Management of anti-HBc-positive patients with rheumatic diseases treated with disease-modifying antirheumatic drugs-a single-center analysis of 2054 patients.

Hepatitis B virus (HBV) reactivation is a common complication of immunosuppressive treatment in high prevalence countries. Biological disease-modifying antirheumatic drugs (bDMARDs) cause this adverse event more often than conventional immunosuppressants. The incidence of HBV reactivation during treatment for rheumatic diseases in Germany is unclear. Furthermore, it remains open how to treat and monitor patients at risk during immunosuppressive therapy with bDMARDs. We examined 2054 patients from a German tertiary rheumatology center in order to analyze the prevalence of HBc-antibody-positivity and the incidence of HBV reactivation in German rheumatology patients treated with immunosuppressants. Of 1317 patients treated with bDMARDs and 737 conventional synthetic DMARD (csDMARDs) patients between 2008 and 2017, 86 had a history of HBV infection (anti-HBc positive). Only two patients were suffering from chronic infection (HBsAg positive). Three patients were treated pre-emptively with entecavir, and eight patients after HBV DNA reappearance. No liver failure occurred due to HBV reactivation. Compared to anti-HBc-positive patients without reactivation, the reactivation group included more patients exposed to three or more classes of bDMARDs (p = 0.017). The median HBs antibody titer was significantly lower in the reactivation group (15.0 IU/l vs. 293.5 IU/l; p = 0.001). This study shows that bDMARDs and csDMARDs can safely be administered to patients with a history of HBV, provided they are closely monitored. Low titers of anti-HBs antibodies and a history of ≥ 3 classes of immunosuppressants increase the risk of HBV reactivation. These data highlight major differences to high prevalence regions.

Effects of structured heart failure disease management on mortality and morbidity depend on patients' mood: results from the Interdisciplinary Network for Heart Failure Study.

AIMS: Depression is common in heart failure (HF) and associated with adverse outcomes. Randomized comparisons of the effectiveness of HF care strategies by patients' mood are scarce. We therefore investigated in a randomized trial a structured collaborative disease management programme (HeartNetCare-HF™; HNC) recording mortality, morbidity, and symptoms in patients enrolled after hospitalization for decompensated systolic HF according to their responses to the 9-item Patient Health Questionnaire (PHQ-9) during an observation period of 180 days. METHODS AND RESULTS: Subjects scoring <12/≥12 were categorized as non-depressed/depressed, and those ignoring the questionnaire as PHQ-deniers. Amongst 715 participants (69 ± 12 years, 29% female), 141 (20%) were depressed, 466 (65%) non-depressed, and 108 (15%) PHQ-deniers. The composite endpoint of mortality and re-hospitalization was neutral overall and in all subgroups. However, HNC reduced mortality risk in both depressed and non-depressed patients [adjusted hazard ratios (HRs) 0.12, 95% confidence interval (CI) 0.03-0.56, P = 0.006, and 0.49, 95% CI 0.25-0.93, P = 0.03, respectively], but not in PHQ-deniers (HR 1.74, 95% CI 0.77-3.96, P = 0.19; P = 0.006 for homogeneity of HRs). Average frequencies of patient contacts in the HNC arm were 12.8 ± 7.9 in non-depressed patients, 12.4 ± 7.1 in depressed patients, and 5.5 ± 7.2 in PHQ-deniers (P < 0.001). CONCLUSIONS: Early after decompensation, HNC reduced mortality risk in non-depressed and even more in depressed subjects, but not in PHQ-deniers. This suggests that differential acceptability and chance of success of care strategies such as HNC might be predicted by appropriate assessment of patients' baseline characteristics including psychological disposition. These post-hoc results should be reassessed by prospective evaluation of HNC in larger HF populations.