Case Report
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World J Hepatol. Mar 27, 2013; 5(3): 133-136
Published online Mar 27, 2013. doi: 10.4254/wjh.v5.i3.133
Mastabol induced acute cholestasis: A case report
Brett M Hymel, David W Victor, Luis Alvarez, Nathan J Shores, Luis A Balart
Brett M Hymel, Department of Gastroenterology, Louisiana State University School of Medicine, New Orleans, LA 70112, United States
Brett M Hymel, David W Victor, Luis Alvarez, Nathan J Shores, Luis A Balart, Department of Gastroenterology and Hepatology, Tulane University School of Medicine, New Orleans, LA 70118, United States
Author contributions: Hymel BM, Victor DW, Alvarez L, Shores NJ and Balart LA contributed to this paper.
Correspondence to: Brett M Hymel, MD, Department of Gastroenterology, Louisiana State University School of Medicine, New Orleans, LA 70112, United States. bretthymel@aol.com
Telephone: +1-504-5684498 Fax: +1-504-5682127
Received: July 9, 2012
Revised: January 6, 2013
Accepted: January 29, 2013
Published online: March 27, 2013
Abstract

A 26-year-old male presented with three weeks of jaundice after the self-initiation of the injectable anabolic steroid, Mastabol [Dromastanolone Di-Propionate (17 beta-Hydroxy-2alpha-methyl-5alpha-androstan-3-one propionate)]. He reported dark urine, light stools, and pruritus. He denied abdominal pain, intravenous drug use, intranasal cocaine, blood transfusions, newly placed tattoos, or sexually transmitted diseases. He used alcohol sparingly. Physical exam revealed jaundice with deep scleral icterus. The liver was palpable 2 cm below the right costal margin with no ascites. The peak bilirubin was 23.6 mg/dL, alkaline phosphatase was 441 units/L, and aspartate aminotransferase/alanine aminotransferase were 70 units/L and 117 units/L respectively. A working diagnosis of acute intrahepatic cholestasis was made. Liver biopsy revealed a centrilobular insult with neutrophilic infiltrates and Ito cell hyperplasia consistent with acute drug induced cholestasis. The patient’s clinical symptoms resolved and his liver enzymes, bilirubin, and alkaline phosphatase normalized. Anabolic steroids with 17 alpha carbon substitutions have been associated with a bland variety of cholestatic injury with little hepatocellular injury. Cholestasis, under these circumstances, may be secondary to the binding of drugs to canalicular membrane transporters, accumulation of toxic bile acids from canalicular pump failure, or genetic defects in canalicular transport proteins. Mastabol is an injectable, 17 beta hydroxyl compound with no alpha alkyl groups at the 17 carbon position. As such, it has been reported to have little potential toxic effects on the liver. This is the first known reported case of Mastabol-induced cholestatic liver injury. It highlights the need for physicians to consider such widely available substances when faced with hepatic injury of unclear etiology.

Keywords: Cholestatic; Mastabol; Hepatic; Anabolic; Steroids