Sleep apnea syndrome and hypothyroidism.

Obstructive sleep apnea syndrome (OSAS) is a serious, prevalent condition that has significant mortality and morbidity when untreated. It is strongly associated with obesity and is characterized by several endocrine and metabolic abnormalities that are frequently more marked than those in obese patients without OSAS, suggesting that factors other than obesity per se have a role in this clinical condition [6]. Obese patients with OSAS show alterations in the GH/IGF-I axis function, PRL secretion, HPA axis and gonadal axis activity. Some derangement in TSH secretion in obesity with or without OSAS has been demonstrated by some authors, whereas a normal thyroid activity has been described by others [5, 6]. The study by Mete and colleagues published on Endocrine in April 2013 examined the relationship between OSAS and thyroid disease. Functional and ultrasonographic examination of the thyroid gland was performed in 150 polysomnographically diagnosed OSAS patients and in 32 control subjects. Aim of the study was to evaluate both thyroid function and thyroid nodule frequency and parenchyma heterogenecity in OSAS patients. The morphologic evaluation of the thyroid gland is peculiar of this study in comparison to other investigations. In fact, regardless of hypothyroidism, large goiters alone can cause pharynx occlusion and thus OSAS. The authors did not find any difference in prevalence of hypothyroidism, numbers of nodules, and parenchyma heterogenecity determined by ultrasound, between OSAS subgroups and controls. Thus this study did not reveal any relationship between OSAS and thyroid disease. The authors concluded that long-term follow-up studies are needed to establish the possible significance of routine evaluation of OSAS patients for thyroid disease [9]. As a matter of fact, the incidence of thyroid deficiency states in patients with OSAS is not clearly known, thus the opportunity to evaluate thyroid function in all patients with the syndrome is still debated. It is well known that OSAS and hypothyroidism have several common signs that create a significant risk of undiagnosed hypothyroidism in OSAS. On the other hand, the suspect of sleep apnea in hypothyroid patients, especially when obese and with persistent sleep-disordered breathing during appropriate replacement therapy, should be taken into account. Endocrinologists and professionals dealing with sleep disturbances and OSAS should bear in mind that hypothyroidism may cause OSAS and that OSAS may be linked to (or even cause) hypothyroidism. A link between hypothyroidism and OSAS is suggested by the high prevalence of sleep apnea among hypothyroid patients, particularly in rare myxedematous cases [3, 7]. The increased prevalence of OSAS appears to be related to obesity and male sex rather than to hypothyroidism per se, although decreased ventilatory responses, extravasation of albumin, and mucopolysaccharides in the tissues of the upper airway and hypothyroid myopathy have been suggested as possible contributing factors for OSAS in hypothyroidism [3]. Moreover, contrasting data are available concerning the efficacy of thyroid replacement therapy in improving sleep apnea in patients with clinical hypothyroidism. Some authors describe a prompt reversal of symptoms, sleep-disordered breathing, and nocturnal hypoxia [12], while little or no improvement in sleep apnea is reported by others [10]. Nocturnal Continuous Positive F. Lanfranco (&) Division of Endocrinology, Diabetology and Metabolism, Department of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126 Turin, Italy e-mail: [email protected]