Endocrine Abstracts

Background: Functional hypogonadotrophic hypogonadism (FHH) occurs in the context of any chronic disease including obese patients with type 2 diabetes (T2DM) and/or metabolic syndrome. FHH is reversible with resolution of the underlying disease process. Reported benefits of bariatric surgery include improvements in lipid profile, blood pressure and resolution of T2DM. Here we report reversal of FHH and T2DM with bariatric surgery-associated weight loss.

Case history: A 47-year-old man was referred with sexual dysfunction. He underwent puberty aged 14. His mood was low, he drank alcohol to excess, was obese (BMI 43), with sparse body hair; testes 15 ml. Baseline biochemistry confirmed hypogonadotrophic hypogonadism: LH 1.7 and FSH 4.4 IU/l; testosterone 7.2 nmol/l (NR: 9–25 nmol/l) and DEXA showed L1-4 spine osteoporosis, but serum ferritin and MRI pituitary were normal.

He was started on testosterone undecanoate 1 g i.m. (3-monthly) with symptomatic and biochemical improvement. However, he eventually became polycythaemic (peak Hb and haematocrit 18.1 g/dl and 55%, respectively) and treatment thus had to be discontinued. Shortly afterwards, he developed T2DM and, in view of his co-morbidities, was referred for lifestyle change (including counselling) and went on to undergo bariatric surgery. Post-operatively, his BMI fell to 30.3, T2DM resolved and hypertension improved. Significantly, FHH had also resolved (LH 3.1 and FSH 4.4 IU/l; testosterone 12.1 nmol/l).

Conclusion: FHH represents a physiologic response to ill health and thus may serve as a useful biological function. Several short-term interventional studies have demonstrated improvements in various surrogate endpoints with testosterone therapy in patients with FHH in relation to obesity and/or metabolic syndrome. Nevertheless, given the paucity of longitudinal safety/efficacy data, it may be more appropriate to target the underlying problem of obesity, rather than opting for testosterone replacement. As demonstrated in our patient, weight loss resulting from bariatric surgery can lead to recovery of pituitary–gonadal axis obviating the requirement for testosterone replacement therapy.