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.

Key clinical point: Hydroxychloroquine for the treatment of rheumatoid arthritis (RA) does not increase the risks for depression, suicidality, or psychosis compared with sulfasalazine.

Major finding: Hydroxychloroquine use was not associated with risks for depression, acute psychosis, or suicidality compared with sulfasalazine. The hazard ratios [HRs] for short-term risks for depression, acute psychosis, and suicidality were 0.96 (95% confidence interval [CI], 0.79-1.16), 1.03 (95% CI, 0.66-1.60), and 0.94 (95% CI, 0.49-1.77), respectively. The corresponding HRs for long-term risks were 0.94 (95% CI, 0.71-1.26), 0.99 (95% CI, 0.72-1.35), and 0.77 (95% CI, 0.56-1.07), respectively.

Study details: Findings from a multinational network cohort study of RA patients using hydroxychloroquine (n=918,144) and sulfasalazine (n=290,383).

Disclosures: This study was supported by the National Institute for Health Research Oxford Biomedical Research Centre, US National Institutes of Health, US Department of Veterans Affairs, Janssen Research & Development, IQVIA, the Korea Health Technology, and the Korea Health Industry Development Institute. Some of the authors reported personal funding/support from pharmaceutical companies and/or research organizations.

Source: Lane JCE et al. Rheumatology (Oxford). 2020 Dec 25. doi: 10.1093/rheumatology/keaa771.

Key clinical point: Hydroxychloroquine for the treatment of rheumatoid arthritis (RA) does not increase the risks for depression, suicidality, or psychosis compared with sulfasalazine.

Major finding: Hydroxychloroquine use was not associated with risks for depression, acute psychosis, or suicidality compared with sulfasalazine. The hazard ratios [HRs] for short-term risks for depression, acute psychosis, and suicidality were 0.96 (95% confidence interval [CI], 0.79-1.16), 1.03 (95% CI, 0.66-1.60), and 0.94 (95% CI, 0.49-1.77), respectively. The corresponding HRs for long-term risks were 0.94 (95% CI, 0.71-1.26), 0.99 (95% CI, 0.72-1.35), and 0.77 (95% CI, 0.56-1.07), respectively.

Study details: Findings from a multinational network cohort study of RA patients using hydroxychloroquine (n=918,144) and sulfasalazine (n=290,383).

Disclosures: This study was supported by the National Institute for Health Research Oxford Biomedical Research Centre, US National Institutes of Health, US Department of Veterans Affairs, Janssen Research & Development, IQVIA, the Korea Health Technology, and the Korea Health Industry Development Institute. Some of the authors reported personal funding/support from pharmaceutical companies and/or research organizations.

Source: Lane JCE et al. Rheumatology (Oxford). 2020 Dec 25. doi: 10.1093/rheumatology/keaa771.

Key clinical point: Hydroxychloroquine for the treatment of rheumatoid arthritis (RA) does not increase the risks for depression, suicidality, or psychosis compared with sulfasalazine.

Major finding: Hydroxychloroquine use was not associated with risks for depression, acute psychosis, or suicidality compared with sulfasalazine. The hazard ratios [HRs] for short-term risks for depression, acute psychosis, and suicidality were 0.96 (95% confidence interval [CI], 0.79-1.16), 1.03 (95% CI, 0.66-1.60), and 0.94 (95% CI, 0.49-1.77), respectively. The corresponding HRs for long-term risks were 0.94 (95% CI, 0.71-1.26), 0.99 (95% CI, 0.72-1.35), and 0.77 (95% CI, 0.56-1.07), respectively.

Study details: Findings from a multinational network cohort study of RA patients using hydroxychloroquine (n=918,144) and sulfasalazine (n=290,383).

Disclosures: This study was supported by the National Institute for Health Research Oxford Biomedical Research Centre, US National Institutes of Health, US Department of Veterans Affairs, Janssen Research & Development, IQVIA, the Korea Health Technology, and the Korea Health Industry Development Institute. Some of the authors reported personal funding/support from pharmaceutical companies and/or research organizations.

Source: Lane JCE et al. Rheumatology (Oxford). 2020 Dec 25. doi: 10.1093/rheumatology/keaa771.

Key clinical point: Patients with endometriosis are at a significantly higher risk of developing rheumatoid arthritis (RA).

Major finding: The risk of RA was significantly higher in patients with endometriosis (adjusted hazard ratio [aHR], 1.75; 95% confidence interval [CI], 1.27-2.41), those aged 45 years or older (aHR, 1.50; 95% CI, 1.06-2.13), and those with autoimmune disease (aHR, 6.99; 95% CI, 2.84-17.21).

Study details: This 13-year Taiwanese population-based study included 14,463 women with and 14,463 women without endometriosis who were propensity score-matched by age, comorbidities, corticosteroids, nonsteroidal anti-inflammatory drugs, and hormonal medications.

Disclosures: The study was supported by the Chung Shan Medical University’s DryLab Team and grants awarded to Chung Shan Medical University. The authors declared no conflicts of interest.

Source: Xue YH et al. Rheumatology (Oxford). 2020 Dec 17. doi: 10.1093/rheumatology/keaa784.

Key clinical point: Patients with endometriosis are at a significantly higher risk of developing rheumatoid arthritis (RA).

Major finding: The risk of RA was significantly higher in patients with endometriosis (adjusted hazard ratio [aHR], 1.75; 95% confidence interval [CI], 1.27-2.41), those aged 45 years or older (aHR, 1.50; 95% CI, 1.06-2.13), and those with autoimmune disease (aHR, 6.99; 95% CI, 2.84-17.21).

Study details: This 13-year Taiwanese population-based study included 14,463 women with and 14,463 women without endometriosis who were propensity score-matched by age, comorbidities, corticosteroids, nonsteroidal anti-inflammatory drugs, and hormonal medications.

Disclosures: The study was supported by the Chung Shan Medical University’s DryLab Team and grants awarded to Chung Shan Medical University. The authors declared no conflicts of interest.

Source: Xue YH et al. Rheumatology (Oxford). 2020 Dec 17. doi: 10.1093/rheumatology/keaa784.

Key clinical point: Patients with endometriosis are at a significantly higher risk of developing rheumatoid arthritis (RA).

Major finding: The risk of RA was significantly higher in patients with endometriosis (adjusted hazard ratio [aHR], 1.75; 95% confidence interval [CI], 1.27-2.41), those aged 45 years or older (aHR, 1.50; 95% CI, 1.06-2.13), and those with autoimmune disease (aHR, 6.99; 95% CI, 2.84-17.21).

Study details: This 13-year Taiwanese population-based study included 14,463 women with and 14,463 women without endometriosis who were propensity score-matched by age, comorbidities, corticosteroids, nonsteroidal anti-inflammatory drugs, and hormonal medications.

Disclosures: The study was supported by the Chung Shan Medical University’s DryLab Team and grants awarded to Chung Shan Medical University. The authors declared no conflicts of interest.

Source: Xue YH et al. Rheumatology (Oxford). 2020 Dec 17. doi: 10.1093/rheumatology/keaa784.

Key clinical point: In patients with active rheumatoid arthritis (RA) who had limited or no prior methotrexate (MTX) exposure, filgotinib (FIL) with MTX reduced signs and symptoms of RA and improved physical function with an acceptable safety profile up to 52 weeks.

Major finding: At week 24, significantly higher proportions of patients receiving FIL200 + MTX (81%; P less than .001) and FIL100 + MTX (80%; P = .017) achieved 20% improvement in American College of Rheumatology criteria (ACR20) vs. MTX (71%). Significant improvements in Health Assessment Questionnaire-Disability Index and 28-joint Disease Activity Score with C-reactive protein less than 2.6 were seen at week 24. Adverse event rates through week 52 were comparable between all treatments.

Study details: In this 52-week phase 3 FINCH 3 trial, 1,252 patients with RA were randomly assigned in a 2:1:1:2 ratio to receive filgotinib 200 mg with MTX (FIL200 + MTX), filgotinib 100 mg with MTX (FIL100+MTX), filgotinib 200 mg monotherapy (FIL200), or MTX.

Disclosures: The study was funded by Gilead Sciences, Inc. The lead author reported receiving grant/research support from and serving as a consultant for Celltrion, Galapagos, and Gilead Sciences.

Source: Westhovens R et al. Ann Rheum Dis. 2021 Jan 15. doi: 10.1136/annrheumdis-2020-219213.

Key clinical point: In patients with active rheumatoid arthritis (RA) who had limited or no prior methotrexate (MTX) exposure, filgotinib (FIL) with MTX reduced signs and symptoms of RA and improved physical function with an acceptable safety profile up to 52 weeks.

Major finding: At week 24, significantly higher proportions of patients receiving FIL200 + MTX (81%; P less than .001) and FIL100 + MTX (80%; P = .017) achieved 20% improvement in American College of Rheumatology criteria (ACR20) vs. MTX (71%). Significant improvements in Health Assessment Questionnaire-Disability Index and 28-joint Disease Activity Score with C-reactive protein less than 2.6 were seen at week 24. Adverse event rates through week 52 were comparable between all treatments.

Study details: In this 52-week phase 3 FINCH 3 trial, 1,252 patients with RA were randomly assigned in a 2:1:1:2 ratio to receive filgotinib 200 mg with MTX (FIL200 + MTX), filgotinib 100 mg with MTX (FIL100+MTX), filgotinib 200 mg monotherapy (FIL200), or MTX.

Disclosures: The study was funded by Gilead Sciences, Inc. The lead author reported receiving grant/research support from and serving as a consultant for Celltrion, Galapagos, and Gilead Sciences.

Source: Westhovens R et al. Ann Rheum Dis. 2021 Jan 15. doi: 10.1136/annrheumdis-2020-219213.

Key clinical point: In patients with active rheumatoid arthritis (RA) who had limited or no prior methotrexate (MTX) exposure, filgotinib (FIL) with MTX reduced signs and symptoms of RA and improved physical function with an acceptable safety profile up to 52 weeks.

Major finding: At week 24, significantly higher proportions of patients receiving FIL200 + MTX (81%; P less than .001) and FIL100 + MTX (80%; P = .017) achieved 20% improvement in American College of Rheumatology criteria (ACR20) vs. MTX (71%). Significant improvements in Health Assessment Questionnaire-Disability Index and 28-joint Disease Activity Score with C-reactive protein less than 2.6 were seen at week 24. Adverse event rates through week 52 were comparable between all treatments.

Study details: In this 52-week phase 3 FINCH 3 trial, 1,252 patients with RA were randomly assigned in a 2:1:1:2 ratio to receive filgotinib 200 mg with MTX (FIL200 + MTX), filgotinib 100 mg with MTX (FIL100+MTX), filgotinib 200 mg monotherapy (FIL200), or MTX.

Disclosures: The study was funded by Gilead Sciences, Inc. The lead author reported receiving grant/research support from and serving as a consultant for Celltrion, Galapagos, and Gilead Sciences.

Source: Westhovens R et al. Ann Rheum Dis. 2021 Jan 15. doi: 10.1136/annrheumdis-2020-219213.

Key clinical point: Cardiovascular (CV) disease (CVD) and CV risk factors were risk factors for incident dementia among rheumatoid arthritis (RA) patients between 65 and 74 years of age; however, this risk attenuated with increasing age.

Major finding: Patients with CVD and CV risk factors between 65 and 74 years of age had an increased risk for dementia vs. those without CVD and CV risk factors (adjusted hazard Ratio [aHR], 1.18; 95% confidence interval [CI], 1.04-1.33; aHR, 1.03; 95% CI, 1.00-1.11, respectively). For patients between 75 and 84 years of age, a trend toward an increased risk of dementia was observed with CVD but was not statistically significant (aHR, 1.03; 95% CI, 0.92-1.14). These associations were not observed among patients aged 85 years and older.

Study details: Longitudinal analysis of 56,567 patients with RA using Center for Medicare & Medicaid claims (CMS) data from 2006 to 2014; 11,789 (20.1%) incident cases of dementia were included in the analysis.

Disclosures: The study was supported by I Navarro-Millan’s IPCI award from Weill Cornell Medicine Division of General Internal Medicine. JR Curtis received research support and consulting fees from AbbVie, Amgen, BMS, Corrona, Eli Lilly, Janssen, Myriad, Pfizer, Regeneron, Roche, and UCB. SB Lieber reported spousal ownership interests in Cigna, Intuitive Surgical, Inc., Merck, and Pfizer. I Navarro-Millán received consulting fees from Sobi. The remaining authors declared no conflicts of interest.

Source: Sattui SE et al. Semin Arthritis Rheum. 2021 Jan 5. doi: 10.1016/j.semarthrit.2020.09.022.

Key clinical point: Cardiovascular (CV) disease (CVD) and CV risk factors were risk factors for incident dementia among rheumatoid arthritis (RA) patients between 65 and 74 years of age; however, this risk attenuated with increasing age.

Major finding: Patients with CVD and CV risk factors between 65 and 74 years of age had an increased risk for dementia vs. those without CVD and CV risk factors (adjusted hazard Ratio [aHR], 1.18; 95% confidence interval [CI], 1.04-1.33; aHR, 1.03; 95% CI, 1.00-1.11, respectively). For patients between 75 and 84 years of age, a trend toward an increased risk of dementia was observed with CVD but was not statistically significant (aHR, 1.03; 95% CI, 0.92-1.14). These associations were not observed among patients aged 85 years and older.

Study details: Longitudinal analysis of 56,567 patients with RA using Center for Medicare & Medicaid claims (CMS) data from 2006 to 2014; 11,789 (20.1%) incident cases of dementia were included in the analysis.

Disclosures: The study was supported by I Navarro-Millan’s IPCI award from Weill Cornell Medicine Division of General Internal Medicine. JR Curtis received research support and consulting fees from AbbVie, Amgen, BMS, Corrona, Eli Lilly, Janssen, Myriad, Pfizer, Regeneron, Roche, and UCB. SB Lieber reported spousal ownership interests in Cigna, Intuitive Surgical, Inc., Merck, and Pfizer. I Navarro-Millán received consulting fees from Sobi. The remaining authors declared no conflicts of interest.

Source: Sattui SE et al. Semin Arthritis Rheum. 2021 Jan 5. doi: 10.1016/j.semarthrit.2020.09.022.

Key clinical point: Cardiovascular (CV) disease (CVD) and CV risk factors were risk factors for incident dementia among rheumatoid arthritis (RA) patients between 65 and 74 years of age; however, this risk attenuated with increasing age.

Major finding: Patients with CVD and CV risk factors between 65 and 74 years of age had an increased risk for dementia vs. those without CVD and CV risk factors (adjusted hazard Ratio [aHR], 1.18; 95% confidence interval [CI], 1.04-1.33; aHR, 1.03; 95% CI, 1.00-1.11, respectively). For patients between 75 and 84 years of age, a trend toward an increased risk of dementia was observed with CVD but was not statistically significant (aHR, 1.03; 95% CI, 0.92-1.14). These associations were not observed among patients aged 85 years and older.

Study details: Longitudinal analysis of 56,567 patients with RA using Center for Medicare & Medicaid claims (CMS) data from 2006 to 2014; 11,789 (20.1%) incident cases of dementia were included in the analysis.

Disclosures: The study was supported by I Navarro-Millan’s IPCI award from Weill Cornell Medicine Division of General Internal Medicine. JR Curtis received research support and consulting fees from AbbVie, Amgen, BMS, Corrona, Eli Lilly, Janssen, Myriad, Pfizer, Regeneron, Roche, and UCB. SB Lieber reported spousal ownership interests in Cigna, Intuitive Surgical, Inc., Merck, and Pfizer. I Navarro-Millán received consulting fees from Sobi. The remaining authors declared no conflicts of interest.

Source: Sattui SE et al. Semin Arthritis Rheum. 2021 Jan 5. doi: 10.1016/j.semarthrit.2020.09.022.

Key clinical point: Higher disease activity and elevated levels of cytokines/chemokines are associated with a greater risk of diabetes mellitus (DM) in patients with rheumatoid arthritis (RA).

Major finding: High Disease activity Score (DAS28)-C reactive protein (CRP) was associated with an increased risk of DM (test for trend: P less than .001). Several cytokines/chemokines analyzed showed independent association with DM risk including interleukin (IL)-1, IL-6, and select macrophage-derived cytokines/chemokines (hazard ratio per standard deviation range, 1.11-1.26). These associations were independent of the DAS28-CRP.

Study details: This longitudinal analysis included 1,866 patients with RA without prevalent DM from Veteran’s Affairs Rheumatoid Arthritis Registry. Thirty cytokines and chemokines were measured in banked serum obtained at the time of enrolment.

Disclosures: No study sponsor was identified. The presenting author has received consulting fees from Bristol-Myers Squibb and Gilead.

Source: Baker JF. Ann Rheum Dis. 2021 Jan 4. doi: 10.1136/annrheumdis-2020-219140

Key clinical point: Higher disease activity and elevated levels of cytokines/chemokines are associated with a greater risk of diabetes mellitus (DM) in patients with rheumatoid arthritis (RA).

Major finding: High Disease activity Score (DAS28)-C reactive protein (CRP) was associated with an increased risk of DM (test for trend: P less than .001). Several cytokines/chemokines analyzed showed independent association with DM risk including interleukin (IL)-1, IL-6, and select macrophage-derived cytokines/chemokines (hazard ratio per standard deviation range, 1.11-1.26). These associations were independent of the DAS28-CRP.

Study details: This longitudinal analysis included 1,866 patients with RA without prevalent DM from Veteran’s Affairs Rheumatoid Arthritis Registry. Thirty cytokines and chemokines were measured in banked serum obtained at the time of enrolment.

Disclosures: No study sponsor was identified. The presenting author has received consulting fees from Bristol-Myers Squibb and Gilead.

Source: Baker JF. Ann Rheum Dis. 2021 Jan 4. doi: 10.1136/annrheumdis-2020-219140

Key clinical point: Higher disease activity and elevated levels of cytokines/chemokines are associated with a greater risk of diabetes mellitus (DM) in patients with rheumatoid arthritis (RA).

Major finding: High Disease activity Score (DAS28)-C reactive protein (CRP) was associated with an increased risk of DM (test for trend: P less than .001). Several cytokines/chemokines analyzed showed independent association with DM risk including interleukin (IL)-1, IL-6, and select macrophage-derived cytokines/chemokines (hazard ratio per standard deviation range, 1.11-1.26). These associations were independent of the DAS28-CRP.

Study details: This longitudinal analysis included 1,866 patients with RA without prevalent DM from Veteran’s Affairs Rheumatoid Arthritis Registry. Thirty cytokines and chemokines were measured in banked serum obtained at the time of enrolment.

Disclosures: No study sponsor was identified. The presenting author has received consulting fees from Bristol-Myers Squibb and Gilead.

Source: Baker JF. Ann Rheum Dis. 2021 Jan 4. doi: 10.1136/annrheumdis-2020-219140

Key clinical point: Use of hydroxychloroquine (HCQ) is not associated with increased risk of developing heart failure (HF) in patients with rheumatoid arthritis (RA).

Major finding: HCQ cumulative dose was not associated with HF (odds ratio [OR], 0.96 [95% confidence interval (CI), 0.90-1.03] per 100 g). No statistically significant association was found for patients with a cumulative dose of 300 g or more (OR, 0.92; 95% CI, 0.41-2.08). Duration of HCQ use prior to index was not associated with HF (OR, 0.98; 95% CI, 0.91-1.05).

Study details: The data come from a nested case-control study of 143 RA cases diagnosed with HF and 143 non-HF RA controls.

Disclosures: The study was funded by grants from the National Institutes of Health. The authors declared no conflicts of interest.

Source: Sorour AA et al. J Rheumatol. 2021 Jan 15. doi: 10.3899/jrheum.201180

Key clinical point: Use of hydroxychloroquine (HCQ) is not associated with increased risk of developing heart failure (HF) in patients with rheumatoid arthritis (RA).

Major finding: HCQ cumulative dose was not associated with HF (odds ratio [OR], 0.96 [95% confidence interval (CI), 0.90-1.03] per 100 g). No statistically significant association was found for patients with a cumulative dose of 300 g or more (OR, 0.92; 95% CI, 0.41-2.08). Duration of HCQ use prior to index was not associated with HF (OR, 0.98; 95% CI, 0.91-1.05).

Study details: The data come from a nested case-control study of 143 RA cases diagnosed with HF and 143 non-HF RA controls.

Disclosures: The study was funded by grants from the National Institutes of Health. The authors declared no conflicts of interest.

Source: Sorour AA et al. J Rheumatol. 2021 Jan 15. doi: 10.3899/jrheum.201180

Key clinical point: Use of hydroxychloroquine (HCQ) is not associated with increased risk of developing heart failure (HF) in patients with rheumatoid arthritis (RA).

Major finding: HCQ cumulative dose was not associated with HF (odds ratio [OR], 0.96 [95% confidence interval (CI), 0.90-1.03] per 100 g). No statistically significant association was found for patients with a cumulative dose of 300 g or more (OR, 0.92; 95% CI, 0.41-2.08). Duration of HCQ use prior to index was not associated with HF (OR, 0.98; 95% CI, 0.91-1.05).

Study details: The data come from a nested case-control study of 143 RA cases diagnosed with HF and 143 non-HF RA controls.

Disclosures: The study was funded by grants from the National Institutes of Health. The authors declared no conflicts of interest.

Source: Sorour AA et al. J Rheumatol. 2021 Jan 15. doi: 10.3899/jrheum.201180