HOW MUCH DOES ALCOHOL CONTRIBUTE TO THE VARIABILITY OF HEPATIC-FIBROSIS IN CHRONIC HEPATITIS-C

In order to determine the contribution of alcohol intake to the severi ty of hepatic fibrosis in patients with chronic hepatitis C, we studie d associations between various levels of alcohol intake, other demogra phic variables and semiquantitative liver histology in 434 cases of ch ronic hepatitis C. Clinical, demographic and disease-related data were entered into a relational database. Liver histology was scored accord ing to Scheuer. The average daily alcohol intake for the year precedin g liver biopsy (recent exposure) and for earlier periods (past exposur e) was categorized into five levels of intake. One-third of patients g ave a history of alcohol intake that had exceeded 40 g/day for at leas t 5 years. By univariate analysis, age, but not recent or past alcohol intake or other baseline variables, was associated with portal score (r = 0.14, P = 0.004), fibrosis score (r = 0.46, P < 0.001), total Sch euer score (r = 0.35, P < 0.001). However, by multivariate analysis, a ge (P < 0.001), past (but not present) alcohol intake (P < 0.001) and birth in Egypt (P = 0.006) were independently associated with fibrosis score. Age, past alcohol and birth place in Egypt contributed 27% to total variance of the hepatic fibrosis score, while age alone accounte d for 23%. Age also independently predicted portal activity (P = 0.02) and total Scheuer score (P < 0.001), whereas past alcohol intake corr elated with total Scheuer score (P = 0.002) but not with other histolo gical indices. A separate multivariate analysis was performed on a mor e homogeneous subgroup of 196 patients who acquired hepatitis C by inj ection drug use. In this subgroup, age (P < 0.05) and past alcohol (P < 0.05) were independently associated with fibrosis score. In both the overall and subgroup analyses, there was a threshold level of past al cohol intake (> 80 g/day) beyond which the risk of fibrosis increased significantly. It is concluded that toxic levels of alcohol exposure f or at least 5 years accentuate hepatic fibrosis in hepatitis C but the influence of alcohol appears to be minor compared with age and other variables and is exerted only at toxic levels of intake.