Hepatic dysfunction accompanying acute cocaine intoxication.
We identified 39 patients with acute cocaine intoxication and rhabdomyolysis over an 8-year period. Twenty-three of the patients (59%) demonstrated biochemical evidence for hepatic dysfunction. Sixteen of these patients had severe liver injury as defined by an alanine aminotransferase (ALT) of greater than 400 U/l (group A). Seven had an ALT between 36-399 U/l (group B) and 16 showed no evidence of liver injury (group C). In contrast to those with normal ALT, the clinical course of the group A patients was more often accompanied by profound hypotension (44 vs. 0%, p less than 0.025), disseminated intravascular coagulation (50 vs. 0%, p less than 0.005), hyperpyrexia (75 vs. 25%, p less than 0.025) and acute renal failure (81 vs. 0%, p less than 0.001). Seven of the group A patients expired (44%). Histologic examination of liver tissue obtained from post-mortem samples demonstrated extensive centrilobular and midzonal necrosis in three cases and panlobular necrosis in two others. A mild lymphocytic infiltrate with bile duct proliferation was present in each specimen. We conclude that cocaine intoxication can be accompanied by liver dysfunction which is most likely multifactorial; the presence of severe dysfunction identifies a patient with potentially significant morbidity and mortality.
Silva
M O
MO
University of Miami School of Medicine, Division of Hepatology, FL 33101.
Roth
D
D
Reddy
K R
KR
Fernandez
J A
JA
Albores-Saavedra
J
J
Schiff
E R
ER
D000328:Adult; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology* / Q000473:pathology; D003042:Cocaine / Q000506:poisoning*; D005260:Female; D006801:Humans; D008099:Liver / Q000473:pathology; D008297:Male; D009336:Necrosis; D012189:Retrospective Studies; D012206:Rhabdomyolysis / Q000139:chemically induced*
D003042:Cocaine