Thyroid Hormone Levels and TSH Activity in Patients with Obstructive Sleep Apnea Syndrome.

Obstructive sleep apnea syndrome (OSAS) is characterized by complete cessation of inspiratory flow (apnea) or upper airway airflow limitation (hypopnea) with increased respiratory muscle activity, which is repeatedly observed during sleep. Hypothyroidism has been described as a rare cause of OSAS, but it is considered to be the main cause of breathing disorders during sleep in patients in whom an improvement of OSAS is observed after thyroid hormone replacement therapy. Nevertheless, euthyreosis due to thyroxine replacement in patients with OSAS often does not improve the breathing disorder and treatment with continuous positive airway pressure is usually applied. The aim of this study was to assess thyroid function in patients with OSAS. We studied 813 patients in whom severe OSAS was diagnosed; the mean apnea-hypopnea index was 44.0. Most of the patients were obese (mean BMI 33.1 ± 6.6 kg/m2) and had excessive daytime sleepiness (ESS 12.8 ± 6.6). With the thyroid stimulating hormone (TSH) concentration as the major criterion, hypothyroidism was diagnosed in 38 (4.7%) and hyperthyroidism was diagnosed in 31 (3.8%) patients. Analysis of basic anthropometric data, selected polysomnography results, and TSH, fT3, and fT4 values did not reveal any significant correlations. In conclusion, the incidence of thyroid function disorders seems to be no different in OSAS than that in the general population. We did not find correlations between TSH activity and the severity of breathing disorders during sleep.

Exercise capacity in patients with obstructive sleep apnea syndrome.

Obstructive sleep apnea syndrome (OSAS) is a common disease characterized by repetitive partial or complete closure of the upper airway during sleep. Cardiovascular disturbances are the most important complications responsible for increased morbidity and mortality. It is suggested that daytime somnolence, chronic fatigue, and nocturnal hypoxemia may further impair muscle function and decrease exercise fitness. The aim of this study was to evaluate cardiopulmonary response to exercise in OSAS patients. One hundred and eleven middle aged (50.2+/-10 yr), obese (BMI 31.0+/-4.6 kg/m2) patients (109 M, 2F) with severe OSAS (AHI 47.2+/-23.1 h(-1)) were enrolled into the study. OSAS was diagnosed with overnight polysomnography and a symptom-limited cardiopulmonary exercise test was performed on a treadmill using Bruce protocol. The results showed that the most frequent reason for exercise termination were: muscle fatigue and/or dyspnea (66+/-), increase in systolic blood pressure>220 mmHg (20%), ECG abnormalities, and chest pain (6%). Although the mean VO2 peak was within the reference value (29.6+/-6 mlO2/kg/min), in 52 patients (46%) VO2 peak was <84% of predicted. Hypertensive response to exercise was diagnosed in 39 of patients (35%). Patients with severe sleep apnea (AHI40>or=h(-1)) were characterized by higher mean blood pressure at rest, at 25%, 50% of maximal work load, at peak exercise and at post-exercise recovery. Several significant correlations between hemodynamic responses to exercise and sleep apnea severity were also noted. We conclude that exercise tolerance can be limited due to hypertensive response in about 20% of patients. Patients with severe OSAS have exaggerated hemodynamic response to exercise and delayed post-exercise blood pressure recovery. Cardiopulmonary response to exercise seems to be related to sleep apnea severity.