Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2002) 4 P14

SFE2002 Poster Presentations Clinical case reports (21 abstracts)

Obstructive Sleep Apnoea- a cause of Pseudophaeochromocytoma

L Hoy 1,2 , M Waterhouse 2 , S Haque 1 , W Wedzicha 2 , A Davison 1 , A Khokar 1 , S Chew 2 , J Monson 2 & K Metcalfe 1,2


1Southend Hospital; 2Barts and The London Hospital.


Obstructive sleep apnoea (OSA)is associated with increased cardiovascular morbidity and mortality and is an independent risk factor for the development of hypertension. A recent study demonstrated elevated urinary catecholamine excretion in hypertensive males with OSA. However, we have recently observed the phenomenum whereby OSA can rarely induce catecholamine production of sufficient severity to mimic the clinical and biochemical presentation of phaeochromocytoma.

Clinical Cases

A 53 year old woman presented with accelerated hypertension, heart failure and elevated urinary noradrenalines of 2145 and 1220nmol/24 hours (normal range 125-500). Plasma noradrenaline of 19.3 nmol/l (normal <5.67) fell to only 12.6 after pentolinium. CT, radioisotopes and venous sampling failed to identify the suspected phaeochromocytoma but CT did reveal massive pulmonary arteries; pulmonary artery pressure measured 80mmHg at echocardiography. A sleep study was consistent with OSA and CPAP was commenced with rapid clinical improvement and near normalisation of catecholamines and pulmonary artery pressure.

A 42 year male with type 1 neurofibromatosis presented with heart failure and accelerated hypertension. Urine catecholamines (noradrenaline 964, adrenaline 236 nmol/24 hours), CT and MIBG suggested an adrenal phaeochromocytoma which was successfully removed. After full recovery from surgery urinary noradrenaline remained high at 1324 nmol/24 hours. Neither imaging nor venous sampling located a further phaeochromocytoma. OSA was then diagnosed on a sleep study and CPAP was commenced.

OSA can cause excessive catecholamine production, presumably as a result of hypoxia and arousal episodes stimulating carotid body chemoreceptors and other sympathetic neurones with subsequent synaptic cleft overflow of noradrenaline. Rarely though OSA can result in massive sympathetic discharge and the presentation of 'pseudophaeochromocytoma'. However, the catecholamine excess and its clinical effects appear to respond well to treatment with CPAP. OSA should be excluded when catecholamines are elevated and a phaeochromocytoma cannot be located.

Volume 4

193rd Meeting of the Society for Endocrinology and Society for Endocrinology joint Endocrinology and Diabetes Day

Society for Endocrinology 

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