LACK OF PLASMA COMPLEMENT ACTIVATION IN SEVERE ACUTE ALCOHOLIC HEPATITIS

To investigate whether complement pathway activation contributes to th e clinical and histological features of acute alcoholic hepatitis, we studied the activation of the classical and alternative pathways in pa tients with alcoholic hepatitis (n = 20), inactive alcoholic cirrhosis (n = 8), heavy drinkers without alcoholic liver disease (n = 10), pat ients with liver disease of nonalcoholic etiology (n = 11), and health y control subjects (n = 18). Complement activation was evaluated in th e alcoholic hepatitis patients by its correlation with a number of cli nical and laboratory features indicative of the severity of liver inju ry, as well as by comparison of the patient groups, There was no signi ficant difference in circulating C3 [1.02 g/liter, confidence interval (CI) = 0.76-1.28] or C4 (0.25 g/liter, CI = 0.17-0.33) in patients wi th alcoholic hepatitis when compared with the four control groups, Fac tor B levels (0.24 g/liter, CI = 0.21-0.27) were higher in the alcohol ic hepatitis patients than the control groups (p < 0.01), However, act ivation of complement (given by the ratios C3d/C3, C4d/C4, and Ba/fact or B) was not different in alcoholic hepatitis patients when compared with the control groups, Univariate analysis of a wide range of clinic al and laboratory features in the alcoholic hepatitis subjects showed a positive correlation between plasma C3 and serum alkaline phosphatas e (r = 0.68, p = 0.0014), AST (r = 0.55, p = 0.015), and gamma-glutamy ltranspeptidase (r = 0.47, p = 0.035), but no correlation with clinica l or laboratory features associated with high morbidity or mortality, There is no relationship between clinical or laboratory indicators of disease severity and complement activation, and it is unlikely that co mplement activation contributes to the clinical and histological featu res of alcoholic liver disease.