icon-folder.gif   Conference Reports for NATAP  
  58th Annual Meeting of the American Association
for the Study of Liver Diseases
November 2-6, 2007
Boston, MA
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Fatty Liver Associated with Metabolics in HBV+
  Spectrum Of Steatosis In Chronic Hepatitis B (CHB) And Its Relation To Biochemical, Metabolic, Virological And Histological Parameters
Reported by Jules Levin
AASLD, Nov 2-6, 2007, Boston, MA
D. K. Singh1; A. Rastogi1; P. Sakhuja1; R. Gondal1; A. Jain1; S. Hissar2; A. Kumar2; S. K. Sarin2
1. Pathology, G B Pant hospital, Delhi, Delhi, India.
2. Gastroenterology, G B Pant Hospital, Delhi, Delhi, India.
Steatosis predicts progression of histologic injury, insulin resistance and reduced response to antiviral therapy in patients with hepatitis C. However, there is limited data in patients with chronic hepatitis B (CHB). This is relevant since response to current antiviral therapies for CHB is poor.
Aim: To assess the spectrum of hepatic steatosis in CHB and to determine its relationship with biochemical, metabolic, virologic and histologic parameters.
Patients and Methods: Liver biopsies of 350 patients with chronic HBV infection were blindly assessed by three experienced pathologists and categorized as: Group 1- no steatosis (≦5%) and group 2- hepatosteatosis (>5%). Demographic, biochemical, metabolic, virologic and histologic parameters were compared between two groups. HBV DNA was quantified by Hybrid capture assay and HBV genotyping was done by multiplex PCR.
Group 1 had 232 (66.3%) and group 2 had 118 (33.7%) patients. In group 2, 65 (55.1%) patients had mild and 53 (44.9%) had moderate to severe steatosis. More than 90% cases showed macrovesicular steatosis.
Group 2 patients showed significantly higher age (35.5±10.5 yrs vs 28.1±13.9 yrs, p=0.000), male preponderance (M:F ratio-8.8:1 vs. 4.8:1, p=0.02), higher BMI (26.2±9.2 Kg/m2 vs. 20.7±3.9 Kg/m2, p=0.000), triglyceride (149.4±62.2 vs. 81.9±31.4, p=0.000) and insulin levels (13.1±9.1 vs 9.1±6.0, p=0.027).
Waist circumference, blood sugar, cholesterol and leptin (2.3±1.9ng/mL vs 2.4±1.3ng/mL, p=0.95) were also higher in group 2 but not statistically significant. Mean HAI and fibrosis scores in group 2 were higher than group 1 (Group 1 vs 2, HAI, 4.5±2.9 vs 4.8±2.6, p=0.28; fibrosis 1.5±1.2 vs 1.7±1.2, p=0.17). More patients in group 1 had higher HBeAg positivity (Group 1 vs 2, 57.2% vs 47.3%, p=0.039). There was no significant difference in ALT (median, 114 vs 99, p=0.36) and HBV DNA levels (2.4E08±4.9E08 vs 1.9E08±4.6E08, p=0.48). In group 2, hepatic steatosis was more frequent in patients with HBV genotype D than in genotype A (58.1% vs. 42.9%, p=0.01).
Conclusions: In our study steatosis was seen in one third cases with chronic HBV infection. These patients showed higher necroinflammatory activity and fibrosis. Association of steatosis with metabolic determinants and its presence in the liver suggests the role of host factors in the etiology of steatosis in chronic hepatitis B. There is no relation to viral factors like viral load and HBeAg status although there is a possibility of relation to genotype D. The efficacy of combined "antiviral and metabolic" approaches versus standard antiviral regimes in patients with steatosis and chronic hepatitis B infection needs to be evaluated.