Endocrine Abstracts

Introduction: The obstructive sleep apnea syndrome (OSAS) has a well-documented association with increase cardiovascular morbidity and mortality. The patients with OSAS have a high prevalence of hypertension and the OSAS may present similar to a pseudo-pheochromocytoma (PPH). We report two cases with PPH caused by OSAS; a common medical condition which is less recognized as a cause of raised catecholamines.

Observations: Case 1: 54 year-old man had a history of recent poorly controlled hypertension and obesity. He had a history of fatigue and drowsiness. Laboratory evaluation was elevated 24-h urinary catecholamine levels (UC) (3.2 times the upper normal levels).

Case 2: 52 year-old woman with a history of poorly controlled resistant hypertension was admitted to our hospital with severe hypertension. She had a history of fatigue and intermittent episodes of palpitations. Laboratory evaluation was significant for elevated UC (3.5 times the upper normal levels).

These patients were previously healthy without any medication and denied any alcohol or illicit drug abuse. Other causes of secondary hypertension such as primary hyperaldosteronism, hyperthyroidism, hypercorticism, and endocrine neoplasms were excluded by hormonal explorations. Computed Tomography-scan showed kidneys with normal size, good cortical index, and normal vessels. In addition, MIBG scintigraphy did not detected any catecholamine-producing tumor. The OSAS was established. Following 4 weeks of overnight continuous positive airway pressure (CPAP) therapy, blood pressure were at 130/80 mm of Hg. Three months later, UC were normalized and symptoms were gone.

Discussion: Twenty-four-hour UC were initially found to be increased in patients with untreated OSAS compared with those with narcolepsy. Evidence is accumulating to suggest a role for sympathetic overactivity in the pathophysiology of these observations. OSAS, however, is not the only cause of PPH as they could be showed in other causes, notably physiological stress, antipsychotic drugs, anti-parkinson drugs, etc. None of these conditions were found in our patients. Mechanisms by which chemoreflex dysfunction may contribute to chronically elevated sympathetic tone and hypertension are discussed.

Conclusion: Finally this cases represent two patients with untreated OSAS and difficult to control HTA, with clinical and biochemical evidence of increased sympathetic activity mimicking a pheochromocytoma. Nasal CPAP therapy allows improvement of hypertension with catecholamine hypersecretion and distinction of this condition from pheochromocytoma. We suggest that a diagnosis of OSAS should be considered in patients with clinical and biochemical evidence of catecholamine excess in whom a catecholamine producing tumor cannot be identified.