Endocrine Abstracts

A 59-year-old lady presented with significant weight gain, and a history of hypertension for investigation of possible Cushing’s syndrome. Her BMI was 29, with mainly central obesity. Initial tests revealed elevated untimed cortisol on two separate occasions, at 905 nmol/l and 893 respectively with detectable midnight cortisol, at 548 and 481. Of 24-hour urinary free cortisol (UFC) was also elevated on two separate occasions, at 931 nmol/24 h and 827 respectively. ACTH was 39 ng/l. She had a normal response to low dose dexamethasone (LDDST) with cortisol suppression to 41 at 48 h. Thyroid function tests, growth hormone, fasting glucose, MRI of the pituitary and adrenals were normal and gonadotrophins consistent with menopausal state. Her overall picture was suggestive of pituitary-dependent Cushing’s disease.

A sleep study was organised which revealed severe OSA with >60 episodes of apnoea on the apnoea-hypopnoea index. CPAP therapy was organised.

Three months after CPAP was commenced, the patient had improved clinically, with weight loss, better sleep and some resolution of hypertension. The 48 h cortisol after LDDST fell to <30 and midnight cortisol was 84 nmol/l. Of 24-hour UFC was repeated and showed normal excretion levels at 42 and 56 nmol/24 h. Pituitary function remained normal.

Chronic OSA causes nocturnal hypoxia, night-time arousal and activation of the sympathetic nervous system, which in turn can cause increased cortisol secretion and interfere with diurnal cortisol rhythm, hence giving a false picture of Cushing’s syndrome. OSA is however a common complicating factor in true Cushing’s syndrome in one-third of a small series. Diagnostic tests must therefore be interpreted with caution, and there should be a low threshold for referring for sleep studies and CPAP treatment before reassessment.