BACKGROUND: Rheumatoid arthritis (RA) patients seropositive for hepatitis B core antibody (HBcAb) and negative for hepatitis B surface antigen (HBsAg) are at risk of hepatitis B virus (HBV) reactivation when treated with biologic or targeted synthetic (b/ts) disease-modifying antirheumatic drugs (DMARDs). The study aims to investigate the risk in this population.
METHODS: From January 2004 through December 2020, 1068 RA patients undergoing b/tsDMARDs therapy and 416 patients with HBsAg-/HBcAb+ were enrolled. Factors associated with HBV reactivation were analysed.
RESULTS: During 2845 person-years of follow-up, 27 of 416 (6.5%,9.5 per 1000 person-years) patients developed HBV reactivation, with a cumulative rate of HBV reactivation of 3.5% at 5 years, 6.1% at 10 years and 24.2% at 17 years. The median interval from beginning b/tsDMARDs to HBV reactivation was 85 months (range: 9-186 months). The risk of HBV reactivation varied by type of b/tsDMARD, with rituximab having the highest risk (incidence rate: 48.3 per 1000 person-years), followed by abatacept (incidence rate: 24.0 per 1000 person-years). In multivariate analysis, rituximab (adjusted hazard ratio [aHR]: 15.77, 95% confidence interval [CI]: 4.12-60.32, p = .001), abatacept (aHR: 9.30, 1.83-47.19, p = .007), adalimumab (aHR: 3.86, 1.05-14.26, p = .04) and negative baseline HBV surface antibody (anti-HBs, <10 mIU/mL) (aHR: 3.89, 1.70-8.92, p < .001) were independent risk factors for HBV reactivation.
CONCLUSIONS: HBsAg-/HBcAb+ RA patients are susceptible to HBV reactivation during b/tsDMARD therapy. Those with negative baseline anti-HBs and those on certain b/tsDMARDs, such as rituximab, abatacept and adalimumab, have high reactivation risks. Risk stratification and management should be based on the patient\'s baseline anti-HBs titre and type of therapy.

OBJECTIVE: This paper aimed to assess and follow up the course of resolved HBV (hepatitis B virus) during and after treatment with direct-acting antiviral drugs (DAAs).
BACKGROUND: Co-infection with hepatitis B and hepatitis C is increasingly recognized in patients with chronic hepatitis. Resolved HBV in patients with chronic HCV (hepatitis C virus) infection has been investigated during interferon therapy, and the investigators suggest a possible correlation with a lower response to anti-viral treatment, higher grades of liver histological changes, and development of hepatocellular carcinoma.
METHODS: Three hundred and thirteen patients were included in our observational and prospective study; two hundred and fifty-three patients had chronic hepatitis C (CHC) (group I), and sixty patients had both CHC and resolved HBV-infection (group II). They all were eligible for treatment with DAAs therapy for chronic HCV in our hepatology unit, Internal Medicine Department, Zagazig University Hospitals from December 2017 to September 2018. They were subjected to thorough history taking, full clinical examination, routine laboratory investigations, HCV antibody, HCV RNA, HBV surface antigen (HBsAg), HBV surface antibody (anti-HBs) HBV core antibody (anti-HBc), and HBV-DNA quantitative levels. All patients were followed up at baseline, at the end of week 4 of anti-viral therapy, at the end of treatment and 12 weeks after treatment.
RESULTS: Assessment at 28 days showed significant decreases in ALT and AST levels in both groups, with stabilization of these levels on follow-up at 12 and 24 weeks. The efficacy of treatment was comparable in both groups. No case of ALT flare was observed in either group. Similar outcomes regarding AST and ALT levels were found in patients with diseases associated with immune derangement.
CONCLUSIONS: The risk of resolved HBV reactivation during or after treatment with DAAs is low.

OBJECTIVE: To identify the incidence and risk factors for hepatitis B virus (HBV) reactivation in rheumatoid arthritis (RA) patients with resolved HBV receiving biological disease-modifying antirheumatic drugs (bDMARDs).
METHODS: Rheumatoid arthritis patients in whom bDMARD therapy was initiated in our departments from April 2009 to July 2016 were reviewed. The patients diagnosed with resolved HBV and whose HBV-DNA levels had been repeatedly measured were enrolled. The endpoint was HBV reactivation (a positive conversion of HBV-DNA or unquantifiable cases with positivity <20 IU/mL). Nucleic acid analogues (NAAs) were administered when the HBV-DNA levels increased beyond 20 IU/mL. The associations between HBV reactivation and the clinical findings were retrospectively analyzed.
RESULTS: One hundred and fifty-two RA patients with resolved HBV were enrolled; 133 (88%) patients had antibodies against HBV surface antigen (anti-HBs). The medicines that were administered included: abatacept (n = 29), golimumab (n = 26), etanercept (n = 25), tocilizumab (n = 25), adalimumab (n = 19), infliximab (n = 17) and certolizumab pegol (n = 11). During the observation period (15 [interquartile range 4.0-34] months), 7 (4.6%) patients developed HBV reactivation. In 5 of these patients, the HBV-DNA levels became negative or remained at <20 IU/mL (+) without NAA therapy. HBV-DNA levels of >20 IU/mL were observed in 2 patients but the HBV-DNA levels became negative after NAA treatment. Patients who were negative for anti-HBs showed a significantly higher incidence of HBV reactivation (P = 0.013).
CONCLUSIONS: HBV reactivation occurred in 4.6% of RA patients with resolved HBV during the treatment with bDMARDs and the absence of anti-HBs may be a risk factor for the reactivation of resolved HBV.