Endocrine effects of nasal continuous positive airway pressure in male patients with obstructive sleep apnoea


Dr Niki Meston, Department of Clinical Laboratory Sciences, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DU UK. (fax: 44 1865 220348; e-mail: nikimeston@hotmail.com).


Abstract. Meston N, Davies RJO, Mullins R, Jenkinson C, Wass JAH, Stradling JR (University of Oxford, John Radcliffe Hospital; Oxford Centre for Respiratory Medicine and University of Oxford, Churchill Hospital; Health Services Research Unit; Oxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Infirmary; Oxford, UK). Endocrine effects of nasal continuous positive airway pressure in male patients with obstructive sleep apnoea. J Intern Med 2003; 254: 447–454.

Objective. Obstructive sleep apnoea (OSA) is a relatively common condition producing disabling somnolence and profound physiological responses to hypoxaemic episodes during sleep, including significant oscillations in blood pressure. This study aimed to provide controlled data on the interaction between OSA and endocrine axes to establish whether overrepresentation of pathology such as hypertension and hypogonadism in OSA subjects might have an endocrine basis.

Design, setting and subjects. Parallel randomized sham placebo controlled 1-month trial of nasal continuous positive airway pressure (nCPAP) in 101 male subjects with OSA presenting to a respiratory sleep clinic.

Methods. Analysis of gonadotrophins, testosterone, sex hormone binding protein (SHBG), prolactin, cortisol, thyroid stimulating hormone (TSH), free thyroxine (free T4), insulin-like growth factor-1 (IGF-1), renin and aldosterone were performed at baseline and after 1 month's active or placebo nCPAP intervention. Quality of life questionnaire scoring was also recorded over the same time period.

Results. Testosterone and SHBG showed significant negative correlations with baseline OSA severity. Active treatment of OSA produced SHBG elevation and TSH reduction (P ≤ 0.03). Both groups showed an increase in aldosterone (P < 0.001) and IGF-1 (P ≤ 0.03), associated with a large improvement in subjective quality of life scoring.

Conclusions. These findings demonstrate significant changes in endocrine axes not previously reported in a placebo-controlled trial. OSA is a recognized reversible cause of testosterone reduction; SHBG suppression correlating to baseline OSA severity supports a diagnosis of secondary hypogonadism. Significant rises in aldosterone and IGF-1 on treatment coincide with increased physical activity and an improved quality of life score.