MDedge Rheumatology

As new COVID-19 cases mount in New York City, Mayor Bill de Blasio began his final week in office watching a sweeping vaccine mandate for private employers take effect.

Business owners were supposed to require all workers to have at least one dose of vaccine by Monday, Dec. 27. Workers won’t be able to opt out of vaccinations, as a proposed federal mandate for private sector employees would allow. Municipal workers were already under a vaccine mandate.

Mayor De Blasio called it the strongest private sector vaccine mandate in the world – and insists it’s absolutely necessary.

“I am 110 percent convinced this was the right thing to do, remains the right thing to do, particularly with the ferocity of Omicron,” the mayor told reporters on Dec. 27. “I don’t know if there’s going to be another variant behind it, but I do know our best defense is to get everyone vaccinated and mandates have worked.”

It’s unclear if Mayor de Blasio’s successor, Mayor-Elect Eric Adams, will continue the vaccine mandate. The New York Times reported that Mr. Adams’ spokesman, Evan Thies, said in a text: “The mayor-elect will make announcements on his administration’s Covid policy this week.”

Mayor De Blasio said enforcement would be light in the first week. Not every business owner is following the law.

The New York Post said Stratis Morfogen, owner of the Brooklyn Dumpling Shop and executive managing director of Brooklyn Chop House, went on Instagram and dared the mayor and Gov. Kathy Hochul to come and arrest him.

“Not going to follow your mandate on threatening my family of employees to get the jab or lose your job!” he said.

Mr. Morfogen said he’s not against vaccines but thinks the mandate violates his employees’ constitutional rights. He said he’s taking more steps toward safety, such as frequent testing of employees.

Union Square Hospitality Group CEO Danny Meyer, who oversees restaurants such as Union Square Cafe and Blue Smoke, requires employees not only to get vaccinated, but to get the booster, too.

“Hospitality is a team sport – it’s kind of like putting on a play on Broadway or playing a basketball game,” Mr. Meyer told CNBC. “If you can’t field a full healthy team, you’re going to have to hit pause.”

Customers at Union Square Hospitality Group restaurants will soon be required to show proof of having received a booster shot.

Also starting Dec. 27, all New Yorkers 12 and up must show they’ve received two doses of vaccine to enter indoor dining, fitness, entertainment, and performance venues unless they’ve gotten the one-dose Johnson & Johnson vaccine.

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

As new COVID-19 cases mount in New York City, Mayor Bill de Blasio began his final week in office watching a sweeping vaccine mandate for private employers take effect.

Business owners were supposed to require all workers to have at least one dose of vaccine by Monday, Dec. 27. Workers won’t be able to opt out of vaccinations, as a proposed federal mandate for private sector employees would allow. Municipal workers were already under a vaccine mandate.

Mayor De Blasio called it the strongest private sector vaccine mandate in the world – and insists it’s absolutely necessary.

“I am 110 percent convinced this was the right thing to do, remains the right thing to do, particularly with the ferocity of Omicron,” the mayor told reporters on Dec. 27. “I don’t know if there’s going to be another variant behind it, but I do know our best defense is to get everyone vaccinated and mandates have worked.”

It’s unclear if Mayor de Blasio’s successor, Mayor-Elect Eric Adams, will continue the vaccine mandate. The New York Times reported that Mr. Adams’ spokesman, Evan Thies, said in a text: “The mayor-elect will make announcements on his administration’s Covid policy this week.”

Mayor De Blasio said enforcement would be light in the first week. Not every business owner is following the law.

The New York Post said Stratis Morfogen, owner of the Brooklyn Dumpling Shop and executive managing director of Brooklyn Chop House, went on Instagram and dared the mayor and Gov. Kathy Hochul to come and arrest him.

“Not going to follow your mandate on threatening my family of employees to get the jab or lose your job!” he said.

Mr. Morfogen said he’s not against vaccines but thinks the mandate violates his employees’ constitutional rights. He said he’s taking more steps toward safety, such as frequent testing of employees.

Union Square Hospitality Group CEO Danny Meyer, who oversees restaurants such as Union Square Cafe and Blue Smoke, requires employees not only to get vaccinated, but to get the booster, too.

“Hospitality is a team sport – it’s kind of like putting on a play on Broadway or playing a basketball game,” Mr. Meyer told CNBC. “If you can’t field a full healthy team, you’re going to have to hit pause.”

Customers at Union Square Hospitality Group restaurants will soon be required to show proof of having received a booster shot.

Also starting Dec. 27, all New Yorkers 12 and up must show they’ve received two doses of vaccine to enter indoor dining, fitness, entertainment, and performance venues unless they’ve gotten the one-dose Johnson & Johnson vaccine.

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

As new COVID-19 cases mount in New York City, Mayor Bill de Blasio began his final week in office watching a sweeping vaccine mandate for private employers take effect.

Business owners were supposed to require all workers to have at least one dose of vaccine by Monday, Dec. 27. Workers won’t be able to opt out of vaccinations, as a proposed federal mandate for private sector employees would allow. Municipal workers were already under a vaccine mandate.

Mayor De Blasio called it the strongest private sector vaccine mandate in the world – and insists it’s absolutely necessary.

“I am 110 percent convinced this was the right thing to do, remains the right thing to do, particularly with the ferocity of Omicron,” the mayor told reporters on Dec. 27. “I don’t know if there’s going to be another variant behind it, but I do know our best defense is to get everyone vaccinated and mandates have worked.”

It’s unclear if Mayor de Blasio’s successor, Mayor-Elect Eric Adams, will continue the vaccine mandate. The New York Times reported that Mr. Adams’ spokesman, Evan Thies, said in a text: “The mayor-elect will make announcements on his administration’s Covid policy this week.”

Mayor De Blasio said enforcement would be light in the first week. Not every business owner is following the law.

The New York Post said Stratis Morfogen, owner of the Brooklyn Dumpling Shop and executive managing director of Brooklyn Chop House, went on Instagram and dared the mayor and Gov. Kathy Hochul to come and arrest him.

“Not going to follow your mandate on threatening my family of employees to get the jab or lose your job!” he said.

Mr. Morfogen said he’s not against vaccines but thinks the mandate violates his employees’ constitutional rights. He said he’s taking more steps toward safety, such as frequent testing of employees.

Union Square Hospitality Group CEO Danny Meyer, who oversees restaurants such as Union Square Cafe and Blue Smoke, requires employees not only to get vaccinated, but to get the booster, too.

“Hospitality is a team sport – it’s kind of like putting on a play on Broadway or playing a basketball game,” Mr. Meyer told CNBC. “If you can’t field a full healthy team, you’re going to have to hit pause.”

Customers at Union Square Hospitality Group restaurants will soon be required to show proof of having received a booster shot.

Also starting Dec. 27, all New Yorkers 12 and up must show they’ve received two doses of vaccine to enter indoor dining, fitness, entertainment, and performance venues unless they’ve gotten the one-dose Johnson & Johnson vaccine.

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

The coronavirus that causes COVID-19 can spread to the heart and brain within days of infection and can survive for months in organs, according to a new study by the National Institutes of Health.

The virus can spread to almost every organ system in the body, which could contribute to the ongoing symptoms seen in “long COVID” patients, the study authors wrote. The study is considered one of the most comprehensive reviews of how the virus replicates in human cells and persists in the human body. It is under review for publication in the journal Nature.

“This is remarkably important work,” Ziyad Al-Aly, MD, director of the Clinical Epidemiology Center at the Veterans Affairs St. Louis Health Care System, told Bloomberg News. Dr. Al-Aly wasn’t involved with the NIH study but has researched the long-term effects of COVID-19.

“For a long time now, we have been scratching our heads and asking why long COVID seems to affect so many organ systems,” he said. “This paper sheds some light and may help explain why long COVID can occur even in people who had mild or asymptomatic acute disease.”

The NIH researchers sampled and analyzed tissues from autopsies on 44 patients who died after contracting the coronavirus during the first year of the pandemic. They found persistent virus particles in multiple parts of the body, including the heart and brain, for as long as 230 days after symptoms began. This could represent infection with defective virus particles, they said, which has also been seen in persistent infections among measles patients.

“We don’t yet know what burden of chronic illness will result in years to come,” Raina MacIntyre, PhD, a professor of global biosecurity at the University of New South Wales, Sydney, told Bloomberg News.

“Will we see young-onset cardiac failure in survivors or early-onset dementia?” she asked. “These are unanswered questions which call for a precautionary public health approach to mitigation of the spread of this virus.”

Unlike other COVID-19 autopsy research, the NIH team had a more comprehensive postmortem tissue collection process, which typically occurred within a day of the patient’s death, Bloomberg News reported. The researchers also used a variety of ways to preserve tissue to figure out viral levels. They were able to grow the virus collected from several tissues, including the heart, lungs, small intestine, and adrenal glands.

“Our results collectively show that, while the highest burden of SARS-CoV-2 is in the airways and lung, the virus can disseminate early during infection and infect cells throughout the entire body, including widely throughout the brain,” the study authors wrote.

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

The coronavirus that causes COVID-19 can spread to the heart and brain within days of infection and can survive for months in organs, according to a new study by the National Institutes of Health.

The virus can spread to almost every organ system in the body, which could contribute to the ongoing symptoms seen in “long COVID” patients, the study authors wrote. The study is considered one of the most comprehensive reviews of how the virus replicates in human cells and persists in the human body. It is under review for publication in the journal Nature.

“This is remarkably important work,” Ziyad Al-Aly, MD, director of the Clinical Epidemiology Center at the Veterans Affairs St. Louis Health Care System, told Bloomberg News. Dr. Al-Aly wasn’t involved with the NIH study but has researched the long-term effects of COVID-19.

“For a long time now, we have been scratching our heads and asking why long COVID seems to affect so many organ systems,” he said. “This paper sheds some light and may help explain why long COVID can occur even in people who had mild or asymptomatic acute disease.”

The NIH researchers sampled and analyzed tissues from autopsies on 44 patients who died after contracting the coronavirus during the first year of the pandemic. They found persistent virus particles in multiple parts of the body, including the heart and brain, for as long as 230 days after symptoms began. This could represent infection with defective virus particles, they said, which has also been seen in persistent infections among measles patients.

“We don’t yet know what burden of chronic illness will result in years to come,” Raina MacIntyre, PhD, a professor of global biosecurity at the University of New South Wales, Sydney, told Bloomberg News.

“Will we see young-onset cardiac failure in survivors or early-onset dementia?” she asked. “These are unanswered questions which call for a precautionary public health approach to mitigation of the spread of this virus.”

Unlike other COVID-19 autopsy research, the NIH team had a more comprehensive postmortem tissue collection process, which typically occurred within a day of the patient’s death, Bloomberg News reported. The researchers also used a variety of ways to preserve tissue to figure out viral levels. They were able to grow the virus collected from several tissues, including the heart, lungs, small intestine, and adrenal glands.

“Our results collectively show that, while the highest burden of SARS-CoV-2 is in the airways and lung, the virus can disseminate early during infection and infect cells throughout the entire body, including widely throughout the brain,” the study authors wrote.

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

The coronavirus that causes COVID-19 can spread to the heart and brain within days of infection and can survive for months in organs, according to a new study by the National Institutes of Health.

The virus can spread to almost every organ system in the body, which could contribute to the ongoing symptoms seen in “long COVID” patients, the study authors wrote. The study is considered one of the most comprehensive reviews of how the virus replicates in human cells and persists in the human body. It is under review for publication in the journal Nature.

“This is remarkably important work,” Ziyad Al-Aly, MD, director of the Clinical Epidemiology Center at the Veterans Affairs St. Louis Health Care System, told Bloomberg News. Dr. Al-Aly wasn’t involved with the NIH study but has researched the long-term effects of COVID-19.

“For a long time now, we have been scratching our heads and asking why long COVID seems to affect so many organ systems,” he said. “This paper sheds some light and may help explain why long COVID can occur even in people who had mild or asymptomatic acute disease.”

The NIH researchers sampled and analyzed tissues from autopsies on 44 patients who died after contracting the coronavirus during the first year of the pandemic. They found persistent virus particles in multiple parts of the body, including the heart and brain, for as long as 230 days after symptoms began. This could represent infection with defective virus particles, they said, which has also been seen in persistent infections among measles patients.

“We don’t yet know what burden of chronic illness will result in years to come,” Raina MacIntyre, PhD, a professor of global biosecurity at the University of New South Wales, Sydney, told Bloomberg News.

“Will we see young-onset cardiac failure in survivors or early-onset dementia?” she asked. “These are unanswered questions which call for a precautionary public health approach to mitigation of the spread of this virus.”

Unlike other COVID-19 autopsy research, the NIH team had a more comprehensive postmortem tissue collection process, which typically occurred within a day of the patient’s death, Bloomberg News reported. The researchers also used a variety of ways to preserve tissue to figure out viral levels. They were able to grow the virus collected from several tissues, including the heart, lungs, small intestine, and adrenal glands.

“Our results collectively show that, while the highest burden of SARS-CoV-2 is in the airways and lung, the virus can disseminate early during infection and infect cells throughout the entire body, including widely throughout the brain,” the study authors wrote.

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

Booster shot protection against symptomatic COVID-19 caused by the Omicron variant appears to fade in about 10 weeks, according to new data from Britain.

U.K. health officials shared the data just before Christmas and noted that there haven’t been enough severe cases of the Omicron variant to calculate how well boosters protect against severe disease. But they believe the extra shots provide significant protection against hospitalization and death.

“It will be a few weeks before effectiveness against severe disease with Omicron can be estimated,” U.K. Health Security Agency officials wrote in the report. “However, based on experience with previous variants, this is likely to be substantially higher than the estimates against symptomatic disease.”

Since countries began reporting Omicron cases in November, multiple studies have suggested the variant is better at escaping antibodies from vaccination and previous infection, according to the New York Times. The U.K. report adds to that, noting that both the initial vaccine series and booster doses were less effective and faded faster against the Omicron variant than the Delta variant.

Among those who received two doses of the AstraZeneca vaccine, a booster of the Pfizer or Moderna vaccine was 60% effective at preventing symptomatic disease 2 to 4 weeks after the shot. But after 10 weeks, the Pfizer booster was 35% effective, and the Moderna booster was 45% effective. (The AstraZeneca vaccine is not authorized in the United States, but the Johnson & Johnson shot uses a similar technology, the New York Times reported.)

Among those who received three Pfizer doses, vaccine effectiveness was 70% about a week after the booster but dropped to 45% after 10 weeks. At the same time, those who received an initial two-dose series of the Pfizer vaccine and then a Moderna booster seemed to have 75% effectiveness up to 9 weeks.

The report was based on an analysis of 148,000 Delta cases and 68,000 Omicron cases in the United Kingdom through Dec. 20. So far, the U.K. health officials wrote, Omicron infections appear to be less severe and less likely to lead to hospitalization than Delta infections. At that time, 132 people with lab-confirmed Omicron had been admitted to hospitals, and 14 deaths had been reported among ages 52-96.

“This analysis is preliminary because of the small numbers of Omicron cases currently in hospital and the limited spread of Omicron into older age groups as yet,” the report said.

The reinfection rate has also increased for the Omicron variant, the report found. Among the 116,000 people who had an Omicron infection, about 11,000 -- or 9.5% -- were linked to a previously confirmed infection, which is likely an undercount of reinfections. In the data analyzed, 69 Omicron cases were a third episode of COVID-19 infection, and 290 cases occurred 60-89 days after a first infection.

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

Booster shot protection against symptomatic COVID-19 caused by the Omicron variant appears to fade in about 10 weeks, according to new data from Britain.

U.K. health officials shared the data just before Christmas and noted that there haven’t been enough severe cases of the Omicron variant to calculate how well boosters protect against severe disease. But they believe the extra shots provide significant protection against hospitalization and death.

“It will be a few weeks before effectiveness against severe disease with Omicron can be estimated,” U.K. Health Security Agency officials wrote in the report. “However, based on experience with previous variants, this is likely to be substantially higher than the estimates against symptomatic disease.”

Since countries began reporting Omicron cases in November, multiple studies have suggested the variant is better at escaping antibodies from vaccination and previous infection, according to the New York Times. The U.K. report adds to that, noting that both the initial vaccine series and booster doses were less effective and faded faster against the Omicron variant than the Delta variant.

Among those who received two doses of the AstraZeneca vaccine, a booster of the Pfizer or Moderna vaccine was 60% effective at preventing symptomatic disease 2 to 4 weeks after the shot. But after 10 weeks, the Pfizer booster was 35% effective, and the Moderna booster was 45% effective. (The AstraZeneca vaccine is not authorized in the United States, but the Johnson & Johnson shot uses a similar technology, the New York Times reported.)

Among those who received three Pfizer doses, vaccine effectiveness was 70% about a week after the booster but dropped to 45% after 10 weeks. At the same time, those who received an initial two-dose series of the Pfizer vaccine and then a Moderna booster seemed to have 75% effectiveness up to 9 weeks.

The report was based on an analysis of 148,000 Delta cases and 68,000 Omicron cases in the United Kingdom through Dec. 20. So far, the U.K. health officials wrote, Omicron infections appear to be less severe and less likely to lead to hospitalization than Delta infections. At that time, 132 people with lab-confirmed Omicron had been admitted to hospitals, and 14 deaths had been reported among ages 52-96.

“This analysis is preliminary because of the small numbers of Omicron cases currently in hospital and the limited spread of Omicron into older age groups as yet,” the report said.

The reinfection rate has also increased for the Omicron variant, the report found. Among the 116,000 people who had an Omicron infection, about 11,000 -- or 9.5% -- were linked to a previously confirmed infection, which is likely an undercount of reinfections. In the data analyzed, 69 Omicron cases were a third episode of COVID-19 infection, and 290 cases occurred 60-89 days after a first infection.

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

Booster shot protection against symptomatic COVID-19 caused by the Omicron variant appears to fade in about 10 weeks, according to new data from Britain.

U.K. health officials shared the data just before Christmas and noted that there haven’t been enough severe cases of the Omicron variant to calculate how well boosters protect against severe disease. But they believe the extra shots provide significant protection against hospitalization and death.

“It will be a few weeks before effectiveness against severe disease with Omicron can be estimated,” U.K. Health Security Agency officials wrote in the report. “However, based on experience with previous variants, this is likely to be substantially higher than the estimates against symptomatic disease.”

Since countries began reporting Omicron cases in November, multiple studies have suggested the variant is better at escaping antibodies from vaccination and previous infection, according to the New York Times. The U.K. report adds to that, noting that both the initial vaccine series and booster doses were less effective and faded faster against the Omicron variant than the Delta variant.

Among those who received two doses of the AstraZeneca vaccine, a booster of the Pfizer or Moderna vaccine was 60% effective at preventing symptomatic disease 2 to 4 weeks after the shot. But after 10 weeks, the Pfizer booster was 35% effective, and the Moderna booster was 45% effective. (The AstraZeneca vaccine is not authorized in the United States, but the Johnson & Johnson shot uses a similar technology, the New York Times reported.)

Among those who received three Pfizer doses, vaccine effectiveness was 70% about a week after the booster but dropped to 45% after 10 weeks. At the same time, those who received an initial two-dose series of the Pfizer vaccine and then a Moderna booster seemed to have 75% effectiveness up to 9 weeks.

The report was based on an analysis of 148,000 Delta cases and 68,000 Omicron cases in the United Kingdom through Dec. 20. So far, the U.K. health officials wrote, Omicron infections appear to be less severe and less likely to lead to hospitalization than Delta infections. At that time, 132 people with lab-confirmed Omicron had been admitted to hospitals, and 14 deaths had been reported among ages 52-96.

“This analysis is preliminary because of the small numbers of Omicron cases currently in hospital and the limited spread of Omicron into older age groups as yet,” the report said.

The reinfection rate has also increased for the Omicron variant, the report found. Among the 116,000 people who had an Omicron infection, about 11,000 -- or 9.5% -- were linked to a previously confirmed infection, which is likely an undercount of reinfections. In the data analyzed, 69 Omicron cases were a third episode of COVID-19 infection, and 290 cases occurred 60-89 days after a first infection.

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

Spesolimab, a humanized, anti–interleukin-36 receptor monoclonal antibody, was associated with rapid improvement in pustules during flares, in a phase 2 study of 53 adults with generalized pustular psoriasis (GPP).

GPP is a life-threatening skin condition involving the widespread eruption of sterile pustules, with a clinical course that “can be relapsing with recurrent flares or persistent with intermittent flares,” Hervé Bachelez, MD, of the Université de Paris and coauthors wrote. GPP patients are often hospitalized, and mortality ranges from 2% to 16% from causes that include sepsis and cardiorespiratory failure.

“The role of the interleukin-36 pathway in GPP is supported by the finding of loss-of-function mutations in the interleukin-36 receptor antagonist gene (IL36RN) and associated genes (CARD14, AP1S3, SERPINA3, and MPO) and by the overexpression of interleukin-36 cytokines in GPP skin lesions,” therefore, IL-36 is a potential treatment target to manage flares, they explained.

In the multicenter, double-blind trial, published in the New England Journal of Medicine, the researchers randomized 35 adults with GPP flares to a single 900-mg intravenous dose of spesolimab and 18 to placebo. Patients in both groups could receive an open-label dose of spesolimab after day 8; all patients were followed for 12 weeks.

The primary study endpoint was the Generalized Pustular Psoriasis Physician Global Assessment (GPPGA) pustulation subscore of 0 at 1 week after treatment. The GPPGA ranges from 0 (no visible pustules) to 4 (severe pustules). At baseline, 46% spesolimab patients and 39% placebo patients had a GPPGA pustulation subscore of 3, and 37% and 33%, respectively, had a pustulation subscore of 4.

After 1 week, 54% of the spesolimab patients had no visible pustules, compared with 6% of placebo patients; the difference was statistically significant (P < .001). The main secondary endpoint was a score of 0 or 1 (clear or almost clear skin) on the GPPGA total score after 1 week. Significantly more spesolimab patients had GPPGA total scores of 0 or 1, compared with placebo patients (43% vs. 11%, respectively; P = .02).

Overall, 6 of 35 spesolimab patients (17%) and 6% of those in the placebo groups developed infections during the first week, and 24 of 51 patients (47%) who had received spesolimab at any point during the study developed infections by week 12. Infections included urinary tract infections (three cases), influenza (three), otitis externa (two), folliculitis (two), upper respiratory tract infection (two), and pustule (two).

In the first week, 6% of spesolimab patients and none of the placebo patients reported serious adverse events; at week 12, 12% of patients who had received at least one spesolimab dose reported a serious adverse event. In addition, antidrug antibodies were identified in 23 (46%) of the 50 patients who received at least one dose of spesolimab.

“Symptoms that were observed in two patients who received spesolimab were reported as a drug reaction with eosinophilia and systemic symptoms (DRESS),” the authors noted. One patient had a RegiSCAR (European Registry of Severe Cutaneous Adverse Reactions) score and the other had a score of 3; a score below 2 indicates no DRESS, and a score of 2 or 3 indicates “possible DRESS,” they added.

“Because 15 of the 18 patients who were assigned to the placebo group received open-label spesolimab, the effect of spesolimab as compared with that of placebo could not be determined after week 1,” the researchers noted.

The study findings were limited by several factors including the short randomization period and small study population, the researchers noted. However, the effect sizes for both the primary and secondary endpoints were large, which strengthened the results.

The results support data from previous studies suggesting a role for IL-36 in the pathogenesis of GPP, and support the need for longer and larger studies of the safety and effectiveness of spesolimab for GPP patients, they concluded.

No FDA-approved therapy

“GPP is a very rare but devastating life-threatening disease that presents with the sudden onset of pustules throughout the skin,” Joel Gelfand, MD, professor of dermatology and director of the psoriasis and phototherapy center at the University of Pennsylvania, Philadelphia, said in an interview. “Without rapid treatment, GPP can result in death. Currently there are no [Food and Drug Administration]–approved treatments for this orphan disease.”

Dr. Gelfand said he was surprised by the degree of efficacy and the speed of the patient response to spesolimab, compared with placebo, which he described as “truly remarkable.” Based on the current study results, “spesolimab offers a tremendous step forward for our patients,” he added. 

Looking ahead, Dr. Gelfand noted that “longer-term studies with a comparator, such as a biologic that targets IL-17, would be helpful to more fully understand the safety, efficacy, and role that spesolimab will have in real-world patients.”

On Dec. 15, Boehringer Ingelheim announced that the FDA had granted priority review for spesolimab for treating GPP flares.

The study was supported by Boehringer Ingelheim. Lead author Dr. Bachelez had no financial conflicts to disclose. Several authors are employees of Boehringer Ingelheim. Dr. Gelfand is a consultant for the study sponsor Boehringer Ingelheim and has received research grants from Boehringer Ingelheim to his institution to support an investigator-initiated study. He also disclosed serving as a consultant and receiving research grants from other manufacturers of psoriasis products.

Spesolimab, a humanized, anti–interleukin-36 receptor monoclonal antibody, was associated with rapid improvement in pustules during flares, in a phase 2 study of 53 adults with generalized pustular psoriasis (GPP).

GPP is a life-threatening skin condition involving the widespread eruption of sterile pustules, with a clinical course that “can be relapsing with recurrent flares or persistent with intermittent flares,” Hervé Bachelez, MD, of the Université de Paris and coauthors wrote. GPP patients are often hospitalized, and mortality ranges from 2% to 16% from causes that include sepsis and cardiorespiratory failure.

“The role of the interleukin-36 pathway in GPP is supported by the finding of loss-of-function mutations in the interleukin-36 receptor antagonist gene (IL36RN) and associated genes (CARD14, AP1S3, SERPINA3, and MPO) and by the overexpression of interleukin-36 cytokines in GPP skin lesions,” therefore, IL-36 is a potential treatment target to manage flares, they explained.

In the multicenter, double-blind trial, published in the New England Journal of Medicine, the researchers randomized 35 adults with GPP flares to a single 900-mg intravenous dose of spesolimab and 18 to placebo. Patients in both groups could receive an open-label dose of spesolimab after day 8; all patients were followed for 12 weeks.

The primary study endpoint was the Generalized Pustular Psoriasis Physician Global Assessment (GPPGA) pustulation subscore of 0 at 1 week after treatment. The GPPGA ranges from 0 (no visible pustules) to 4 (severe pustules). At baseline, 46% spesolimab patients and 39% placebo patients had a GPPGA pustulation subscore of 3, and 37% and 33%, respectively, had a pustulation subscore of 4.

After 1 week, 54% of the spesolimab patients had no visible pustules, compared with 6% of placebo patients; the difference was statistically significant (P < .001). The main secondary endpoint was a score of 0 or 1 (clear or almost clear skin) on the GPPGA total score after 1 week. Significantly more spesolimab patients had GPPGA total scores of 0 or 1, compared with placebo patients (43% vs. 11%, respectively; P = .02).

Overall, 6 of 35 spesolimab patients (17%) and 6% of those in the placebo groups developed infections during the first week, and 24 of 51 patients (47%) who had received spesolimab at any point during the study developed infections by week 12. Infections included urinary tract infections (three cases), influenza (three), otitis externa (two), folliculitis (two), upper respiratory tract infection (two), and pustule (two).

In the first week, 6% of spesolimab patients and none of the placebo patients reported serious adverse events; at week 12, 12% of patients who had received at least one spesolimab dose reported a serious adverse event. In addition, antidrug antibodies were identified in 23 (46%) of the 50 patients who received at least one dose of spesolimab.

“Symptoms that were observed in two patients who received spesolimab were reported as a drug reaction with eosinophilia and systemic symptoms (DRESS),” the authors noted. One patient had a RegiSCAR (European Registry of Severe Cutaneous Adverse Reactions) score and the other had a score of 3; a score below 2 indicates no DRESS, and a score of 2 or 3 indicates “possible DRESS,” they added.

“Because 15 of the 18 patients who were assigned to the placebo group received open-label spesolimab, the effect of spesolimab as compared with that of placebo could not be determined after week 1,” the researchers noted.

The study findings were limited by several factors including the short randomization period and small study population, the researchers noted. However, the effect sizes for both the primary and secondary endpoints were large, which strengthened the results.

The results support data from previous studies suggesting a role for IL-36 in the pathogenesis of GPP, and support the need for longer and larger studies of the safety and effectiveness of spesolimab for GPP patients, they concluded.

No FDA-approved therapy

“GPP is a very rare but devastating life-threatening disease that presents with the sudden onset of pustules throughout the skin,” Joel Gelfand, MD, professor of dermatology and director of the psoriasis and phototherapy center at the University of Pennsylvania, Philadelphia, said in an interview. “Without rapid treatment, GPP can result in death. Currently there are no [Food and Drug Administration]–approved treatments for this orphan disease.”

Dr. Gelfand said he was surprised by the degree of efficacy and the speed of the patient response to spesolimab, compared with placebo, which he described as “truly remarkable.” Based on the current study results, “spesolimab offers a tremendous step forward for our patients,” he added. 

Looking ahead, Dr. Gelfand noted that “longer-term studies with a comparator, such as a biologic that targets IL-17, would be helpful to more fully understand the safety, efficacy, and role that spesolimab will have in real-world patients.”

On Dec. 15, Boehringer Ingelheim announced that the FDA had granted priority review for spesolimab for treating GPP flares.

The study was supported by Boehringer Ingelheim. Lead author Dr. Bachelez had no financial conflicts to disclose. Several authors are employees of Boehringer Ingelheim. Dr. Gelfand is a consultant for the study sponsor Boehringer Ingelheim and has received research grants from Boehringer Ingelheim to his institution to support an investigator-initiated study. He also disclosed serving as a consultant and receiving research grants from other manufacturers of psoriasis products.

Spesolimab, a humanized, anti–interleukin-36 receptor monoclonal antibody, was associated with rapid improvement in pustules during flares, in a phase 2 study of 53 adults with generalized pustular psoriasis (GPP).

GPP is a life-threatening skin condition involving the widespread eruption of sterile pustules, with a clinical course that “can be relapsing with recurrent flares or persistent with intermittent flares,” Hervé Bachelez, MD, of the Université de Paris and coauthors wrote. GPP patients are often hospitalized, and mortality ranges from 2% to 16% from causes that include sepsis and cardiorespiratory failure.

“The role of the interleukin-36 pathway in GPP is supported by the finding of loss-of-function mutations in the interleukin-36 receptor antagonist gene (IL36RN) and associated genes (CARD14, AP1S3, SERPINA3, and MPO) and by the overexpression of interleukin-36 cytokines in GPP skin lesions,” therefore, IL-36 is a potential treatment target to manage flares, they explained.

In the multicenter, double-blind trial, published in the New England Journal of Medicine, the researchers randomized 35 adults with GPP flares to a single 900-mg intravenous dose of spesolimab and 18 to placebo. Patients in both groups could receive an open-label dose of spesolimab after day 8; all patients were followed for 12 weeks.

The primary study endpoint was the Generalized Pustular Psoriasis Physician Global Assessment (GPPGA) pustulation subscore of 0 at 1 week after treatment. The GPPGA ranges from 0 (no visible pustules) to 4 (severe pustules). At baseline, 46% spesolimab patients and 39% placebo patients had a GPPGA pustulation subscore of 3, and 37% and 33%, respectively, had a pustulation subscore of 4.

After 1 week, 54% of the spesolimab patients had no visible pustules, compared with 6% of placebo patients; the difference was statistically significant (P < .001). The main secondary endpoint was a score of 0 or 1 (clear or almost clear skin) on the GPPGA total score after 1 week. Significantly more spesolimab patients had GPPGA total scores of 0 or 1, compared with placebo patients (43% vs. 11%, respectively; P = .02).

Overall, 6 of 35 spesolimab patients (17%) and 6% of those in the placebo groups developed infections during the first week, and 24 of 51 patients (47%) who had received spesolimab at any point during the study developed infections by week 12. Infections included urinary tract infections (three cases), influenza (three), otitis externa (two), folliculitis (two), upper respiratory tract infection (two), and pustule (two).

In the first week, 6% of spesolimab patients and none of the placebo patients reported serious adverse events; at week 12, 12% of patients who had received at least one spesolimab dose reported a serious adverse event. In addition, antidrug antibodies were identified in 23 (46%) of the 50 patients who received at least one dose of spesolimab.

“Symptoms that were observed in two patients who received spesolimab were reported as a drug reaction with eosinophilia and systemic symptoms (DRESS),” the authors noted. One patient had a RegiSCAR (European Registry of Severe Cutaneous Adverse Reactions) score and the other had a score of 3; a score below 2 indicates no DRESS, and a score of 2 or 3 indicates “possible DRESS,” they added.

“Because 15 of the 18 patients who were assigned to the placebo group received open-label spesolimab, the effect of spesolimab as compared with that of placebo could not be determined after week 1,” the researchers noted.

The study findings were limited by several factors including the short randomization period and small study population, the researchers noted. However, the effect sizes for both the primary and secondary endpoints were large, which strengthened the results.

The results support data from previous studies suggesting a role for IL-36 in the pathogenesis of GPP, and support the need for longer and larger studies of the safety and effectiveness of spesolimab for GPP patients, they concluded.

No FDA-approved therapy

“GPP is a very rare but devastating life-threatening disease that presents with the sudden onset of pustules throughout the skin,” Joel Gelfand, MD, professor of dermatology and director of the psoriasis and phototherapy center at the University of Pennsylvania, Philadelphia, said in an interview. “Without rapid treatment, GPP can result in death. Currently there are no [Food and Drug Administration]–approved treatments for this orphan disease.”

Dr. Gelfand said he was surprised by the degree of efficacy and the speed of the patient response to spesolimab, compared with placebo, which he described as “truly remarkable.” Based on the current study results, “spesolimab offers a tremendous step forward for our patients,” he added. 

Looking ahead, Dr. Gelfand noted that “longer-term studies with a comparator, such as a biologic that targets IL-17, would be helpful to more fully understand the safety, efficacy, and role that spesolimab will have in real-world patients.”

On Dec. 15, Boehringer Ingelheim announced that the FDA had granted priority review for spesolimab for treating GPP flares.

The study was supported by Boehringer Ingelheim. Lead author Dr. Bachelez had no financial conflicts to disclose. Several authors are employees of Boehringer Ingelheim. Dr. Gelfand is a consultant for the study sponsor Boehringer Ingelheim and has received research grants from Boehringer Ingelheim to his institution to support an investigator-initiated study. He also disclosed serving as a consultant and receiving research grants from other manufacturers of psoriasis products.

The antiviral remdesivir, an intravenous drug given mostly to seriously ill COVID-19 patients in hospitals, could keep unvaccinated people who become infected out of the hospital if given on an outpatient basis, a new study says.

Researchers studied 562 unvaccinated people from September 2020 to April 2021, according to the study published in the New England Journal of Medicine. The study determined the risk of hospitalization or death was 87% lower in study participants who were given remdesivir than participants who received a placebo.

All participants were at high risk of developing severe COVID-19 because of their age – they were over 60 – or because they had an underlying medical condition such as diabetes or obesity.

An important caveat: The findings are based on data collected before the Delta variant surged in the summer of 2021 or the Omicron variant surged late in the year, the Washington Post reported.

The new study says the drug could be helpful in keeping vaccinated as well as unvaccinated people out of the hospital – an important factor as the Omicron surge threatens to overwhelm health systems around the world.

Remdesivir could be a boon for COVID-19 patients in parts of the world that don’t have vaccines or for patients with immunocompromised systems.

“These data provide evidence that a 3-day course of remdesivir could play a critical role in helping COVID-19 patients stay out of the hospital,” Robert L. Gottlieb, MD, PhD, the therapeutic lead for COVID-19 research at Baylor Scott & White Health in Dallas, said in a news release from Gilead Pharmaceuticals. “While our hospitals are ready to assist patients in need, prevention and early intervention are preferable to reduce the risk of disease progression and allow patients not requiring oxygen to recover from home when appropriate.”

Remdesivir was the first antiviral for COVID-19 authorized by the Food and Drug Administration. It was given to then-President Donald Trump when he was hospitalized with COVID-19 in October 2020.

Gilead released the study findings in September.

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

The antiviral remdesivir, an intravenous drug given mostly to seriously ill COVID-19 patients in hospitals, could keep unvaccinated people who become infected out of the hospital if given on an outpatient basis, a new study says.

Researchers studied 562 unvaccinated people from September 2020 to April 2021, according to the study published in the New England Journal of Medicine. The study determined the risk of hospitalization or death was 87% lower in study participants who were given remdesivir than participants who received a placebo.

All participants were at high risk of developing severe COVID-19 because of their age – they were over 60 – or because they had an underlying medical condition such as diabetes or obesity.

An important caveat: The findings are based on data collected before the Delta variant surged in the summer of 2021 or the Omicron variant surged late in the year, the Washington Post reported.

The new study says the drug could be helpful in keeping vaccinated as well as unvaccinated people out of the hospital – an important factor as the Omicron surge threatens to overwhelm health systems around the world.

Remdesivir could be a boon for COVID-19 patients in parts of the world that don’t have vaccines or for patients with immunocompromised systems.

“These data provide evidence that a 3-day course of remdesivir could play a critical role in helping COVID-19 patients stay out of the hospital,” Robert L. Gottlieb, MD, PhD, the therapeutic lead for COVID-19 research at Baylor Scott & White Health in Dallas, said in a news release from Gilead Pharmaceuticals. “While our hospitals are ready to assist patients in need, prevention and early intervention are preferable to reduce the risk of disease progression and allow patients not requiring oxygen to recover from home when appropriate.”

Remdesivir was the first antiviral for COVID-19 authorized by the Food and Drug Administration. It was given to then-President Donald Trump when he was hospitalized with COVID-19 in October 2020.

Gilead released the study findings in September.

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

The antiviral remdesivir, an intravenous drug given mostly to seriously ill COVID-19 patients in hospitals, could keep unvaccinated people who become infected out of the hospital if given on an outpatient basis, a new study says.

Researchers studied 562 unvaccinated people from September 2020 to April 2021, according to the study published in the New England Journal of Medicine. The study determined the risk of hospitalization or death was 87% lower in study participants who were given remdesivir than participants who received a placebo.

All participants were at high risk of developing severe COVID-19 because of their age – they were over 60 – or because they had an underlying medical condition such as diabetes or obesity.

An important caveat: The findings are based on data collected before the Delta variant surged in the summer of 2021 or the Omicron variant surged late in the year, the Washington Post reported.

The new study says the drug could be helpful in keeping vaccinated as well as unvaccinated people out of the hospital – an important factor as the Omicron surge threatens to overwhelm health systems around the world.

Remdesivir could be a boon for COVID-19 patients in parts of the world that don’t have vaccines or for patients with immunocompromised systems.

“These data provide evidence that a 3-day course of remdesivir could play a critical role in helping COVID-19 patients stay out of the hospital,” Robert L. Gottlieb, MD, PhD, the therapeutic lead for COVID-19 research at Baylor Scott & White Health in Dallas, said in a news release from Gilead Pharmaceuticals. “While our hospitals are ready to assist patients in need, prevention and early intervention are preferable to reduce the risk of disease progression and allow patients not requiring oxygen to recover from home when appropriate.”

Remdesivir was the first antiviral for COVID-19 authorized by the Food and Drug Administration. It was given to then-President Donald Trump when he was hospitalized with COVID-19 in October 2020.

Gilead released the study findings in September.

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

Key clinical point: Circulating biomarkers for inflammation, abnormal extracellular matrix remodeling, congestion, and myocardial injury were associated with alterations in cardiac structure and function that affected prognosis in patients with rheumatoid arthritis (RA).

Major finding: Left ventricular mass index (LVMi), left atrial volume index (LAVi), and diastolic function (E/e′) were associated with biomarkers of inflammation (tumor necrosis factor receptor superfamily member 11a, bone morphogenetic protein 9, and pentraxin-related protein 3), extracellular matrix remodeling (placental growth factor), congestion (N-terminal probrain natriuretic peptide and adrenomedullin), and myocardial injury (troponin; all P < .05). Higher LVMi (adjusted hazard ratio [aHR] 1.03; P < .001) and E/e¢ (aHR 1.06; P = .042) were associated with poor prognosis.

Study details: This study included 355 adult patients with RA from the RA Porto cohort.

Disclosures: No information on funding was provided. The authors declared no conflict of interests.

Source: Kobayashi M et al. Front Cardiovasc Med. 2021;8:754784 (Nov 18). Doi: 10.3389/fcvm.2021.754784.

Key clinical point: Circulating biomarkers for inflammation, abnormal extracellular matrix remodeling, congestion, and myocardial injury were associated with alterations in cardiac structure and function that affected prognosis in patients with rheumatoid arthritis (RA).

Major finding: Left ventricular mass index (LVMi), left atrial volume index (LAVi), and diastolic function (E/e′) were associated with biomarkers of inflammation (tumor necrosis factor receptor superfamily member 11a, bone morphogenetic protein 9, and pentraxin-related protein 3), extracellular matrix remodeling (placental growth factor), congestion (N-terminal probrain natriuretic peptide and adrenomedullin), and myocardial injury (troponin; all P < .05). Higher LVMi (adjusted hazard ratio [aHR] 1.03; P < .001) and E/e¢ (aHR 1.06; P = .042) were associated with poor prognosis.

Study details: This study included 355 adult patients with RA from the RA Porto cohort.

Disclosures: No information on funding was provided. The authors declared no conflict of interests.

Source: Kobayashi M et al. Front Cardiovasc Med. 2021;8:754784 (Nov 18). Doi: 10.3389/fcvm.2021.754784.

Key clinical point: Circulating biomarkers for inflammation, abnormal extracellular matrix remodeling, congestion, and myocardial injury were associated with alterations in cardiac structure and function that affected prognosis in patients with rheumatoid arthritis (RA).

Major finding: Left ventricular mass index (LVMi), left atrial volume index (LAVi), and diastolic function (E/e′) were associated with biomarkers of inflammation (tumor necrosis factor receptor superfamily member 11a, bone morphogenetic protein 9, and pentraxin-related protein 3), extracellular matrix remodeling (placental growth factor), congestion (N-terminal probrain natriuretic peptide and adrenomedullin), and myocardial injury (troponin; all P < .05). Higher LVMi (adjusted hazard ratio [aHR] 1.03; P < .001) and E/e¢ (aHR 1.06; P = .042) were associated with poor prognosis.

Study details: This study included 355 adult patients with RA from the RA Porto cohort.

Disclosures: No information on funding was provided. The authors declared no conflict of interests.

Source: Kobayashi M et al. Front Cardiovasc Med. 2021;8:754784 (Nov 18). Doi: 10.3389/fcvm.2021.754784.

Key clinical point: Herpes zoster (HZ) events occur in tofacitinib-treated patients with rheumatoid arthritis (RA), but most of them are nonserious, mild, or moderate with HZ events resolving in most patients.

Major finding: Overall, 11.1% and 8.0% of patients with RA experienced at least 1 or recurring HZ events, respectively. Most events were nonserious, mild, or moderate in severity, with the majority of the first (97.6%) and second (96.8%) HZ events resolved in most patients. Tofacitinib treatment remained unchanged in 47.3% of patients with the first HZ event and was temporarily or permanently discontinued in 42.8% and 9.1% of patients, respectively.

Study details: The data come from a post hoc analysis of pooled data from 21 RA and 3 psoriatic arthritis (PsA) clinical studies involving 7,061 and 783 tofacitinib-treated patients with RA and PsA, respectively.

Disclosures: These studies were sponsored by Pfizer Inc. T Hirose, J L Rivas, and K Kwok reported being employees and shareholders of Pfizer Inc. Other authors reported receiving grant/research support and speaker/consultancy fees from various companies including Pfizer.

Source: Winthrop KL et al. Rheumatol Ther. 2021 (Dec 6). Doi: 10.1007/s40744-021-00390-0.

Key clinical point: Herpes zoster (HZ) events occur in tofacitinib-treated patients with rheumatoid arthritis (RA), but most of them are nonserious, mild, or moderate with HZ events resolving in most patients.

Major finding: Overall, 11.1% and 8.0% of patients with RA experienced at least 1 or recurring HZ events, respectively. Most events were nonserious, mild, or moderate in severity, with the majority of the first (97.6%) and second (96.8%) HZ events resolved in most patients. Tofacitinib treatment remained unchanged in 47.3% of patients with the first HZ event and was temporarily or permanently discontinued in 42.8% and 9.1% of patients, respectively.

Study details: The data come from a post hoc analysis of pooled data from 21 RA and 3 psoriatic arthritis (PsA) clinical studies involving 7,061 and 783 tofacitinib-treated patients with RA and PsA, respectively.

Disclosures: These studies were sponsored by Pfizer Inc. T Hirose, J L Rivas, and K Kwok reported being employees and shareholders of Pfizer Inc. Other authors reported receiving grant/research support and speaker/consultancy fees from various companies including Pfizer.

Source: Winthrop KL et al. Rheumatol Ther. 2021 (Dec 6). Doi: 10.1007/s40744-021-00390-0.

Key clinical point: Herpes zoster (HZ) events occur in tofacitinib-treated patients with rheumatoid arthritis (RA), but most of them are nonserious, mild, or moderate with HZ events resolving in most patients.

Major finding: Overall, 11.1% and 8.0% of patients with RA experienced at least 1 or recurring HZ events, respectively. Most events were nonserious, mild, or moderate in severity, with the majority of the first (97.6%) and second (96.8%) HZ events resolved in most patients. Tofacitinib treatment remained unchanged in 47.3% of patients with the first HZ event and was temporarily or permanently discontinued in 42.8% and 9.1% of patients, respectively.

Study details: The data come from a post hoc analysis of pooled data from 21 RA and 3 psoriatic arthritis (PsA) clinical studies involving 7,061 and 783 tofacitinib-treated patients with RA and PsA, respectively.

Disclosures: These studies were sponsored by Pfizer Inc. T Hirose, J L Rivas, and K Kwok reported being employees and shareholders of Pfizer Inc. Other authors reported receiving grant/research support and speaker/consultancy fees from various companies including Pfizer.

Source: Winthrop KL et al. Rheumatol Ther. 2021 (Dec 6). Doi: 10.1007/s40744-021-00390-0.

Key clinical point: Consumption of flaxseed for 12 weeks improved disease activity and reduced pain, morning stiffness, and disease feeling in patients with rheumatoid arthritis (RA).

Major finding: Disease Activity Score 28-joints-erythrocyte sedimentation rate improved significantly in patients receiving flaxseed plus regular diet (RF; P = .001), but not in patients receiving flaxseed plus anti-inflammatory diet (AIF; P = .057) and roasted wheat plus regular diet (RW; P = .110). Significant reductions in pain severity (P ≤ .001), morning stiffness (P < .05), and disease feeling (P < .01) were observed in the AIF and RF groups.

Study details: This randomized controlled trial included 120 patients with RA who were randomly assigned to 12-week intervention with AIF, RF, or RW diet groups.

Disclosures: This study was funded by the Shiraz University of Medical Sciences, Shiraz, Iran. No disclosures were reported.

Source: Ghaseminasab-Parizi M et al. Eur J Nutr. 2021 (Nov 27). Doi: 10.1007/s00394-021-02707-9.

Key clinical point: Consumption of flaxseed for 12 weeks improved disease activity and reduced pain, morning stiffness, and disease feeling in patients with rheumatoid arthritis (RA).

Major finding: Disease Activity Score 28-joints-erythrocyte sedimentation rate improved significantly in patients receiving flaxseed plus regular diet (RF; P = .001), but not in patients receiving flaxseed plus anti-inflammatory diet (AIF; P = .057) and roasted wheat plus regular diet (RW; P = .110). Significant reductions in pain severity (P ≤ .001), morning stiffness (P < .05), and disease feeling (P < .01) were observed in the AIF and RF groups.

Study details: This randomized controlled trial included 120 patients with RA who were randomly assigned to 12-week intervention with AIF, RF, or RW diet groups.

Disclosures: This study was funded by the Shiraz University of Medical Sciences, Shiraz, Iran. No disclosures were reported.

Source: Ghaseminasab-Parizi M et al. Eur J Nutr. 2021 (Nov 27). Doi: 10.1007/s00394-021-02707-9.

Key clinical point: Consumption of flaxseed for 12 weeks improved disease activity and reduced pain, morning stiffness, and disease feeling in patients with rheumatoid arthritis (RA).

Major finding: Disease Activity Score 28-joints-erythrocyte sedimentation rate improved significantly in patients receiving flaxseed plus regular diet (RF; P = .001), but not in patients receiving flaxseed plus anti-inflammatory diet (AIF; P = .057) and roasted wheat plus regular diet (RW; P = .110). Significant reductions in pain severity (P ≤ .001), morning stiffness (P < .05), and disease feeling (P < .01) were observed in the AIF and RF groups.

Study details: This randomized controlled trial included 120 patients with RA who were randomly assigned to 12-week intervention with AIF, RF, or RW diet groups.

Disclosures: This study was funded by the Shiraz University of Medical Sciences, Shiraz, Iran. No disclosures were reported.

Source: Ghaseminasab-Parizi M et al. Eur J Nutr. 2021 (Nov 27). Doi: 10.1007/s00394-021-02707-9.

Key clinical point: Patients with rheumatoid arthritis (RA) do not exhibit an elevated risk for acute or 1-year postoperative surgical site infection following total knee arthroplasty (TKA) compared with patients with osteoarthritis.

Major finding: The risk for surgical site infection at 90 days (adjusted odds ratio [aOR] 0.81; P = .598) and 1 year (aOR 0.463; P = .26) post-TKA was not significantly different between patients with RA and osteoarthritis.

Study details: This retrospective cohort study included patients with RA (n = 1,126) and osteoarthritis (n = 63,215) who underwent primary TKA.

Disclosures: No external funding was received for this study. The authors declared no conflict of interests.

Source: Chung HK et al. Sci Rep. 2021;11:22704 (Nov 22). Doi: 10.1038/s41598-021-02153-x.

Key clinical point: Patients with rheumatoid arthritis (RA) do not exhibit an elevated risk for acute or 1-year postoperative surgical site infection following total knee arthroplasty (TKA) compared with patients with osteoarthritis.

Major finding: The risk for surgical site infection at 90 days (adjusted odds ratio [aOR] 0.81; P = .598) and 1 year (aOR 0.463; P = .26) post-TKA was not significantly different between patients with RA and osteoarthritis.

Study details: This retrospective cohort study included patients with RA (n = 1,126) and osteoarthritis (n = 63,215) who underwent primary TKA.

Disclosures: No external funding was received for this study. The authors declared no conflict of interests.

Source: Chung HK et al. Sci Rep. 2021;11:22704 (Nov 22). Doi: 10.1038/s41598-021-02153-x.

Key clinical point: Patients with rheumatoid arthritis (RA) do not exhibit an elevated risk for acute or 1-year postoperative surgical site infection following total knee arthroplasty (TKA) compared with patients with osteoarthritis.

Major finding: The risk for surgical site infection at 90 days (adjusted odds ratio [aOR] 0.81; P = .598) and 1 year (aOR 0.463; P = .26) post-TKA was not significantly different between patients with RA and osteoarthritis.

Study details: This retrospective cohort study included patients with RA (n = 1,126) and osteoarthritis (n = 63,215) who underwent primary TKA.

Disclosures: No external funding was received for this study. The authors declared no conflict of interests.

Source: Chung HK et al. Sci Rep. 2021;11:22704 (Nov 22). Doi: 10.1038/s41598-021-02153-x.

Key clinical point: Positive correlations between circulating inflammatory cytokines and coinhibitory checkpoint molecules modulated by anticitrullinated peptide antibodies (ACPA) or joint damage stage existed in patients with rheumatoid arthritis (RA).

Major finding: Serum levels of interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-α) were positively associated with RA disease activity and galectin-9, independent of ACPA titers (all P < .05) and with soluble T-cell immunoglobulin and mucin-domain containing-3 in patients with ACPA <200 U/mL (P < .05). Galectin-9 was positively correlated with IL-6 (P = .005) only in patients without advanced joint damage and with TNF-a (P = .001) and IL-6 (P = .02) in patients with advanced joint damage.

Study details: This retrospective analysis included 132 patients with RA.

Disclosures: The work was funded by the Japan Grant-in-Aid for Scientific Research. K Migita received grants from Chugai, Pfizer, and AbbVie. Other authors declared no conflict of interests.

Source: Matsumoto H et al. PLoS One. 2021;16(11):e0260254 (Nov 18). Doi: 10.1371/journal.pone.0260254.

Key clinical point: Positive correlations between circulating inflammatory cytokines and coinhibitory checkpoint molecules modulated by anticitrullinated peptide antibodies (ACPA) or joint damage stage existed in patients with rheumatoid arthritis (RA).

Major finding: Serum levels of interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-α) were positively associated with RA disease activity and galectin-9, independent of ACPA titers (all P < .05) and with soluble T-cell immunoglobulin and mucin-domain containing-3 in patients with ACPA <200 U/mL (P < .05). Galectin-9 was positively correlated with IL-6 (P = .005) only in patients without advanced joint damage and with TNF-a (P = .001) and IL-6 (P = .02) in patients with advanced joint damage.

Study details: This retrospective analysis included 132 patients with RA.

Disclosures: The work was funded by the Japan Grant-in-Aid for Scientific Research. K Migita received grants from Chugai, Pfizer, and AbbVie. Other authors declared no conflict of interests.

Source: Matsumoto H et al. PLoS One. 2021;16(11):e0260254 (Nov 18). Doi: 10.1371/journal.pone.0260254.

Key clinical point: Positive correlations between circulating inflammatory cytokines and coinhibitory checkpoint molecules modulated by anticitrullinated peptide antibodies (ACPA) or joint damage stage existed in patients with rheumatoid arthritis (RA).

Major finding: Serum levels of interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-α) were positively associated with RA disease activity and galectin-9, independent of ACPA titers (all P < .05) and with soluble T-cell immunoglobulin and mucin-domain containing-3 in patients with ACPA <200 U/mL (P < .05). Galectin-9 was positively correlated with IL-6 (P = .005) only in patients without advanced joint damage and with TNF-a (P = .001) and IL-6 (P = .02) in patients with advanced joint damage.

Study details: This retrospective analysis included 132 patients with RA.

Disclosures: The work was funded by the Japan Grant-in-Aid for Scientific Research. K Migita received grants from Chugai, Pfizer, and AbbVie. Other authors declared no conflict of interests.

Source: Matsumoto H et al. PLoS One. 2021;16(11):e0260254 (Nov 18). Doi: 10.1371/journal.pone.0260254.