Steatosis Accelerates the Progression of Liver Damage of... : Hepatology (original) (raw)
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Steatosis Accelerates the Progression of Liver Damage of Chronic Hepatitis C Patients and Correlates With Specific Hcv Genotype and Visceral Obesity
Adinolfi, Luigi E. M.D.*,1; Gambardella, Michele1; Andreana, Augusto1; Tripodi, Marie-françoise1; Utili, Riccardo1; Ruggiero, Giuseppe1
1_From Internal Medicine & Hepatology, Second University of Naples, Naples, Italy_
* Istituto di Terapia Medica - Facoltà di Medicina, Seconda Università di Napoli, Via Cotugno, 1 (c/o Ospedale Gesù e Maria), 80135 Napoli, Italy. fax: (39) 081–566–6230.; E-mail: [email protected].
Received: 4 October 2000; Accepted: 5 March 2001
Abstract
The role of steatosis in the progression of liver damage in chronic hepatitis C (CHC) was studied. Enrolled were 180 consecutive liver biopsy–proven CHC patients and 41 additional subjects with a known duration of infection. We evaluated the histological activity index (HAI), grade of fibrosis and steatosis, body mass index (BMI; kg/m2), distribution of body fat, HCV genotype, and levels of HCV RNA. Eighty six (48%) patients showed steatosis, and a higher prevalence was observed in genotype 3a infection (P < .01). A correlation between the grade of steatosis and fibrosis was observed (_P_ < .001). Fibrosis was also associated with age (_P_ < .001). After adjusting for age, the association between steatosis and fibrosis remained significant. The grade of steatosis also correlated with the HAI (_P_ < .007) with a significant increase in periportal necrosis. No relation was found between steatosis and age, gender, iron storage, or levels of HCV RNA. Patients with a high grade of steatosis (>30%) showed higher serum levels of γ–GT and ALT (P < .001). Overall, steatosis was not significantly associated to BMI. Analysis by single genotype showed a significant association between the grade of steatosis and BMI in type 1 infection r = .689; P < .001) and with levels of HCV RNA in type 3a infection r = .786; P < .001). Visceral fat distribution rather than BMI proved to be associated with steatosis (P < .001). Data obtained from patients with a known date of infection confirmed that steatosis grades 3–4 were associated with a higher annual rate of fibrosis progression, and showed that alcohol and steatosis act together in increasing fibrosis (P < .05). Our data indicate that steatosis is an important cofactor in increasing liver necroinflammatory activity and in accelerating fibrosis in CHC. Visceral obesity and genotype 3a play a role in the development of steatosis.
Copyright © 2001 American Association for the Study of Liver Diseases.