Endocrine Abstracts

This 60-year-old male was reviewed remotely for follow up in the general endocrine outpatient clinic having originally been referred for erectile dysfunction and low libido. He had a past medical history of hypertension and dyslipidaemia and was prescribed amlodipine and atorvastatin. On previous clinical assessments, he had increased muscle bulk, normal secondary sexual characteristics with testes measuring 15mls and 12mls. There had been no evidence of gynaecomastia. He worked as a gym instructor. The patient reported a long history of using testosterone, other anabolic steroids and tamoxifen for athletic performance enhancement, but described stopping these several years earlier. Serum testosterone concentration was low on serial measurements (1.0-7.2 nmol/l) with sex hormone binding globulin (SHBG) below the reference range. Gonadotrophins were consistently low (LH <0.1 IU/l – 0.9 IU/l, FSH <0.1 IU/l – 1.2 IU/l). Pituitary profile was otherwise within normal limits. The patient had undergone a CT head (due to contraindication to MRI) which demonstrated no evidence of pituitary pathology. Polycythaemia had been noted on serial testing with no genetic cause or other secondary causes identified following haematology specialty review. At a previous review, testosterone replacement was felt be to inappropriate due to the risk of cardiovascular and thromboembolic disease given the presence of polycythaemia (Haemoglobin 173-195g/l; Haematocrit 0.54-0.60L/l). However, testosterone replacement with a long-acting injected preparation had been subsequently initiated on a 14-weekly basis which the patient was receiving in the community. Up to date pathology results demonstrated polycythaemia (Haemoglobin 188g/l; Haematocrit 0.56L/l) and elevated serum testosterone (58.7 nmol/l). It was recommended that prescribed testosterone replacement was stopped and the rationale for discontinuation explained. The patient was concerned about deterioration in sexual function. Urgent haematological advice was sought, and venesection subsequently arranged. Testosterone stimulates erythrocytosis and replacement therapy can lead to polycythaemia. Increasing haematocrit concentrations can usually be managed by reducing the dose of testosterone replacement, increasing the interval between injections of long-acting testosterone preparations, or converting to a transdermal preparation. In cases where haematocrit is markedly elevated, haematological advice should be sought and, rarely, venesection may be required.