Glucocorticosteroids for viral hepatitis C

Hepatitis C virus may cause liver inflammation and fibrosis. It is not known whether glucocorticosteroids are beneficial or harmful for patients with hepatitis C infection.

The objectives were to evaluate the beneficial and harmful effects of glucocorticosteroids for patients with acute or chronic hepatitis C infection with or without hepatitis C related autoimmune disorders.

Searches of The Cochrane Hepato-Biliary Controlled Trials Register, The Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, and reference lists of relevant articles and hand searches of relevant journals were performed in July 2003. Principal authors of clinical trials were approached.

Randomised clinical trials dealing with glucocorticosteroids for viral hepatitis C - acute or chronic with or without autoimmune disorders.

Data were extracted by one reviewer and validated by another. Further information was sought by correspondence with the principal investigator of the trial in case the relevant data were not published. Disagreements were solved by discussion before the meta-analysis.

Eight trials randomised 384 patients with chronic hepatitis C to glucocorticosteroids plus interferon versus interferon plus placebo/no intervention, glucocorticosteroids versus interferon, or glucocorticosteroids versus placebo. Glucocorticosteroids treatment given as short pre-treatment followed by interferon or as long-term parallel treatment combined with interferon versus interferon monotherapy had no significant effect on mortality (no deaths occurred; 342 patients), virological response at six months follow-up (RR 0.85; 95% CI 0.52 to 1.38; 38 patients), or biochemical response at six months follow-up (RR 0.95; 95% CI 0.84 to 1.06; 307 patients). There was no significant difference in serious adverse events between combination therapy versus interferon monotherapy (RR 4.76; 95% CI 0.24 to 93.19; 342 patients). Glucocorticosteroids versus interferon had no significant effect on mortality (RR 2.33; 95% CI 0.27 to 17.80; 13 patients) or virological response at follow-up (RR 1.17; 95% CI 0.86 to 1.58; 13 patients). We found no trials on glucocorticosteroids for acute hepatitis C.

There is insufficient evidence neither to confirm nor exclude both beneficial and harmful effects of glucocorticosteroids for chronic hepatitis C with or without autoimmune disorders. This Review is not able to rule out potential serious adverse effects of glucocorticosteroids. Therefore, this Review cannot establish whether glucocorticosteroids treatment can be safely administrated for indications requiring glucocorticosteroids without analysing for hepatitis C virus. The effect of glucocorticosteroids for acute hepatitis C has not been examined in randomised trials.