more significant risk among RA patients age 65-74, perhaps because of a general increase in dementia in older adults. As RA disease activity was not obtainable in this study, the effects of systemic inflammation are difficult to attribute. In addition, there may be some misclassification of data regarding coding of dementia subtypes (i.e. vascular and Alzheimer dementia). However, as there are limited studies in this area, this study provides credible evidence for an increase in dementia in RA patients with CVD, which should be further investigated.

Finally, hydroxychloroquine (HCQ) has come under increased scrutiny in the past year in terms of its potential use outside of treatment of lupus and RA as well as potential side effects. Cardiac toxicity related to HCQ is thought to be rare; Sorour et al looked at the association between chronic HCQ use in patients with RA and the development of heart failure (HF) using a retrospective study comparing patients who developed HF after RA diagnosis to those who did not develop HF. HCQ use was similar in both groups and a higher cumulative HCQ dose was not associated with increased risk of HF. As it is small and retrospective, larger prospective studies would be helpful, but this remains reassuring as to the safety of HCQ in RA patients.

Daily treatment with tofacitinib (Xeljanz) led to more malignancies and adverse cardiovascular events in older rheumatoid arthritis patients compared with treatment with a tumor necrosis factor (TNF) inhibitor, according to the partial results of a safety study announced last week by Pfizer.

The postmarketing study known as ORAL Surveillance began in 2014 to evaluate the safety of the Janus kinase (JAK) inhibitor tofacitinib compared to a TNF inhibitor in RA patients 50 years of age or older with at least one additional cardiovascular risk factor. Its 4,362 participants were randomized to either daily doses of 5 mg (n = 1,455) or 10 mg (n = 1,456) of tofacitinib or the TNFi (n = 1,451), which was adalimumab for patients in the United States, Canada, and Puerto Rico, and etanercept elsewhere. During analysis, adverse events were pooled for all patients on tofacitinib.

Overall, 135 patients developed major adverse cardiovascular events (MACE) and 164 developed malignancies – excluding nonmelanoma skin cancer. The incidence of adjudicated malignancies was significantly higher in the tofacitinib group, compared with the TNFi group (1.13 vs. 0.77 per 100 person-years; hazard ratio, 1.48; 95% confidence interval, 1.04-2.09). The rate of MACE was also higher in the combined tofacitinib group (0.98 vs. 0.73 per 100 person-years; HR, 1.33; 95% CI, 0.91-1.94). Both rates for tofacitinib did not meet the trial’s noninferiority criteria.

Among the patients on tofacitinib, the most reported MACE was myocardial infarction and the most reported malignancy was lung cancer. Study participants with noted risk factors – including older age and smoking – were more likely to experience adverse events.

In February 2019, patients in the 10-mg tofacitinib group were switched to the 5-mg because of a safety signal indicating increased risk of pulmonary embolism and death.

Tofacitinib was approved for RA in November 2012, though concerns about serious side effects had been noted during clinical trials and a boxed warning was ultimately added to the drug’s label. Tofacitinib is also approved for adults with active psoriatic arthritis, adults with moderately to severely active ulcerative colitis, and patients aged 2 years or older with active polyarticular course juvenile idiopathic arthritis. Other JAK inhibitors such as baricitinib and upadacitinib have been approved for RA in the interim as well, though the higher dose of baricitinib was rejected in committee because of safety concerns and both their boxes also warn against infections, thrombosis, and cancer.

A postmarketing safety study on baricitinib is expected to be completed in 2025.

The full results of the ORAL Surveillance study – which should address safety regarding pulmonary embolism and mortality, as well as efficacy data – have not yet been released. “Pfizer is working with the [FDA] and other regulatory agencies to review the full results and analyses as they become available,” the press release said.

Daily treatment with tofacitinib (Xeljanz) led to more malignancies and adverse cardiovascular events in older rheumatoid arthritis patients compared with treatment with a tumor necrosis factor (TNF) inhibitor, according to the partial results of a safety study announced last week by Pfizer.

The postmarketing study known as ORAL Surveillance began in 2014 to evaluate the safety of the Janus kinase (JAK) inhibitor tofacitinib compared to a TNF inhibitor in RA patients 50 years of age or older with at least one additional cardiovascular risk factor. Its 4,362 participants were randomized to either daily doses of 5 mg (n = 1,455) or 10 mg (n = 1,456) of tofacitinib or the TNFi (n = 1,451), which was adalimumab for patients in the United States, Canada, and Puerto Rico, and etanercept elsewhere. During analysis, adverse events were pooled for all patients on tofacitinib.

Overall, 135 patients developed major adverse cardiovascular events (MACE) and 164 developed malignancies – excluding nonmelanoma skin cancer. The incidence of adjudicated malignancies was significantly higher in the tofacitinib group, compared with the TNFi group (1.13 vs. 0.77 per 100 person-years; hazard ratio, 1.48; 95% confidence interval, 1.04-2.09). The rate of MACE was also higher in the combined tofacitinib group (0.98 vs. 0.73 per 100 person-years; HR, 1.33; 95% CI, 0.91-1.94). Both rates for tofacitinib did not meet the trial’s noninferiority criteria.

Among the patients on tofacitinib, the most reported MACE was myocardial infarction and the most reported malignancy was lung cancer. Study participants with noted risk factors – including older age and smoking – were more likely to experience adverse events.

In February 2019, patients in the 10-mg tofacitinib group were switched to the 5-mg because of a safety signal indicating increased risk of pulmonary embolism and death.

Tofacitinib was approved for RA in November 2012, though concerns about serious side effects had been noted during clinical trials and a boxed warning was ultimately added to the drug’s label. Tofacitinib is also approved for adults with active psoriatic arthritis, adults with moderately to severely active ulcerative colitis, and patients aged 2 years or older with active polyarticular course juvenile idiopathic arthritis. Other JAK inhibitors such as baricitinib and upadacitinib have been approved for RA in the interim as well, though the higher dose of baricitinib was rejected in committee because of safety concerns and both their boxes also warn against infections, thrombosis, and cancer.

A postmarketing safety study on baricitinib is expected to be completed in 2025.

The full results of the ORAL Surveillance study – which should address safety regarding pulmonary embolism and mortality, as well as efficacy data – have not yet been released. “Pfizer is working with the [FDA] and other regulatory agencies to review the full results and analyses as they become available,” the press release said.

Daily treatment with tofacitinib (Xeljanz) led to more malignancies and adverse cardiovascular events in older rheumatoid arthritis patients compared with treatment with a tumor necrosis factor (TNF) inhibitor, according to the partial results of a safety study announced last week by Pfizer.

The postmarketing study known as ORAL Surveillance began in 2014 to evaluate the safety of the Janus kinase (JAK) inhibitor tofacitinib compared to a TNF inhibitor in RA patients 50 years of age or older with at least one additional cardiovascular risk factor. Its 4,362 participants were randomized to either daily doses of 5 mg (n = 1,455) or 10 mg (n = 1,456) of tofacitinib or the TNFi (n = 1,451), which was adalimumab for patients in the United States, Canada, and Puerto Rico, and etanercept elsewhere. During analysis, adverse events were pooled for all patients on tofacitinib.

Overall, 135 patients developed major adverse cardiovascular events (MACE) and 164 developed malignancies – excluding nonmelanoma skin cancer. The incidence of adjudicated malignancies was significantly higher in the tofacitinib group, compared with the TNFi group (1.13 vs. 0.77 per 100 person-years; hazard ratio, 1.48; 95% confidence interval, 1.04-2.09). The rate of MACE was also higher in the combined tofacitinib group (0.98 vs. 0.73 per 100 person-years; HR, 1.33; 95% CI, 0.91-1.94). Both rates for tofacitinib did not meet the trial’s noninferiority criteria.

Among the patients on tofacitinib, the most reported MACE was myocardial infarction and the most reported malignancy was lung cancer. Study participants with noted risk factors – including older age and smoking – were more likely to experience adverse events.

In February 2019, patients in the 10-mg tofacitinib group were switched to the 5-mg because of a safety signal indicating increased risk of pulmonary embolism and death.

Tofacitinib was approved for RA in November 2012, though concerns about serious side effects had been noted during clinical trials and a boxed warning was ultimately added to the drug’s label. Tofacitinib is also approved for adults with active psoriatic arthritis, adults with moderately to severely active ulcerative colitis, and patients aged 2 years or older with active polyarticular course juvenile idiopathic arthritis. Other JAK inhibitors such as baricitinib and upadacitinib have been approved for RA in the interim as well, though the higher dose of baricitinib was rejected in committee because of safety concerns and both their boxes also warn against infections, thrombosis, and cancer.

A postmarketing safety study on baricitinib is expected to be completed in 2025.

The full results of the ORAL Surveillance study – which should address safety regarding pulmonary embolism and mortality, as well as efficacy data – have not yet been released. “Pfizer is working with the [FDA] and other regulatory agencies to review the full results and analyses as they become available,” the press release said.

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

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

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

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

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

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

Key clinical point: Increased prevalence for temporomandibular (TMD) pain is reported in individuals at risk for rheumatoid arthritis (RA). It is recommended to be alert to TMD pain disorders in such cases.

Major finding: The prevalence of TMD pain was higher in individuals at risk for RA vs. controls (P = .046). However, patients with early RA showed no difference in the prevalence of TMD pain vs. control individuals.

Study details: The data come from a cross-sectional study involving 50 individuals each with early RA, those at risk for RA, and controls.

Disclosures: The authors have not declared a specific grant for this research from any funding agency in the public, commercial, or not-for-profit sectors. The authors declared no conflicts of interest.

Source: Kroese JM et al. RMD Open. 2021 Jan 11. doi: 10.1136/rmdopen-2020-001485.

Key clinical point: Increased prevalence for temporomandibular (TMD) pain is reported in individuals at risk for rheumatoid arthritis (RA). It is recommended to be alert to TMD pain disorders in such cases.

Major finding: The prevalence of TMD pain was higher in individuals at risk for RA vs. controls (P = .046). However, patients with early RA showed no difference in the prevalence of TMD pain vs. control individuals.

Study details: The data come from a cross-sectional study involving 50 individuals each with early RA, those at risk for RA, and controls.

Disclosures: The authors have not declared a specific grant for this research from any funding agency in the public, commercial, or not-for-profit sectors. The authors declared no conflicts of interest.

Source: Kroese JM et al. RMD Open. 2021 Jan 11. doi: 10.1136/rmdopen-2020-001485.

Key clinical point: Increased prevalence for temporomandibular (TMD) pain is reported in individuals at risk for rheumatoid arthritis (RA). It is recommended to be alert to TMD pain disorders in such cases.

Major finding: The prevalence of TMD pain was higher in individuals at risk for RA vs. controls (P = .046). However, patients with early RA showed no difference in the prevalence of TMD pain vs. control individuals.

Study details: The data come from a cross-sectional study involving 50 individuals each with early RA, those at risk for RA, and controls.

Disclosures: The authors have not declared a specific grant for this research from any funding agency in the public, commercial, or not-for-profit sectors. The authors declared no conflicts of interest.

Source: Kroese JM et al. RMD Open. 2021 Jan 11. doi: 10.1136/rmdopen-2020-001485.

Key clinical point: Treat-to-target strategy (T2T) was associated with higher probability of achieving the treatment target in patients with rheumatoid arthritis (RA) who could not reach treatment target within 6 months.

Major finding: RA patients following T2T had a 2.8 times higher likelihood for remission/low disease activity at 12 months than those not following the T2T strategy (P = .005).

Study details: Data from ATTRA registry were assessed. Seventy-five patients with RA following T2T were matched with 75 patients who continued initial treatment despite not reaching the treatment target within 6 months.

Disclosures: The work was supported by the project (Ministry of Health, Czech Republic) for conceptual development of research organization (Institute of

Rheumatology). The authors declared no conflicts of interest.

Source: Nekvindová L et al. Arthritis Res Ther. 2021 Jan 6. doi: 10.1186/s13075-020-02393-8.

Key clinical point: Treat-to-target strategy (T2T) was associated with higher probability of achieving the treatment target in patients with rheumatoid arthritis (RA) who could not reach treatment target within 6 months.

Major finding: RA patients following T2T had a 2.8 times higher likelihood for remission/low disease activity at 12 months than those not following the T2T strategy (P = .005).

Study details: Data from ATTRA registry were assessed. Seventy-five patients with RA following T2T were matched with 75 patients who continued initial treatment despite not reaching the treatment target within 6 months.

Disclosures: The work was supported by the project (Ministry of Health, Czech Republic) for conceptual development of research organization (Institute of

Rheumatology). The authors declared no conflicts of interest.

Source: Nekvindová L et al. Arthritis Res Ther. 2021 Jan 6. doi: 10.1186/s13075-020-02393-8.

Key clinical point: Treat-to-target strategy (T2T) was associated with higher probability of achieving the treatment target in patients with rheumatoid arthritis (RA) who could not reach treatment target within 6 months.

Major finding: RA patients following T2T had a 2.8 times higher likelihood for remission/low disease activity at 12 months than those not following the T2T strategy (P = .005).

Study details: Data from ATTRA registry were assessed. Seventy-five patients with RA following T2T were matched with 75 patients who continued initial treatment despite not reaching the treatment target within 6 months.

Disclosures: The work was supported by the project (Ministry of Health, Czech Republic) for conceptual development of research organization (Institute of

Rheumatology). The authors declared no conflicts of interest.

Source: Nekvindová L et al. Arthritis Res Ther. 2021 Jan 6. doi: 10.1186/s13075-020-02393-8.

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

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

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

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

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

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

Key clinical point: In patients with rheumatoid arthritis (RA), baseline magnetic resonance imaging (MRI) osteitis and tenosynovitis independently predicted 2-year MRI damage. Following the MRI-targeted treatment strategy was a positive predictor for stringent remission.

Major finding: Baseline osteitis independently predicted MRI erosion (odds ratio [OR], 1.13), joint space narrowing (OR, 1.15), and combined damage progression (OR, 1.23; P less than .001 for all). Tenosynovitis independently predicted MRI erosion progression (OR, 1.13; P = .01). MRI-targeted treatment strategy predicted Clinical Disease Activity Index remission (OR, 2.94; P = .01), Simplified Disease Activity Index remission (OR, 2.50; P = .047), and Boolean remission (OR, 5.47; P less than .001).

Study details: The data come from the IMAGINE-RA study, a 2-year, investigator-initiated, randomized clinical Danish multicenter trial on 200 RA patients.

Disclosures: The work was supported by AbbVie, who supported the IMAGINE-RA primary study. Some authors received grants/personal fees/nonfinancial support from various research organizations and/or pharmaceutical companies, including AbbVie.

Source: Møller-Bisgaard S et al. Rheumatology (Oxford). 2021 Jan 5. doi: 10.1093/rheumatology/keaa496.

Key clinical point: In patients with rheumatoid arthritis (RA), baseline magnetic resonance imaging (MRI) osteitis and tenosynovitis independently predicted 2-year MRI damage. Following the MRI-targeted treatment strategy was a positive predictor for stringent remission.

Major finding: Baseline osteitis independently predicted MRI erosion (odds ratio [OR], 1.13), joint space narrowing (OR, 1.15), and combined damage progression (OR, 1.23; P less than .001 for all). Tenosynovitis independently predicted MRI erosion progression (OR, 1.13; P = .01). MRI-targeted treatment strategy predicted Clinical Disease Activity Index remission (OR, 2.94; P = .01), Simplified Disease Activity Index remission (OR, 2.50; P = .047), and Boolean remission (OR, 5.47; P less than .001).

Study details: The data come from the IMAGINE-RA study, a 2-year, investigator-initiated, randomized clinical Danish multicenter trial on 200 RA patients.

Disclosures: The work was supported by AbbVie, who supported the IMAGINE-RA primary study. Some authors received grants/personal fees/nonfinancial support from various research organizations and/or pharmaceutical companies, including AbbVie.

Source: Møller-Bisgaard S et al. Rheumatology (Oxford). 2021 Jan 5. doi: 10.1093/rheumatology/keaa496.

Key clinical point: In patients with rheumatoid arthritis (RA), baseline magnetic resonance imaging (MRI) osteitis and tenosynovitis independently predicted 2-year MRI damage. Following the MRI-targeted treatment strategy was a positive predictor for stringent remission.

Major finding: Baseline osteitis independently predicted MRI erosion (odds ratio [OR], 1.13), joint space narrowing (OR, 1.15), and combined damage progression (OR, 1.23; P less than .001 for all). Tenosynovitis independently predicted MRI erosion progression (OR, 1.13; P = .01). MRI-targeted treatment strategy predicted Clinical Disease Activity Index remission (OR, 2.94; P = .01), Simplified Disease Activity Index remission (OR, 2.50; P = .047), and Boolean remission (OR, 5.47; P less than .001).

Study details: The data come from the IMAGINE-RA study, a 2-year, investigator-initiated, randomized clinical Danish multicenter trial on 200 RA patients.

Disclosures: The work was supported by AbbVie, who supported the IMAGINE-RA primary study. Some authors received grants/personal fees/nonfinancial support from various research organizations and/or pharmaceutical companies, including AbbVie.

Source: Møller-Bisgaard S et al. Rheumatology (Oxford). 2021 Jan 5. doi: 10.1093/rheumatology/keaa496.

Key clinical point: Patients with incident rheumatoid arthritis (RA) have increased risks for venous thromboembolism (VTE), pulmonary embolism (PE), and deep vein thrombosis (DVT) than the general population.

Major finding: RA patients showed higher overall risks for VTE (adjusted hazard ratio [aHR], 1.28; 95% confidence interval [CI], 1.20-1.36), PE (aHR, 1.25; 95% CI, 1.13-1.39), and DVT (aHR, 1.30; 95% CI, 1.21-1.40) after adjusting for VTE risk factors.

Study details: The data come from a population-based study involving 39,142 patients with incident RA and 78,078 matched non-RA controls.

Disclosures: The study was supported by the Canadian Institutes of Health Research. The authors declared no conflicts of interest.

Source: Li L et al. Rheumatology (Oxford). 2021 Jan 5. doi: 10.1093/rheumatology/keaa262.

Key clinical point: Patients with incident rheumatoid arthritis (RA) have increased risks for venous thromboembolism (VTE), pulmonary embolism (PE), and deep vein thrombosis (DVT) than the general population.

Major finding: RA patients showed higher overall risks for VTE (adjusted hazard ratio [aHR], 1.28; 95% confidence interval [CI], 1.20-1.36), PE (aHR, 1.25; 95% CI, 1.13-1.39), and DVT (aHR, 1.30; 95% CI, 1.21-1.40) after adjusting for VTE risk factors.

Study details: The data come from a population-based study involving 39,142 patients with incident RA and 78,078 matched non-RA controls.

Disclosures: The study was supported by the Canadian Institutes of Health Research. The authors declared no conflicts of interest.

Source: Li L et al. Rheumatology (Oxford). 2021 Jan 5. doi: 10.1093/rheumatology/keaa262.

Key clinical point: Patients with incident rheumatoid arthritis (RA) have increased risks for venous thromboembolism (VTE), pulmonary embolism (PE), and deep vein thrombosis (DVT) than the general population.

Major finding: RA patients showed higher overall risks for VTE (adjusted hazard ratio [aHR], 1.28; 95% confidence interval [CI], 1.20-1.36), PE (aHR, 1.25; 95% CI, 1.13-1.39), and DVT (aHR, 1.30; 95% CI, 1.21-1.40) after adjusting for VTE risk factors.

Study details: The data come from a population-based study involving 39,142 patients with incident RA and 78,078 matched non-RA controls.

Disclosures: The study was supported by the Canadian Institutes of Health Research. The authors declared no conflicts of interest.

Source: Li L et al. Rheumatology (Oxford). 2021 Jan 5. doi: 10.1093/rheumatology/keaa262.