AB0360G DETECTABLE HBV DNA AT TREATMENT BASELINE PREDICTED HEPATITIS B VIRUS REACTIVATION IN INFLAMMATORY ARTHRITIS PATIENTS WITH NEGATIVE HEPATITIS B SURFCE ANTIGEN BUT POSITIVE ANTI-HEPATITIS B CORE ANTIGEN
Authors: Grace Chup-Hei Ho
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Hepatitis B virus (HBV) reactivation in inflammatory arthritis IA (rheumatoid arthritis, psoriatic arthritis, and peripheral spondyloarthritis) patients with positive hepatitis B surface antigen (HBsAg+) is one of the treatment-related complications. The risk of reactivation in patients with negative hepatitis B surface antigen but positive anti-hepatitis B core antibody (HBsAg+/anti-HBc-) is less well defined. <h3>Objectives</h3> This retrospective, single centre study aimed to study the prevalence of HBV reactivation (defined as HBV DNA becoming detectable during treatment if it was untectable at baseline, or an increase in HBV DNA titre if detectable at baseline) among IA patients with HBsAg+/anti-HBc+ status, and to investigate any factors predicting reactivation. <h3>Methods</h3> IA patients attending the rheumatology specialist clinic in a local tertiary hospital between 1<sup>st</sup>January 2011 and 31<sup>st</sup> December 2016 were included if they had HBsAg-/anti-HBc+ status. Demographic data, clinical parameters including treatments for IA and any use of antiviral prophylaxis, and laboratory results including anti-hepatitis B surface antibody (anti-HBs) and serial HBV DNA levels were obtained. Logistic regression was used to identify factors predicting HBV reactivation. <h3>Results</h3> Around 1/3 (68%) of the 206 included patients included were female and the mean age was 61.7-year-old. 75% had rheumatoid arthritis and the remaining had psoriatic arthritis or peripheral spondyloarthritis. Most patients (94%, n=194) were on conventional synthetic DMARD csDMARD (25 on monotherapy and 169 on combination therapy). 35% patients (n=72) were on biologic DMARD (with or without csDMARD). As antiviral prophylaxis was not mandatory in HBsAg-/anti-HBc+ patients according to local protocol, only 17 patients (8.3%) were on preemptive antiviral against HBV. Thirteen patients (6.3%) experienced HBV reactivation during their disease course and four of them were on antiviral prophylaxis. All of these reactivations were only transient low-grade viraemia with HBV DNA level &lt; 20IU/ml. Spontaneous resolution of viraemia were observed in all these patients. None of the reactivation resulted in acute hepatitis, hepatic failure or mortality. Presence of detectable HBV DNA at baseline predicted HBV reactivation (OR 21.0, p&lt;0.005). Other parameters including age, the lack of antiviral prophylaxis, negative anti-HBs status and anti-HBs titre were not significant predictors of HBV reactivation. None of the synthetic and biologic DMARDs were associated with HBV reactivation. <h3>Conclusion</h3> HBV reactivation was infrequent among IA patients with HBsAg-/anti-HBc+ status and was unlikely to be associated with adverse clinical outcome. It could occur in patients with positive anti-HBs or on antiviral prophylaxis. Detectable HBV DNA at baseline was a predictor of HBV reactivation. <h3>References</h3> [1] Mod Rheumatol. 2018Jan22:1-6 [2] Clin Exp Rheumatol. 2017 Sep-Oct;35(5):831-836 <h3>Disclosure of Interests</h3> None declared