We report a case of primary hypogonadism induced by amiodarone and review the relevant literature. Amiodarone has a well-established and extensive profile of side effects including thyroid toxicity, corneal deposits and skin discoloration. In rare cases, epididymitis or orchitis may occur. This inflammation can lead to testicular atrophy, inducing primary hypogonadism. We present the case of a 57-year-old patient, treated with amiodarone for several years, initially presenting with testicular pain followed by gynaecomastia, and finally loss of libido indicative of hypergonadotropic hypogonadism. Imaging confirmed bilateral testicular atrophy. Amiodarone was discontinued, and androgen replacement therapy was initiated. This case, combined with data from the literature, highlights the importance of careful monitoring of patients on amiodarone to identify symptoms or clinical signs suggesting testicular dysfunction, to diagnose and treat consequent hypogonadism.
Learning points: This case highlights the causal relationship between prolonged amiodarone use and the development of hypogonadism.The underlying mechanism involves the destructive effect of amiodarone on testicular tissue, leading to primary hypogonadism through testicular atrophy.It is crucial to monitor patients for clinical signs of hypogonadism after prescribing amiodarone to ensure timely diagnosis and treatment of any resulting hypogonadism.
Keywords: Amiodarone; epididymitis; gynaecomastia; hypergonadotropic hypogonadism; testicular dysfunction.
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