TY - JOUR
T1 - Hepatic dysfunction accompanying acute cocaine intoxication
AU - Silva, Marcelo O.
AU - Roth, David
AU - Reddy, K. Rajender
AU - Fernandez, John A.
AU - Albores-Saavedra, Jorge
AU - Schiff, Eugene R.
PY - 1991/5
Y1 - 1991/5
N2 - 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 > 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 < 0.025), disseminated intravascular coagulation (50 vs. 0%, p < 0.005), hyperpyrexia (75 vs. 25%, p < 0.025) and acute renal failure (81 vs. 0%, p < 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.
AB - 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 > 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 < 0.025), disseminated intravascular coagulation (50 vs. 0%, p < 0.005), hyperpyrexia (75 vs. 25%, p < 0.025) and acute renal failure (81 vs. 0%, p < 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.
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U2 - 10.1016/0168-8278(91)90832-V
DO - 10.1016/0168-8278(91)90832-V
M3 - Article
C2 - 1940259
AN - SCOPUS:0025793416
VL - 12
SP - 312
EP - 315
JO - Journal of Hepatology
JF - Journal of Hepatology
SN - 0168-8278
IS - 3
ER -