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A new study found RA patients with concomitant Sjögren’s disease were more likely to fail TNFi treatment than the treatments of other mode of action biologics and JAKi.
A study found rheumatoid arthritis (RA) patients with concomitant Sjögren’s disease have a severe RA phenotype and respond less to treatment, especially with the tumor necrosis factor-a-inhibitors (TNFi).1
“CoRASS is the first study to assess the treatment response to different treatment modalities in RA with regard to the presence or absence of [Sjögren’s disease],” wrote investigators, led by Lisa Christ, from the department of rheumatology and immunology at the University Hospital and University of Bern in Switzerland. “Patients with concomitant [Sjögren’s disease] revealed a more aggressive phenotype including higher disease activity, a higher ultrasound [power doppler]-score, and more erosive disease in this multicenter cohort.”
Although it is known Sjögren’s disease may occur with RA, patients with both RA and Sjögren’s disease often remain undetected and undertreated.2 So far, treatment options for RA do not allow for personalized medicine, as there are no validated biomarkers to aid individualized treatment.1
To better understand concomitant Sjögren’s disease with RA, investigators conducted an observational cohort study to assess the clinical phenotype and treatment response in RA patients with and without Sjögren’s disease. They leveraged participants from the Swiss Clinical Quality Management in Rheumatic Diseases registry.
The study included 337 patients ≥ 18 years old with concomitant Sjögren’s disease and 5974 without. Patients with Sjögren’s disease were more likely to be female, non-smokers, have a positive rheumatoid factor, a greater disease activity score, erosive bone damage, anti-cyclic citrullinated peptide antibodies, a longer RA disease duration, worse patient-reported outcomes, and more signs of synovitis.
The team assessed treatment effectiveness by 3 ways: drug retention time of TNFi (n =3788); other mode of action biologics including abatacept, IL-6Ri, and rituximab (n = 2225); and Janus kinase-inhibitors (JAKi) (n = 768). They used an adjusted hazard ratio to compare the time for drug discontinuation between the treatment options. In total, they analyzed 6781 treatment responses.
RA patients with Sjögren’s disease had shorter drug retention rates than patients without Sjögren’s disease for TNFi (518; 95% confidence interval [CI], 391 – 721 vs 777; 95% CI, 728 – 866), other mode of action (619; 95% CI, 525 – 979 vs 894; 95% CI, 796 – 1016), and JAKi (817; 95% CI, 436 – 1570 vs 812; 95% CI, 684 – 949).
Furthermore, an adjusted Cox model showed RA patients with Sjögren’s disease had a greater risk for stopping TNFi Treatment than patients without Sjögren’s disease (crude hazard ratio [HR], 1.24; 95% CI, 1.06 – 1.44). The team observed a trend for other mode of action (crude HR, 1.16; 95% CI, 0.96 – 1.39) but not for JAKi (crude HR, 1.06; 95% CI, 0.71 – 1.57). After adjusting, they found stopping TNFi was still greater for patients with Sjögren’s disease (HR, 1.30; 95% CI, 1.07 – 1.60) but not for other mode of action and JAKi (HR, 1.12; 95% CI, 0.91 – 1.37 and HR, 0.97; 95% CI, 0.62 – 1.53, respectively).
After a year, patients with Sjögren’s disease were less likely to reach a DAS28 remission with all 3 treatment options. Additionally, these individuals had a greater risk for stopping all treatment forms (TNFi: adjusted hazard ratio [HR], 1.3; 95% CI, 1.07 – 1.6; other mode of action: HR, 1.12; 95% CI, 0.91 – 1.37; JAKi: HR, 0.97; 95% CI, 0.28 – 0.96).
The team highlighted 2 limitations, including the observational study design, and relying on a physician’s diagnosis for the definition of RA and Sjögren’s disease, leaving room for some cases of Sjögren’s disease to be undetected.
“...Patients with RA should be assessed for the presence of [Sjögren’s disease], and non-TNFi treatment modalities may be considered early,” investigators concluded.
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