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Winning Abstracts from the 2008 Medical Student Abstract Competition: Cocaine-induced Hepatotoxicity

Authors: Monica Dandona and Adam Mitchell, MD

Cocaine is the second most commonly used illicit drug in the United States. Hospital-related admissions have predominantly been due to complications from cardiovascular, central nervous system, neuromuscular, renal, and pulmonary injury. Recent clinical evidence, however, demonstrates that the liver is also a target organ of cocaine-related toxicity.

Case Presentation
A previously healthy 28 year-old man with a ten-year history of polysubstance abuse was brought to the emergency department with cocaine intoxication. His abdomen was diffusely tender to palpation with localization to the right upper quadrant. Liver-related tests upon admission showed an ALT of 759 U/L (30-65 U/L), AST of 2280 U/L (15-37 U/L), and prothrombin time of 17.3 s (10.9-13.1 s). Total and direct bilirubin peaked four days after admission to 3.8 mg/dL (less than 1.0 mg/dL) and 1.5 mg/dL (0.0-0.3 mg/dL), respectively, with an albumin of 2.7 g/dL (3.4-5.0 g/dL). Serologic tests for viral, autoimmune, metabolic, and hereditary causes of liver dysfunction were negative. Infectious workup was also negative. The urine drug screen was positive for cocaine metabolites, benzodiazepines, and phencyclidine hydrochloride (PCP). Ethanol was not detected in serum, but the patient did admit to drinking 2-4 ounces of hard liquor every other day. Abdominal ultrasound showed normal liver size and echogenicity. Aggressive IV hydration was immediately initiated secondary to the patientís elevated creatinine. The patient was discharged after 9 days with downward trending serum creatinine and liver-associated enzymes. At 14-day follow-up, his complete blood count and metabolic panel returned to within normal limits. His ALT was 149 U/L and AST was 66 U/L, still slightly elevated from baseline.

This case illustrates an uncommon presentation of cocaine-induced hepatotoxicity. Biomechanistic studies on this phenomenon have increased our understanding of the causality between the formation of reactive cocaine intermediates and acute hepatocyte injury. Animal studies have confirmed that risk factors contributing to liver injury include concurrent alcohol, phencyclidine, and/or phenobarbital use. Other predisposing factors are glutathione deficiency, glucose-6-phosphate dehydrogenase deficiency, and low plasma pseudocholinesterase activity. It is therefore thought that the concurrent use of PCP catalyzed the hepatotoxicity observed in our otherwise healthy young patient. The follow-up ALT/AST elevation found in our patient is commonly noted in chronic PCP and alcohol users. Of note, no studies to date have been performed investigating the contribution of prior liver disease to cocaine-induced hepatotoxicity. The question thus remains whether the presence of metabolic defects, hereditary liver disease, and viral or autoimmune hepatitis play a significant role in contributing to cocaine-associated liver injury. Further investigation is needed to determine whether such testing is necessary in patients presenting with cocaine-induced hepatotoxicity.

Back to March 2009 Issue of IMpact

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