Role of genotype G hepatitis B virus mixed infection on the progression of hepatic fibrosis in HIV positive patients over 5 years of follow-up.

BACKGROUND: Due to common routes of transmission, HIV and HBV are frequently found as concomitant infections. The dynamic of liver disease in co-infected patients is important to understand for appropriate clinical management. Conflicting data surround the role played by genotype-G HBV (HBV-G) during the course of HIV co-infection. OBJECTIVES: This study aims to assess, using non-invasive methods, liver disease progression in HIV-HBV genotype-G co-infected patients. STUDY DESIGN: Co-infected patients with residual HBV replication (n=125) were screened for HBV-G infection by specific real-time PCR. The impact of HBV-G on liver fibrosis progression, as assessed by a non invasive biomarker (Fibrotest), was evaluated first, by a cross sectional analysis comparing fibrosis between HBV-G (n=23) and non-G (n=55) infected patients and second, by a longitudinal study performed over a 5 year period. RESULTS: Selected patients were mostly male (90%), with homogenous characteristics between the HBV-G and non-G infected groups, in terms of age, known duration of HIV disease, immune and virological status and duration of HIV/HBV treatment. HBV-G infected patients were exclusively from Western Europe with homosexual intercourses (83%) as principal risk of transmission. Cross sectional analysis revealed comparable liver disease severity distribution between HBV-G and non-G infected patients. Co-infection with other hepatitis viruses and low CD4-nadir, but not HBV-G co-infection, were associated with a 5-year risk of fibrosis progression. CONCLUSIONS: This study suggests that HBV-G infection is not significantly associated with a more severe liver disease and does not have a deleterious impact on fibrosis progression in efficiently treated HIV-HBV co-infected patients.

Efficacy and tolerance of telaprevir in HIV-hepatitis C virus genotype 1-coinfected patients failing previous antihepatitis C virus therapy: 24-week results.

The efficacy and tolerance of telaprevir (TVR) was examined in 20 mostly cirrhotic HIV-hepatitis C genotype 1 (HCV-G1)-infected patients failing previous treatment with pegylated-interferon and ribavirin (PR). HCV-RNA less than 12 IU/ml was observed in 35.3% of patients at W2, 55.0% at W4, 65.0% at W12 and 55.0% at W24. All patients with virological failure (n = 9) exhibited V36M/R155K mutations. Early virological response was a determinant of HCV-RNA less than 12 IU/ml at W24 (P < 0.001). No grade 3-4 dermatological side-effects were reported. TVR-PR tritherapy appeared to be rather effective and well tolerated among difficult-to-treat HIV-HCV-G1 patients.

Lateral rectus muscle paralysis induced by ribavirin and pegylated interferon-α2a in a patient with HIV/HCV co-infection.

We report a lateral rectus muscle paralysis occurring 2 weeks after initiation of an interferon-α and ribavirin treatment in a patient with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) virus co-infection. This patient presented with horizontal diplopia that appeared rapidly and without any other neurological symptoms. Symptoms fully resolved with treatment interruption without any ophthalmological sequelae. This side effect is rare and has never been reported in a HIV-HCV co-infected patient.

Insulin resistance is associated with a higher risk of hepatocellular carcinoma in cirrhotic HIV/HCV-co-infected patients: results from ANRS CO13 HEPAVIH.

BACKGROUND & AIMS: Compared to HCV-mono-infected patients, hepatocellular carcinoma (HCC) occurs at younger age in HIV/HCV-co-infected patients, is markedly more advanced at diagnosis, is less amenable to curative treatment, and has a more severe outcome. The aim of this study was to identify factors predictive of HCC occurrence in a large cohort of HIV/HCV-co-infected patients with cirrhosis. METHODS: This study involved 244 HIV/HCV-co-infected patients included in the ANRS CO13 HEPAVIH cohort, who had HCV-related cirrhosis (clinically or histologically proven cirrhosis, or liver stiffness ≥12.5 kPa) and no signs of HCC at baseline. Cox proportional hazards models were used to identify factors associated with HCC occurrence. RESULTS: During a median follow-up of 2.6 (IQR, 1.8-3.5) years, 21 patients (8.6%) developed HCC. Diagnosis of HCC was based on histology in 5 patients (24%) and non-invasive criteria in 16 patients (76%). In univariate analyses, the following factors were related to HCC occurrence: age, previous cirrhosis decompensation, a HOMA value >3.8 (patients with treated diabetes were excluded from the HOMA calculation), a lower platelet count, a lower prothrombin level, and higher alpha-fetoprotein levels. The HOMA value was >3.8 at baseline in 66.7% of patients who developed HCC and in 35.3% of the remaining patients (p=0.016). In multivariate analysis, age over 50 years (adjusted RR 3.2, 95% CI 1.2-9.0; p=0.02) and a HOMA value >3.8 (adjusted RR 3.4, 95% CI 1.1-10.3; p=0.03) remained significantly associated with HCC occurrence. CONCLUSIONS: As in HCV-mono-infected patients with HCV-related cirrhosis, insulin resistance appears to play a key role in HCC occurrence in HCV/HIV-co-infected patients with cirrhosis. This finding calls for specific screening strategies for patients with a particularly high risk of developing HCC.

Six-year follow-up of hepatitis B surface antigen concentrations in tenofovir disoproxil fumarate treated HIV-HBV-coinfected patients.

BACKGROUND: Quantitative measurement of hepatitis B surface antigen (HBsAg) has been proposed as a surrogate marker of treatment efficacy when HBV DNA load becomes undetectable. Our main objective was to study the kinetics of HBsAg level in HIV-HBV-coinfected patients with undetectable HBV DNA load under treatment containing tenofovir disoproxil fumarate (TDF). METHODS: A retrospective analysis was performed on frozen serum samples of 33 HIV-HBV-coinfected patients who were treated with TDF and had undetectable HBV DNA for ≥1 year. Baseline and serial follow-up samples were assayed for HBsAg levels. RESULTS: The characteristics of the patients at TDF initiation were median age 43.6 years, median HBV DNA load 2 log(10) IU/ml and median HBsAg concentration 3.4 log(10) IU/ml. Ten patients were positive for hepatitis B e antigen. Baseline median HBsAg concentration, defined 1 year after HBV DNA became undetectable, was 3.1 log(10) IU/ml. Overall, from years 1 to 6 and a median duration of TDF treatment of 2.6 years, the median HBsAg concentration decreased slowly. Notably, only 13 (39%) patients presented a constant decrease of HBsAg concentration, whereas the remaining had fluctuating or increasing HBsAg concentrations. The slope was not influenced by HBeAg status, HIV infection duration and CD4(+) T-cell count at baseline or at nadir. CONCLUSIONS: Despite control of HBV DNA replication under efficient TDF treatment, HBsAg levels persistently decreased in only 39% of HIV-HBV-coinfected patients. Larger follow-up studies are needed to determine whether HBsAg concentration monitoring under analogue treatment can be used as a reliable marker for HBV clearance.