title: Serum HCV RNA levels correlate with histological liver damage and concur with steatosis in progression of chronic hepatitis C.
abstract: The role of HCV RNA levels and host factors in the severity of liver injury was studied. Enrolled were 298 consecutive liver biopsy-proven chronic hepatitis (CH) C patients (179 men; median age: 52 years, range 19-68; CH, 198; cirrhosis, 100) and 18 chronic hepatitis C with normal ALT. HCV genotypes were: 1a, 4.3%; 1b, 53%; 2a/c, 28%; 3a, 7%; 4, 1.3%, and mixed 6.4%. Serum HCV RNA levels were similar for all genotypes (median: 2.8 x 10(6) eq/ml; range <0.2-69). In patients with chronic hepatitis without cirrhosis, the serum HCV RNA levels reflected the grade of liver necroinflammatory activity (R = 0.45; P < 0.001) and the stage of fibrosis (R = 0.51; P < 0.001), regardless of age, gender, HCV genotype, hepatic steatosis, and hepatic iron overload. Patients with high serum HCV RNA levels (> or =3 x 10(6) eq/ml) had higher ALT values (P < 0.002) than those with lower HCV RNA levels. Patients with normal ALT showed low HCV RNA levels (median: 0.82 x 10(6) eq/ml) and histological features of minimal or mild chronic hepatitis. Cirrhotic patients showed significantly lower levels of viremia than those with chronic hepatitis with a similar HAI. The data of a subgroup of 62 patients with an established time of infection showed that for a similar duration of disease, patients with serum HCV RNA levels > or =3 x 10(6) eq/ml had a significantly higher fibrosis score than those with lower levels. HAI and fibrosis score were significantly higher in patients with HCV RNA levels > or =3 x 10(6) eq/ml and grade 3-4 steatosis than those with lower HCV RNA levels and steatosis grades. The data indicate that the liver damage is correlated with the HCV RNA levels and that a high viral load acts together with steatosis in accelerating the progression of liver injury.
authors.affiliation: Institute of Medical Therapy, Faculty of Medicine, Second University of Naples, Italy.
authors.forename: L E
authors.initials: LE
authors.lastname: Adinolfi
authors.forename: R
authors.initials: R
authors.lastname: Utili
authors.forename: A
authors.initials: A
authors.lastname: Andreana
authors.forename: M F
authors.initials: MF
authors.lastname: Tripodi
authors.forename: M
authors.initials: M
authors.lastname: Marracino
authors.forename: M
authors.initials: M
authors.lastname: Gambardella
authors.forename: M
authors.initials: M
authors.lastname: Giordano
authors.forename: G
authors.initials: G
authors.lastname: Ruggiero
mesh_terms: D000328:Adult; D000368:Aged; D018450:Disease Progression; D005234:Fatty Liver / Q000209:etiology / Q000473:pathology*; D016679:Genome, Viral; D016174:Hepacivirus / Q000235:genetics* / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000150:complications / Q000378:metabolism / Q000473:pathology* / Q000821:virology; D006801:Humans; D007501:Iron / Q000378:metabolism; D008099:Liver / Q000378:metabolism / Q000473:pathology*; D008103:Liver Cirrhosis / Q000473:pathology / Q000821:virology; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood*; D019562:Viral Load
chemical_list: D012367:RNA, Viral; D007501:Iron