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Sleep Apnea in Acromegaly

Ronald R. Grunstein, MB, BS; Kian Y. Ho, MD; and Colin E. Sullivan, MB, BS, PhD
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Grant Support: by the National Health and Medical Research Council of Australia and the New South Wales Department of Health.

Requests for Reprints: R. Grunstein, MB, BS, Sleep Disorders Centre, Royal Prince Alfred Hospital, Missenden Road, Camperdown, Sydney, New South Wales, 2050 Australia.

Current Author Addresses: Dr. Grunstein: Sleep Disorders Centre, Royal Prince Alfred Hospital, Missenden Road. Camperdown, Sydney, New South Wales, 2050 Australia.

Dr. Ho: Garvan Institute of Medical Research, St. Vincent's Hospital, Darlinghurst, Sydney, New South Wales, 2010 Australia.

Dr. Sullivan: David Read Laboratory, Department of Medicine, University of Sydney, New South Wales, 2006 Australia.

© 1991 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1991;115(7):527-532. doi:10.7326/0003-4819-115-7-527
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Objective: To provide information on the nature, prevalence, and severity of sleep apnea in patients with acromegaly.

Design: Consecutive case series.

Setting: Tertiary referral hospital.

Patients: Fifty-three patients with acromegaly were consecutively referred: 33 patients were referred because of clinical suspicion of sleep apnea and 20 patients were referred without suspected apnea.

Measurements: Sleep studies as well as growth hormone and insulin-like growth factor 1 (IGF-1) measurements were done.

Main Results: Thirty-one patients (93%; 95% Cl, 85% to 100%) referred because of suspicion of sleep apnea had sleep apnea compared with 12 patients (60%; Cl, 37% to 83%) referred without suspected sleep apnea. Patients with sleep apnea did not have biochemical evidence of increased disease activity (random growth hormone, 12.7 ± 4.4 μg/L; mean growth hormone at 24-hour sampling, 10.8 ± 8.4 μg/L; IGF-1, 90.0 ± 7.5 nmol/L) compared with patients without sleep apnea (random growth hormone, 14.2 ± 4.9 μg/L, P > 0.2; mean growth hormone, 12.4 ± 3.5 μg/L, P > 0.2; IGF-1, 90.0 ± 10.0 nmol/L, P > 0.2). Central sleep apnea was the predominant type of apnea in 33% (Cl, 18% to 47%) of patients and was associated with higher random growth hormone and IGF-1 levels than was obstructive apnea (random growth hormone, 23.4 ± 3.9 compared with 8.8 ± 3.1 μg/L, P < 0.001; IGF-1, 126 ± 17.5 compared with 72.5 ± 7.5 nmol/L, P < 0.01).

Conclusions: Sleep apnea is common in acromegaly. The rate of central sleep apnea was unexpectedly high in patients with acromegaly, and biochemical evidence of increased disease activity was associated with the presence of central apnea rather than with the degree of sleep apnea. Altered respiratory control is a possible mechanism producing sleep apnea in acromegaly.





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