Does the control of alanine aminotransferase levels lead to a regression of liver fibrosis in chronic hepatitis C patients?

M. Yagura et al., Does the control of alanine aminotransferase levels lead to a regression of liver fibrosis in chronic hepatitis C patients?, HEPATOL RES, 19(2), 2001, pp. 144-157
Citations number
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
ISSN journal
1386-6346 → ACNP
Year of publication
144 - 157
SICI code
The aim of this study was to investigate the effect of various medications other than interferon (IFN) on liver fibrosis in chronic hepatitis C (CII-C ) patients, and the results were compared with those obtained in CH-C patie nts without therapy. Fifty CH-C patients (31 men and 18 women; mean age 58. 5 years) without previous IFN therapy, who randomly received medicines othe r than IFN such as Stronger Neo-Minophagen C, Ursodeoxycholic acid and a he rbal medicine, Sho-saiko-to (TJ-9) (Group I), and as a control group, 45 CI I-C patients (27 men and 18 women; mean age 56.6 years) without therapy (Gr oup TT) were examined. All patients had persistent alanine aminotransferase (ALT) elevation more than 6 months before this study and were also subdivi ded into three subgroups according to different pattern of ALT during the o bservation period, i.e. (a): persistently ALT < 60 IU/l (below about twice the upper limit of normal range); (b): persistently ALT <greater than or eq ual to> 60 IU/l; and (c) other than (a) and (b). All patients were biopsied twice before starting this study and during observation period and the liv er fibrosis was compared between them by staging in each case. When the fib rosis stage was the same between two specimens, we determined whether the d egree of fibrosis had improved or worsened by computed image analysis. Bloo d tests for fibrosis marker, serum aminoterminal peptide of type III procol lagen (P III P) and liver enzyme such as albumin (Alb) and zinc turbidity t est (ZTT) levels, and platelet (Plt) counts were also examined on the two t imes of liver biopsy. As a result, there were no significant differences in fibrotic improvement rate when assessed by both staging only and staging t ogether with Fibrotic ratio, determined by computed image analysis and also in yearly change of P III P (P/Y) and fibrosis (F/Y), the changed rate of Alb, ZTT levels and Pit counts between Group I and Group II, except for P/Y in subgroup (a) which was rather higher in Group I than in Group Il. There were also no significant relationship between the changes of histological activity and fibrosis staging in both groups. In conclusion, other medicati ons than IFN could not significantly improve both liver fibrosis and its as sociated laboratory data irrespective of ALT levels in CII-C patients as co mpared to the control group during average 3 years' follow-up period. (C) 2 001 Elsevier Science Ireland Ltd. All rights reserved.