Background Reactivation of hepatitis B virus (HBV) in patients undergoing immunosuppressive therapy, can be transient and clinically silent, but is often severe, resulting in acute hepatic failure. However, there have not fully elucidated about the factors involved in both suppressing and promoting the reactivation of HBV in patients with collagen disease including RA.
Objectives To determine the factors influential in the prevention of HBV reactivation in patients with collagen diseases.
Methods A search of the electronic databases Medline (PubMed), Embase Cochrane and Japan Medical Abstract Society (search terms: hepatitis B virus, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, systemic lupus erythematosus, polymyalgia rheumatic, systemic scleroderma, polymyositis, dermatomyositis, mixed connective tissue disease, Behçet disease, vasculitis and collagen disease) was performed in August 2013 to identify trials and studies addressing HBV reactivation in collagen disease, regardless of definition or duration. Selection criteria were English and Japanese language and contrastive study of the two groups with or without HBV reactivation. Among HBsAg-positive patients, HBV reactivation was defined as a 10-fold rise in HBV-DNA or a change to positive hepatitis B e antigen (HBeAg) in previously HBeAg-negative patients. Among patients with resolved HBV, HBV reactivation was defined as a change from HBsAg-negative to HBsAg-positive and/or serum titre >2.1 log copies/ml for HBV. In addition to a narrative overview of the studies found in this systemic review, a meta-analysis was performed by pooling the results of the studies comparing the effects of two groups with or without HBV reactivation by subgroups.
Results 27 studied with 1266 patients (rheumatoid arthritis, 1060; ankylosing spondylitis, 82; psoriatic arthritis,45; systemic lupus erythematosus, 18; polymyalgia rheumatic, 6; systemic scleroderma, 5; polymyositis/dermatomyositis, 3; other, 9 patinets.) were selected by all authors and narrative overview was done. The cumulative prevalence of HBV reactivation were follows; HBsAg-positive patients, 17.6% (39/221); HBsAg-positive with nucleoside analogue (NA) prophylaxis, 9.0% (9/100); HBsAg-positive with lamivudine (LAM) prophylaxis, 18.8% (9/48); HBsAg-positive with prophylaxis entecavir (ETV) 0% (0/24); HBsAg-positive without NA prophylaxis, 24.8% (30/121); resolved HBV, 3.3% (33/1007). The pooled effect of anti-HBs positivity, NA prophylaxis use, ETV prophylaxis use, and neutrophil counts>2480 on HBV reactivation in HBsAg-positive patients with collagen disease remained significant under the fixed effects model (RR 3.04; 0.30; 1.23x10–7; 1.11x10–8; P<0.05). Logistic regression model predicting HBV reactivation in collagen disease with HBsAg-positive was revealed the neutrophil counts >2480 (RR7.64x10–16; P=0.003).
Conclusions Through a comprehensive literature review and meta-analysis, we found that neutrophil is an important factor preventing HBV reactivation for patients with collagen disease.
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Acknowledgements Through a comprehensive literature review and meta-analysis, we found that neutrophil is an important factor preventing HBV reactivation for patients with collagen disease.
Disclosure of Interest : None declared