Hepatocellular fat accumulation and low serum cholesterol in patients infected with HCV-3a.
OBJECTIVE
The aim of this study was to prospectively investigate the prevalence of hepatic steatosis in chronic hepatitis C patients with respect to viral genotype, hepatic iron concentration, total body iron, body mass index, and serum lipid parameters. Furthermore, the effect of hepatitis C virus (HCV) eradication by antiviral therapy on serum cholesterol levels was studied.


METHODS
Hepatocellular fat and hepatic iron were determined in liver biopsies obtained from 137 interferon-naïve patients with chronic hepatitis C (100 men, 37 women, mean age 40.8 +/- 10.7 yr) enrolled in two prospective clinical trials of interferon/ribavirin therapy. Body mass index and fasting cholesterol levels were determined at baseline, during, and after therapy.


RESULTS
Marked steatosis (>20% of fat-containing hepatocytes) was found in 74.5% of patients infected with HCV-3a compared with 17.9% in HCV-1 and 21.7% in HCV-4-infected patients (p < 0.01). Steatosis in HCV-3a-infected patients did not correlate with the body mass index, hepatic iron content, ferritin, or transferrin saturation. At baseline, serum cholesterol was lower in patients infected with HCV-3a (147 +/- 42 mg/dl; p < 0.01) compared with HCV-1 (188 +/- 36) or HCV-4 (172 +/- 35). In contrast to HCV-1- or HCV-4-infected patients, serum cholesterol increased in HCV-3a virological responders at the end of treatment and 6 months after therapy (baseline 146 +/- 38, end of treatment 166 +/- 29, p < 0.05, sustained virological response 200 +/- 34, p < 0.01). However, serum cholesterol remained unchanged in HCV-3a nonresponders.


CONCLUSIONS
Our data suggest that, in addition to inducing steatosis, HCV-3a lowers serum cholesterol. This metabolic effect is fully reversible after successful HCV-3a eradication. This unique property is not shared by other HCV genotypes.
Hofer
Harald
H
Department of Internal Medicine IV, University of Vienna, Austria.
Bankl
Hans C
HC
Wrba
Friedrich
F
Steindl-Munda
Petra
P
Peck-Radosavljevic
Markus
M
Osterreicher
Christoph
C
Mueller
Christian
C
Gangl
Alfred
A
Ferenci
Peter
P
D000328:Adult; D000998:Antiviral Agents / Q000008:administration & dosage / Q000494:pharmacology; D005234:Fatty Liver / Q000150:complications* / Q000378:metabolism; D005260:Female; D005293:Ferritins / Q000378:metabolism; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy / Q000821:virology; D022781:Hepatocytes / Q000378:metabolism*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000008:administration & dosage / Q000494:pharmacology; D007501:Iron / Q000378:metabolism*; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009752:Nutritional Status; D011092:Polyethylene Glycols / Q000008:administration & dosage / Q000494:pharmacology; D015995:Prevalence; D011446:Prospective Studies; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins; D012720:Severity of Illness Index; D014168:Transferrin / Q000378:metabolism
D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D008055:Lipids; D012367:RNA, Viral; D011994:Recombinant Proteins; D014168:Transferrin; D011092:Polyethylene Glycols; D005293:Ferritins; D007501:Iron; C100416:peginterferon alfa-2a