Endocrine Abstracts

A 44-year-old man referred with erectile dysfunction was found to have hypogonadotrophic hypogonadism (HH), but otherwise apparently normal anterior pituitary function (LH 1.6 & FSH 2.7 IU/l; T 3.4 & cortisol 516 nmol/l; PRL 103, GH 5.5 & TSH 2.8 mU/l; f-T4 13, f-T3 4.8 & f-T 128 pmol/l; ferritin 103 ug/l). He appeared normally virilised, with central obesity (BMI 36 kg.m⁻², collar size 46 cm) and symptomatic sleep apnoea (SA). MRI showed a right-sided microadenoma (10×4×7 mm), so the initial diagnosis was HH secondary to SA with pituitary “incidentaloma”. However, the presence of both SA and pituitary adenoma raised the possibility of acromegaly and a more detailed evaluation was undertaken.

Baseline glucose tolerance test: ½-hourly blood sampling: mean daytime GH level only 5.5 mU/l, but with absence of physiological troughs in GH secretion. Immunohistochemistry following endoscopic trans-sphenoidal surgery confirmed a GH-expressing pituitary adenoma.

Post-operative evaluation: These indicated improved GH dynamics, but without complete operative cure.

Discussion: Acromegaly is a rare disease, though the reported annual incidence of ∼3 per million necessarily excludes individuals with early or subclinical disease. The prevalence of pituitary tumours is rather higher at 1 – 2 per 100 000 population (though some autopsy series have indicated a prevalence up to 3 orders of magnitude greater). Overt acromegaly can go undiagnosed for years; detecting early disease is thus particularly challenging.

Even without obvious clinical features or abnormal baseline biochemistry, acromegaly should be formally screened for in patients with pituitary adenomas, so as to detect sub-clinical disease. A single random GH levels may be falsely reassuring, so a fasting level with IGF1 should always be performed, if not an OGTT.