L. Mazzoran et al., EFFECTS OF INTERFERON THERAPY ON FIBROSIS SERUM MARKERS IN HCV-POSITIVE CHRONIC LIVER-DISEASE, European journal of gastroenterology & hepatology, 10(2), 1998, pp. 125-131
Objective To evaluate serum levels of prolyl-hydroxylase and helical d
omain of Type IV degrees collagen, markers of hepatic fibrogenesis, in
patients with HCV-positive chronic liver disease and the effects of i
nterferon therapy on these markers. Design Prolyl-hydroxylase and Type
IV degrees collagen were determined before therapy and each month dur
ing the treatment and follow-up. Methods Fifty-seven HCV-positive pati
ents were studied. All the subjects received alpha 2a recombinant inte
rferon, 6 MU subcutaneously three times a week for 4 weeks, followed b
y 3 MU thrice weekly for 5 months. After cessation of treatment, each
patient was followed for 12 months. Prolyl-hydroxylase and helical dom
ain of Type IV degrees collagen were measured by using immunoenzymatic
methods. HCV-RNA and HCV genotype were determined according to the me
thod of Okamoto. Results In the patients prolyl-hydroxylase (39.8 +/-
8.9 ng/ml) was not different from controls (39.1 +/- 5.9 ng/ml). On th
e contrary, the patients showed a mean Type IV degrees collagen (133.6
+/- 93.3 ng/ml) significantly (P < 0.01) higher than controls (100.2
+/- 10.5 ng/ml). A good relationship between the degree of liver fibro
sis and the Type IV degrees collagen serum level was found (r = 0.68;
P < 0.005). In both responders and non-responders the Type IV degrees
collagen levels decreased during interferon therapy. During the follow
-up, in responders the Type IV degrees collagen did not show modificat
ions, while in nonresponders/relapsers it returned rapidly to the pret
reatment levels (139.1 +/- 100.7 ng/ml). Conclusion In HCV-positive ch
ronic liver disease, prolylhydroxylase is not a good marker of hepatic
fibrosis, while Type IV degrees collagen is a useful tool for evaluat
ing fibrogenic activity. Interferon seems to be able to reduce the liv
er fibrosis even without the inhibition of viral replication and indep
endently from liver necrosis. (C) 1998 Rapid Science Ltd.