DISORDERED BREATHING DURING SLEEP IN HYPOTHYROIDISM

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Abstract
A 56 yr old man with hypothyroidism and sleep apnea syndrome was studied to determine the cause of the nocturnal obstructive apnea and O2 desaturation. Control studies showed free thyroxine (T4) concentration of 0.7 ng/dl (normal, 0.8-2.3 ng/dl), and TSH of 32 .mu.IU/ml (normal, < 12 .mu.IU/ml). Weight, pulmonary function, arterial blood gases, minute ventilation to CO2 production ratio (.ovrhdot.VE/.ovrhdot.VCO2) and the ventilatory response to exercise (.DELTA..ovrhdot.VE/.DELTA..ovrhdot.VCO2) were normal. Episodes of obstructive apnea (4/h during non-rapid eye movement (NREM) and 10/h during REM) and O2 desaturation (9/h during NREM and 11/h during REM) were common during sleep. O2 saturation ranged between 72-99% and 70-97% during NREM and REM sleep, respectively. Medroxyprogesterone acetate (MPA) therapy for 4 wk caused a reduction in awake PaCO2 (38-33 mm Hg), and an increase in .ovrhdot.VE/.ovrhdot.VCO2 (17%), mouth occlusion pressure (50%) and .DELTA..ovrhdot.VE/.ovrhdot.VCO2 (23%). During sleep, apneas were completely eliminated and only 1 episode of O2 desaturation occurred. L-Thyroxine therapy for 2 mo. after a placebo period caused an awake isocapnic hyperpnea with no change in PaCO2 and .ovrhdot.VE/.ovrhdot.VCO2 despite a 23% increase in .ovrhdot.VE. Mouth occlusion pressure increased 37% but .DELTA..ovrhdot.VE/.DELTA..ovrhdot.VCO2 was unchanged. Obstructive apnea and O2 desaturation during sleep were completely eliminated with L-thyroxine. The patient noted complete relief of symptoms with both MPA and L-thyroxine. The sleep apnea syndrome was the presenting manifestation of hypothyroidism in this patient and was solely responsible for his symptoms and disability.

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