Endocrine Abstracts

Background: Commercial “testosterone optimisation” services and online supplement providers increasingly market treatment for young men presenting with non-specific symptoms, often without adequate diagnostic work-up. Unregulated testosterone or “booster” supplements can suppress the hypothalamic–pituitary–gonadal (HPG) axis, mimicking hypogonadotropic hypogonadism. Misdiagnosis may expose patients to unnecessary treatments, fertility impairment, and complications including erythrocytosis, testicular atrophy, and metabolic consequences. This case series illustrates these risks and emphasises the importance of specialist assessment in centres with full diagnostic capability.

Case Series: A 35-year-old man presented with progressive reduced libido and energy. He’d sought private hCG therapy due to long NHS waiting times. Baseline testing revealed low testosterone with inappropriately low gonadotrophins, while other pituitary hormones were normal. Given obesity, normal prior fertility, and absence of pituitary pathology, functional hypogonadotrophic hypogonadism was diagnosed. hCG was discontinued, lifestyle modification implemented, and pituitary MRI was normal. Follow-up demonstrated normalisation of hormones with symptomatic improvement, illustrating recovery of HPG function without long-term hormonal therapy. A 33-year-old man with a historical diagnosis of hypogonadotrophic hypogonadism had received Nebido for eight years. He had azoospermia. Therapy withdrawal demonstrated recovery of gonadotrophins and testosterone within six months, leading to fertility restoration with spontaneous partner pregnancy. Circadian disruption from shiftwork contributed to reduced testosterone and was addressed in management. A 27-year-old man with long-standing gynecomastia, fatigue, and poor sleep was referred for raised prolactin. Cannulated sampling showed mild stress-related hyperprolactinaemia, with suppressed gonadotrophins but normal testosterone. He reported use of over-the-counter testosterone boosters. Following discontinuation, gonadotrophins and prolactin normalised. Persistent symptoms were attributed to mild REM- and positional-predominant sleep-disordered breathing, managed with CPAP and sleep hygiene. A 35-year-old man accessed private testosterone and hCG therapy for presumed hypogonadism without full evaluation. After 18 months, he developed testicular atrophy and erythrocytosis requiring venesection. Other pituitary hormones were normal on assessment. All therapy was ceased, and serial monitoring demonstrated recovery of gonadotrophins and testosterone, with normalisation of haematologic parameters.

Discussion and Learning Points: These cases demonstrate how misdiagnosis or unregulated treatments can suppress gonadotrophins, mimic central hypogonadism, and threaten fertility while causing haematologic and metabolic complications. Recovery of the HPG axis is possible but requires structured monitoring and careful counselling. Hypogonadism should be assessed only in specialist centres with validated investigations. Persistent fatigue with normal gonadal function warrants evaluation for alternative causes. Clinicians must educate patients on the risks of private or unregulated therapy and ensure safe, evidence-based management.