Patients with rheumatoid arthritis (RA) receiving immunosuppressant therapy who were also diagnosed with chronic hepatitis B virus (HBV) infection demonstrated greater radiographic progression and poorer clinical response at 1 year compared with patients with RA without chronic HBV, according to findings published in Arthritis Research & Therapy.
Despite recognition by clinicians of an association between RA and HBV infection, the mechanism behind this connection has remained unclear. This was the first longitudinal study to explore the relationship between HBV infection and RA disease progression and treatment outcomes in patients taking disease-modifying antirheumatic drugs.
RA was defined primarily by a Disease Activity Score 28-joint assessment based on C-reactive protein (DAS28-CRP) ≥2.6. There were 32 patients with RA and chronic HBV and 128 matched patients with RA without chronic HBV (84% women; mean age, 49 years; mean DAS28-CRP score, 4.6) retrospectively enrolled and followed at baseline and at 1, 3, 6, and 12 months. The therapeutic target was DAS28-CRP <2.6, or <3.2 for participants with RA disease duration >24 months. Bilateral hand and wrist radiographs were taken at baseline and at 12 months and were evaluated for change in modified total Sharp score (mTSS). The primary outcome was the proportion of patients displaying radiographic progression (≥0.5 units on mTSS) after 12 months.
Significantly more individuals with RA and chronic HBV showed radiographic progression after 1 year vs those without HBV (53% vs 17%; P <.001). Clinical responses were also significantly poorer in patients with chronic HBV vs those without HBV at both 6 months (53% vs 82%; P =.003) and 12 months (53% vs 75%; P =.034).
Improvements in American College of Rheumatology response criteria (20% and 50%) and European League Against Rheumatism scores also showed similar differences between the groups at 6 and 12 months (P <.05 for all). After confounder adjustment and multivariate analysis, odds ratios (ORs) revealed that the presence of chronic HBV infection was still an independent risk factor for 1-year radiographic progression (OR, 2.403; 95% CI, 1.218-4.743; P =.011) and poorer clinical response at 6 months (OR, 2.844; 95% CI, 1.245-6.498; P =.013).
The main adverse events during the trial included infections, gastrointestinal discomfort, and aminotransferase elevation. In addition, HBV reactivation occurred in 34% of patients with RA and chronic HBV, and 2 patients experienced hepatitis flares.
Study limitations included the real-world, observational design, the use of a single center, the various medication regimens used among participants, the lack of sufficient participation by patients without bony erosions at baseline, and the small sample of patients with chronic HBV.
Chronic HBV infection may negatively affect patients with RA taking immunosuppressants in terms of disease activity and progression, and HBV reactivation is also a serious consideration for clinicians treating this population. The authors noted, “that HBV infection might directly or indirectly contribute to joint damage.” Future investigations should involve multiple centers, more participants, and placebo control participants.
Chen YL, Lin JZ, Mo YQ, et al. Deleterious role of hepatitis B virus infection in therapeutic response among patients with rheumatoid arthritis in a clinical practice setting: a case-control study. Arthritis Res Ther. 2018;20(1):81.
This article originally appeared on Rheumatology Advisor