Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to ascertain the occurrence of the sleep apnoea syndrome (SAS) in patients after pituitary afunctional adenoma operation or in patients with other affection in sella turcica region except acromegaly patients. Eighty-one patients were addressed. Sixteen patients (eight men, eight women) underwent the examination; the rest of them had no interest to be explored. Afunctional pituitary adenoma was diagnosed in twelve patients, afunctional pituitary adenoma and subsequently optic glioma in one patient, craniopharyngioma in one patient, prolactinoma in one patient and undifferentiated cystic pituitary tumour in one patient. Neurological examination was done in all patients (standardized sleep questionnaire was included). SAS was quantified using PolyMESAM. Severity of SAS were set up from the value of M index (M = ODI.delta saturation; ODI--oxygen desaturation index). Mild SAS: 40 < M < 100; middle SAS: 100 < M < 210; severe SAS: M > 210. SAS was diagnosed in 13 patients: mild SAS in three of them (average value of M index: 81.0 +/- 12.7), moderate SAS in seven patients (average value of M index: 129.0 +/- 18.7) and severe SAS in three patients (average value of M index: 790.0 +/- 563.0). Therapy by continuous positive airway pressure (CPAP) was recommended in six patients. Five of them continue in using of CPAP--four patients with good compliance. The occurrence of SAS was 16.05% in measured group, higher than in normal population.
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PMID:[The sleep apnea syndrome in hypophyseal disorders with the exception of acromegaly]. 1170 81

A bidirectional interaction exists between the electrophysiological and neuroendocrine components of sleep. The first is represented by the nonrapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS) cycles, the latter by distinct patterns of the secretion of various hormones. Certain hormones (neuropeptides and steroids) play a specific role in sleep regulation. Changes in their activity contribute to the pathophysiology of sleep disorders. A reciprocal interaction of the peptides growth hormone-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) plays a key role in sleep regulation. GHRH promotes growth hormone secretion and, at least in males, NREMS, whereas CRH impairs NREMS, promotes REMS and stimulates the secretion of adrenocorticotropic hormone and cortisol. Changes in the CRH:GHRH ratio in favor of CRH contribute to impaired sleep, elevated cortisol secretion and blunted GH levels during depression and normal aging. However, in women, GHRH exerts CRH-like effects. Galanin, ghrelin and neuropeptide Y are other sleep-promoting peptides, whereas somatostatin impairs sleep. A decline of orexin activity causes narcolepsy. In addition to CRH overactivity, hypercortisolism appears to be involved in the pathophysiology of sleep- electroencephalogram (EEG) changes in depression. Various neuroactive steroids exert specific effects on sleep. The changes of sleep EEG in women after the menopause are related to the decline of estrogen and progesterone. Furthermore, sleep-EEG changes in dwarfism, acromegaly, Addison's disease, Cushing's disease, brain injury, sleep apnea syndrome, primary insomnia, prolactinoma and dementia appear to be related to changes in the activity of peptides and steroids.
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PMID:Roles of peptides and steroids in sleep disorders. 3075 93