A 56-yr-old man with hypothyroidism and sleep apnea syndrome was studied to determine the cause of the nocturnal obstructive apnea and oxygen desaturation. Control studies showed free thyroxine (T 4) concentration of 0.7 ng/dl (normal, 0.8 to 2.3 ng/dl), and thyroid-stimulating hormone of 32 μIU/ml (normal, less than 12 μIU/ml). Weight, pulmonary function, arterial blood gases, minute ventilation to carbon dioxide production ratio (V̇E/V̇(CO 2)), and the ventilatory response to exercise (ΔV̇E/ΔV̇(CO 2)) were normal. Episodes of obstructive apnea (4 per hour during non-REM (NREM) and 10 per hour during REM) and oxygen desaturation (9 per hour during NREM and 11 per hour during REM) were common during sleep. Oxygen saturation ranged between 72 and 99% and 70 and 97% during NREM and REM sleep, respectively. Medroxyprogesterone acetate (MPA) therapy for 4 wk caused a reduction in awake Pa(CO 2) (38 to 33 mm Hg), and an increase in V̇E/V̇(CO 2) (17%), mouth occlusion pressure (50%), and ΔV̇E/V̇(CO 2) (23%). During sleep, apneas were completely eliminated and only one episode of oxygen desaturation occurred. L-thyroxine therapy for 2 months after a placebo period caused an awake isocapnic hyperpnea with no change in Pa(CO 2) and V̇E/V̇(CO 2) despite a 23% increase in V̇E. Mouth occlusion pressure increased 37% but ΔV̇E/ΔV̇(CO 2) was unchanged. Obstructive apnea and oxygen desaturation during sleep were completely eliminated with L-thyroxine. The patient noted complete relief of symptoms with both MPA and L-thyroxine. We concluded that the sleep apnea syndrome was the presenting manifestation of hypothyroidism in this patient and was solely responsible for his symptoms and disability.
|Original language||English (US)|
|Number of pages||5|
|Journal||American Review of Respiratory Disease|
|State||Published - Nov 13 1981|