Abstract

BackgroundContinuous use of anabolic androgenic steroid in high-doses is associated with substantial health risks, including hepatocellular adenoma. Malignant transformation from hepatocellular adenoma to hepatocellular carcinoma after anabolic androgenic steroid abuse has been rarely reported. The morphological distinction of adenoma from well-differentiated hepatocellular carcinoma is challenging and requires elaborated imaging techniques and histology.Case presentationWe report about a 29-year old male professional bodybuilder who presented with mid-epigastric pain at the emergency unit. Ultrasound showed a severe hepatomegaly with multiple lesions. Contrast-enhanced ultrasound revealed a heterogeneous pattern with signs of hepatocellular carcinoma. CT scan of the abdomen confirmed multiple hypervascular lesions and central areas of necrosis without contrast enhancement. Subsequent diagnostics included fine needle aspiration (FNA) of suspicious lesions and mini-laparoscopy to establish the diagnosis of a β-catenin and testosterone-receptor positive hepatocellular carcinoma embedded in multiple adenomas. The patient was subsequently treated by liver transplantation and remains tumor-free 27 month after surgery.ConclusionHepatocellular carcinoma occurring in association with anabolic androgenic steroid abuse should sensitize physicians and especially professional bodybuilders for the harmful use of high doses of steroids.

Highlights

  • Continuous use of anabolic androgenic steroid in high-doses is associated with substantial health risks, including hepatocellular adenoma

  • Hepatocellular carcinoma occurring in association with anabolic androgenic steroid abuse should sensitize physicians and especially professional bodybuilders for the harmful use of high doses of steroids

  • Clinical history We describe a case of a 29-year old male professional bodybuilder who presented at the emergency unit with midepigastric-pain

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Summary

Conclusion

6 years of chronic anabolic androgenic steroid abuse lead to HCA and HCC development with almost no normal liver tissue left. Authors’ contributions PS carried out the concept and design of the case report, responsible for the acquisition, analysis and interpretation of data and drafted the manuscript. BS was responsible for the acquisition, analysis and interpretation of data, technical support and for the revision of the manuscript for content. MG was responsible for the acquisition, analysis and interpretation of data, sonography and for the revision of the manuscript for content. MM was responsible for the acquisition, analysis and interpretation of data, technical support and for the revision of the manuscript for content and study supervision. AV carried out the concept and design of the case report and was responsible for the acquisition, analysis and interpretation of data, technical support and for the final revision of the manuscript for content. Author details 1Department of Gastroenterology, Hepatology and Endocrinology, Medizinische Hochschule, OE 6810 Carl-Neuberg-Str. 1, 30625 Hannover, Germany. 2Department of Diagnostic and Interventional Radiology, Medizinische Hochschule Hannover, Hannover, Germany. 3Department of Pathology, Medizinische Hochschule Hannover, Hannover, Germany

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