Poor efficacy of nucleic acid testing in identifying occult HBV infection and consequences for safety of blood supply in Italy.

BACKGROUND & AIMS: In Italy, DNA screening of blood donations for hepatitis B virus (HBV) was introduced to prevent the transmission of window period and occult HBV infection. Anti-HBc screening is not recommended in order to avoid shortage of the blood supply. To contain costs, donor samples are generally pooled before testing. We evaluated the safety of this national policy using a prospective repository of donors/recipient pairs. METHODS: We used highly sensitive nucleic acid testing (NAT) assays to test repository and follow-up samples from donors who were initially classified as negative by minipool NAT assays (6-MP), but were later found to carry occult HBV DNA. When available, we also analysed recipients' pre- and post-transfusion samples, collected in the context of a repository financed by the European Commission (the BOTIA project). RESULTS: Between 2008 and 2011 6-MP NAT assays identified 18 carriers of occult HBV infection among 12,695 donors; 28 samples from previous donations were available from 13 of these carriers. Highly sensitive HBV DNA detection methods showed that 6-MP HBV DNA screening failed to identify 14/28 (50%) viraemic donations, that were released for transfusion. HBV marker testing of such blood product recipients revealed two cases of transfusion transmitted HBV infection, documented by donor-recipient sequence identity. CONCLUSIONS: Viraemic blood donations from occult HBV infection carriers remain undetected by current minipool HBV DNA screening, and transfusion transmission of HBV continues to occur in susceptible patients. More effective individual HBV DNA screening and/or tests for antibodies to HBV core antigen should be considered to improve blood safety.

Portal pressure reduction after entecavir treatment in compensated HBV cirrhosis.

A Caucasian male aged 54 year was referred to our liver centre for the management of HBV-related cirrhosis. Prior treatment with recombinant alpha-interferon followed by lymphoblastoid interferon was only temporarily effective and the patient refused antiviral treatment with lamivudine. When admitted to our unit, the patient had a Child-Pugh score of A6, high HBV DNA load (4 x 10(6) IU/ml) and evidence of cirrhotic cardiomyopathy. Hepatic venous pressure gradient (HVPG) was 29mm Hg, indicative of clinically severe portal hypertension. Following 3 months of treatment with entecavir, tests for HBV DNA were negative, and 9 months after therapy started, HVPG was measured as 24mm Hg, a reduction from baseline of 17%. These findings indicate that sustained suppression of HBV DNA replication by entecavir in compensated cirrhosis with severe portal hypertension leads to a portal pressure reduction, without the need for vaso-active drugs, as measured using the transjugular HVPG approach described here.