ABSTRACT: BACKGROUND: The role of occult hepatitis B virus infection as a cause of liver disease is still debated although many studies found a higher prevalence of this condition in subjects than those without liver disease compared. A recent meta-analysis showed an increased risk of hepatocellular carcinoma for occult hepatitis B virus infection. AIMS: We carried out a meta-analysis of observational studies to summarize the existing evidence and assess quantitatively the association between occult hepatitis B virus infection and chronic liver disease. METHODS: We searched the available literature on this issue published up to May 2012 using PubMed and EMBASE. All articles that provided enough information to estimate the chronic liver disease risk associated with occult hepatitis B virus infection were selected. Fourteen studies were retrieved. RESULTS: A total of 1503 subjects with (cases) and 2052 without chronic liver disease (controls) were included. The summary odds ratio for chronic liver disease from all studies was 8.9 (95% confidence interval: 4.1-19.5). The meta-analysis restricted to 7 studies with more precise effect estimate (wt%>8%) provided a lower odds ratio estimate (odds ratio=3.9; 95% confidence interval: 1.7-9.0). CONCLUSIONS: These findings suggest a relevant association between occult hepatitis B virus infection and chronic liver disease, confirming the hypothesis that hepatitis B virus may play a pathogenic role even in the "occult" status.
Digestive and Liver Disease 11/2012; · 3.05 Impact Factor
ABSTRACT: The role of insulin resistance in predicting virological response to therapy of chronic hepatitis C is debated. We assessed the association between basal (defined as homeostasis model assessment of insulin resistance (HOMA-IR)>2) and post-load insulin resistance (as oral glucose insulin sensitivity index<9.8 mg/kg/min) with the rapid and sustained virological responses in chronic hepatitis C.
Observational prospective study of 124 treatment-naïve patients with chronic hepatitis C not fulfilling the metabolic syndrome criteria, adherent to a standard treatment with pegylated interferon alpha plus ribavirin.
Insulin resistance was detected in 50% (by HOMA-IR) and 29% (by oral glucose insulin sensitivity index) of patients. Independent predictors of rapid virologic response were hepatitis C virus (HCV) genotype 2 (odds ratio 5.66; 95% confidence interval 1.88-17.01), HCV genotype 3 (odds ratio 5.23; 95% confidence interval 1.84-14.84) and lower basal ferritin levels (odds ratio 0.99; 95% confidence interval 0.993-0.998). Independent predictors of sustained virologic response were HCV genotype 2 (odds ratio 19.54; 95% confidence interval 2.29-166.41) and HCV genotype 3 (odds ratio 3.24; 95% confidence interval 1.10-9.58). Rapid virologic response was by itself predictive of sustained virologic response (odds ratio 40.90; 95% confidence interval 5.37-311.53).
Insulin resistance, measured by both static and dynamic methods, does not predict rapid or sustained virologic response in chronic hepatitis C patients without the metabolic syndrome.
Digestive and Liver Disease 01/2012; 44(5):419-25. · 3.05 Impact Factor
ABSTRACT: To investigate the independent association between the homeostasis model assessment of the insulin resistance (HOMA-IR) score and rapid virological response (RVR) and sustained virological response (SVR) in chronic hepatitis C (CHC).
Observational prospective cohort study of 412 CHC patients [59% males; mean age 45 years; genotype 1 (44%), 2 (32%), 3 (19%) and 4 (5%)] treated with pegylated interferon α plus ribavirin.
A HOMA-IR ≥2.0 was present in 49% and a metabolic syndrome in 4% of patients. By multivariate analysis, independent predictors of SVR were the lack of advanced fibrosis (≥F3) in genotype 1 and a lower body mass index in genotype 3 patients. In the subgroup of patients in whom HCV-RNA was evaluated at week 4 (n = 281), independent predictors of RVR were HCV-RNA <700,000 IU/ml, age <40 years and lower aspartate aminotransferase:alanine aminotransferase ratio in genotype 1 and baseline HOMA-IR ≤2 in genotype 3 patients. No predictive factor of RVR was identified among genotype 2 patients. RVR was the strongest predictor of SVR among genotype 1 or 3 patients.
In this series of treatment-naïve, Caucasian CHC patients at a low risk for the metabolic syndrome, HOMA-IR is not a predictor of SVR, irrespective of the HCV genotype, although it may predict RVR in genotype 3 infection.
Liver international: official journal of the International Association for the Study of the Liver 01/2011; 31(1):66-74. · 3.82 Impact Factor