Taylor Hooton Foundation > Hoot’s Corner > General > Severe and Prolonged Jaundice Associated with Body Building Supplements (BBS)
November 17, 2015
Severe and Prolonged Jaundice Associated with Body Building Supplements (BBS)
  Review of 44 Cases from the Drug-Induced Liver Injury Network (DILIN) Background & Aim: The use of body building supplements (BBS) containing anabolic steroids (AS) continues to rise despite efforts to curtail their availability. We sought to characterize the clinical features and outcomes of presumed AS-induced jaundice in patients taking BBS prospectively enrolled in the DILIN. Methods: 44 (5%) out of 847 cases of liver injury attributed to drug or herbal dietary supplements enrolled between Sept 2004 and March 2013 were attributed solely to BBS. The presence of various natural and synthetic androgens in consumed products was quantified by LC/MS compared with 18 known standards with an average assay sensitivity [limit of quantitation] ~ 38 fmoles/mg of product. Liver biopsies were interpreted by the study hepatopathologist without clinical information. Results: All 44 were men, ages 21 to 59 (mean = 32) years with 81% self-identified as Caucasian and the remainder African-American. 2 subjects had chronic HCV infection. The BBS products were used for body building and purported to contain various AS with different chemical structures and commercial names. All were were taken orally in otherwise healthy males. Median latency to onset was 1.8 (range 0.4 to 14) months, but the exact dates of starting and stopping were not always available. All 44 cases were jaundiced and symptomatic at presentation and 43 patients had pruritus that was frequently severe, prolonged and debilitating. Initial median bilirubin was 9.8 mg/dL, ALT 168 U/L, Alk P 111 U/L and INR 1. Subsequently, median ALT fell steadily, while Alk P and bilirubin levels increased 2-3 fold before falling. Peak median bilirubin in first 6 months was 25.8 (range 7.3- 63). 64% were hospitalized and 18% had evidence of hepatic dysfunction (e.g. elevated INR). Liver biopsy in 22 patients reviewed revealed canalicular cholestasis often with only mild portal and lobular inflammation, in contrast to the classic “bland cholestasis” often described in association with AS. Symptomatic hepatic failure was not observed and no patient died or required liver transplantation. Seven of the 44 patients (16%) had creatinine elevation > 1.5 mg/dL during their episode which trended down as the bilirubin improved. Of 14 BBS products available for analysis, 71% had identifiable AS along with other non-defined steroid containing compounds. Conclusion: Jaundice associated with BBS containing AS is a distinct clinical syndrome marked by severe and prolonged cholestasis in previously healthy men but which did not lead to hepatic failure or chronic liver injury in this study. AS were often identified in BBS despite efforts to limit their availability. http://onlinelibrary.wiley.com/doi/10.1002/hep.28237/full