This study assessed the effect of alcoholic cirrhosis in man and of experimental liver injury in rats on the disposition and elimination of clindamycin. In 7 cirrhotics a statistically significant, although modest, prolongation of clindamycin half-life (T1/2β) was observed as compared to values in 7 agematched normal controls (mean ±SD: 4.46±0.93, hr vs 3.42±0.45 hr, P=0.02). This was primarily due to a decrease in clindamycin serum clearance in the cirrhotics, since the volume of distribution of the drug was similar in both groups (P<0.05). Serum protein binding of clindamycin was of the order of 79% and was comparable in both groups (P>0.05). There was a significant correlation between the T1/2β of the drug and both total serum bilirubin and SGOT. The T1/2β of clindamycin was also prolonged in rats with acute hepatic necrosis induced by administration of carbon tetrachloride and those with acute cholestasis caused by common bile duct ligation. These data suggest that liver damage, both chronic and acute, impairs the elimination of clindamycin but that this effect is small.
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