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Hepatitis B virus and HIV coinfection: relationship of different serological patterns to survival and liver disease

HIV MEDICINE, Issue 5 2007
MK Osborn
Objectives Eighty per cent of HIV-positive patients show evidence of past or current infection with hepatitis B virus (HBV). The impact of chronic HBV infection or the presence of isolated HBV core antibody on survival in the era of highly active antiretroviral therapy (HAART) has not been well studied. Methods This retrospective analysis included patients from the HIV Atlanta Veterans Affairs Cohort Study (HAVACS). This cohort comprises 2818 HIV-positive patients followed since 1982. For this analysis, 1685 patients with available HBV serologies were included, based on laboratory records available since 1992. Adjusted survival analyses were performed for patients showing any of four serological patterns for HBV: (1) surface antigen positive (chronic HBV infection), (2) isolated core antibody, (3) surface antibody with or without core antibody (resolved/vaccinated) and (4) no HBV markers (negative group). Risk factors for liver disease were identified. Results A trend was seen for a lower survival rate from AIDS to death in the chronic HBV infection group compared with the negative group [hazard ratio (HR) 1.43; P=0.118]. The only independent predictor of lower survival rate was hepatitis C virus positivity (HR 1.62; P=0.008). Protective factors were use of HAART (HR 0.40; P=0.0003), use of lamivudine (HR 0.36; P<0.0001) and use of tenofovir (HR 0.23; P<0.0001). Survival from HIV diagnosis to death was not different among the HBV groups. Isolated core antibody patients did not have a lower survival rate compared with those with resolved HBV infection. Patients with chronic HBV infection were 3.5 times more likely to have liver disease than those with no HBV infection (P<0.02). Conclusions There is a trend towards a lower survival rate in patients with HIV and chronic HBV infection, but the difference did not reach statistical significance. The presence of isolated core antibody was not associated with a lower survival rate. [source]

Occult hepatitis B virus infection in patients with autoimmune liver diseases

LIVER INTERNATIONAL, Issue 3 2009
Sarah P. Georgiadou
Abstract Background: Occult hepatitis B virus (HBV) infection is characterized by undetectable serum HBV surface antigen (HBsAg) but detectable HBV-DNA in serum or liver. Aims: To determine the prevalence and clinical impact of occult HBV in autoimmune liver diseases as similar data are missing. Methods: One hundred and ninety-six sera samples from HBsAg-negative patients, including 66 autoimmune hepatitis (AIH), 93 primary biliary cirrhosis (PBC) and 37 primary sclerosing cholangitis (PSC), were investigated for HBV-DNA using the polymerase chain reaction (PCR) before treatment initiation. One hundred and three serial samples from 38 AIH patients under immunosuppression and 282 selected blood donors (HBsAg negative; antibodies to HBV-core antigen positive) were also investigated. Fourteen available paraffin-embedded AIH liver samples were also investigated for HBV-DNA by nested-PCR. Results: Hepatitis B virus DNA was detected in the serum of 24/196 patients (12.2%) and 0/282 donors (P=0.0000). Nine patients had AIH (13.6%), eight had PBC (8.6%) and seven had PSC (18.9%) (P=0.0000 vs healthy). HBV-DNA detection in AIH livers was higher than in serum. HBV-DNA was associated neither with HBV markers nor with epidemiological, laboratory and clinical data. Serial testing of AIH patients revealed two HBV-DNA-negative patients before treatment becoming positive during treatment, while all HBV-DNA-positive patients before immunosuppression became negative. Conclusion: Based mainly on serum HBV-DNA, we found a significant proportion of autoimmune liver disease patients with occult HBV compared with donors. However, taking into account our results in a small number of liver tissues, it should be emphasized that occult HBV could be even higher when both serum and liver specimens are investigated. Occult HBV does not seem to affect the clinical and laboratory features of the diseases, while AIH patients with occult HBV under immunosuppression do not deteriorate during follow-up. [source]

Hepatitis B prophylaxis post-liver transplant without maintenance hepatitis B immunoglobulin therapy

CLINICAL TRANSPLANTATION, Issue 2 2006
Dilip S. Nath
Abstract: Background: We examined outcomes in recipients who underwent a liver transplant for HBV-induced liver disease and received a protocol for prophylaxis that did not use HBIG maintenance. Results: Between October 2002 and July 2005, a total of 14 liver transplant recipients were identified that met the study criteria. Mean recipient age was 47.6 yr; mean donor age was 37.2 yr. Category of transplant was as follows: cadaveric liver (n=10, 71%), cadaveric split-liver (n=2, 14%), and cadaveric liver,kidney (n=2, 14%). Liver disease was diagnosed at a mean of 7.3 yr before transplant; three (21%) had a coexisting hepatocellular cancer at the time of transplant. Pre-transplant, all 14 (100%) recipients were hepatitis B surface antigen (HBsAg) positive, and 11 (79%) were HBV DNA positive (mean viral load of 251.2 pg/mL). Three (21%) were E antigen positive, and one (7%) was D antigen positive. Pre-transplant, seven patients (50%) were on anti-viral therapy and there was documented diminution in viral loads after initiating anti-viral therapy in 3 cases. Three (21%) were hepatitis C virus (HCV) antigen positive and all had low-RNA titers. With mean follow-up of 14.1 months, all 14 patients are alive with a functioning graft. Mean ALT, AST and total bilirubin values are currently at 43.2, 32.2, and 0.84, respectively. One recipient remains HBsAg surface antigen positive post-transplant but has normal lab values. The remaining recipients have no evidence of HBV recurrence by serology and protocol biopsies. The regimen has been well tolerated without the need for drug reduction or discontinuation because of side-effects. Conclusion: Longer follow-up is needed, but this regimen may represent an alternative to chronic HBIG maintenance therapy. [source]