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Background Anabolic androgenic steroids (AASs) are known to cause hepatotoxicity, with significant concern for inducing cholestasis and vanishing bile duct syndrome (VBDS). The risk is increased when combined with other supplements, such as the X-39 patch, containing copper. VBDS is a rarely reported but serious complication of AAS use, characterized by cholestasis and histological evidence of intrahepatic bile duct loss. Diagnostic confirmation requires a liver biopsy, showing the loss of at least 50% portal tracts.
Case Presentation A 27-year-old male with a history of low testosterone levels, being treated with testosterone supplementation, presented to the emergency department with symptoms of pruritus and jaundice. The patient was also reportedly using the X-39 patch for general wellness support. On physical examination, the patient appeared icteric. Laboratory studies revealed elevated liver enzymes – aspartate transaminase (AST) 152 U/L, alanine transaminase (ALT) 227 U/L, alkaline phosphatase (ALP) 216 U/L, total bilirubin level of 32.6 mg/dL, elevated WBC (17.6×109/L), and platelet count (657×109/L). His initial copper level was markedly elevated at 3,248 μg/dL. USG, MRI, and MRCP of the abdomen were unremarkable. Liver biopsy was negative for malignancy but demonstrated cholestatic hepatitis with mild focal portal chronic inflammation with stage-1 fibrosis. The infectious and autoimmune workups were unremarkable. Cytomegalovirus PCR depicted low-level viremia. The hepatitis panel was negative. Anti-nuclear antibodies were negative, with a mildly elevated anti-smooth muscle antibody. Ceruloplasmin level was within normal limits, while alpha-1 antitrypsin was slightly elevated. The patient was managed with immediate cessation of testosterone supplementation, along with penicillamine to chelate copper. Supportive care for symptom relief was provided – colestipol, hydroxyzine, and gabapentin for pruritus, and ursodeoxycholic acid for prevention of gallstone formation. Following treatment, the patient's copper level decreased to 402 μg/dL. Serial liver function tests showed gradual improvement over weeks, with normalization of bilirubin and significant reductions in AST and ALT levels.
Discussion: VBDS is often a diagnosis of exclusion in patients with elevated ALP levels (≥2 times the upper limit of normal) when other causes of cholestasis are ruled out. Our case is only the fourth documented instance linking AAS use to this condition, and the first case ever to report the association of VBDS to the X-39 wellness patch, alongside AAS. While most cases improve with time, severe VBDS can lead to acute liver failure and death. Clinicians should maintain a high index of suspicion for drug-induced liver injury, particularly in patients using testosterone and wellness supplements.