A glandular problem.

Accessible online at: www.karger.com/res In a recent issue of Respiration, Bottini and Tantucci [1] review some of the endocrine diseases in which sleep apnea syndrome is common. They focus on five conditions: acromegaly, hypothyroidism, diabetes with peripheral neuropathy, Cushing’s disease and syndrome, and hyperandrogenism in which sleep apnea occurs frequently and evidence for sleep disturbance should be sought and if present treated. Often the predisposition to sleep apnea is a result of anatomical and functional changes in the upper airway caused by the disease [1, 2]. Patients with acromegaly tend to develop airway obstruction because the disease produces mucosal thickening, macroglossia, hypertrophy of the vocal cords, impaired mobility of the cricoarytenoid joints, myopathic changes in the vocal cords, and at times by paralysis of the recurrent laryngeal nerve. Bromocriptine or octreotide treatment may improve the sleep apnea observed in acromegaly but continuous positive airway pressure is more effective. Narrowing of the upper airway by myxomatous changes in the tissues of the pharyngeal wall and tongue contribute to the obstructive apneas seen in hypothyroidism. In the neuropathy occurring with diabetes, impaired respiratory sensation and/or poor muscle strength may contribute to apneas during sleep [1, 2]. In other cases, the cause of the apneas is still obscure but may involve hormonal effects on the respiratory pattern generator and the response to chemical and mechanical stimulations. Somatostatin, for example, has been reported to inhibit breathing while progesterone, growth hormone, and corticotropin-releasing hormone have been reported to stimulate breathing [2]. Relationships are complex. Hormones affect sleep. For example prolactins seem to stimulate sleep; thus patients with prolactinomas have enhanced slow-wave sleep [3], but coticotropin-releasing hormone may have an arousing action [2]. On the other hand release of hormones like thyrotropin, melatonin, growth hormone, prolactin and cortisol wax and wane with the sleep-wake cycle. Sleep deprivation alters considerably the daily rhythm of release of thyrotropin, growth hormone and prolactin. In patients with sleep apnea, sleeping levels of growth hormone and prolactin are reduced, but continuous positive airway pressure normalizes them [4]. It is now recognized that sleep, respiration and metabolism are closely linked not just by nerve pathways but in addition by a complex network of neurohumoral chemicals that include, in addition to the traditional hormones, cytokines and peptides such as the leptins and hypocretins (also known as orexins) and ghrelin. Some of these substances are produced in both the brain and peripheral tissues [5–9]. Cytokines such as IL-1 and TNF-· increase with sleep deprivation and, when injected into the cerebrospinal fluid of animals, produce sleep [5]. Hypocretins, produced in the lateral hypothalamus, are arousal producing, and abnormalities in hypocretin neurotransmission are