Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased spontaneous activity of the hypothalamic-pituitary-adrenal (HPA)-axis is frequently reported in major depressed inpatients. The aim of the present study was to determine whether there are differences in spontaneous HPA-axis activity between major depressed inpatients and outpatients. Toward this end, the authors measured basal 9:00 a.m. plasma cortisol and the integrated assessment of plasma morning cortisol secretion over 2 (AUC 120) hours in 48 major depressed inpatients, 17 major depressed outpatients and 73 normal volunteers. Major depressed inpatients exhibit significantly higher plasma cortisol values than healthy controls and major depressed outpatients. The cortisol data from the latter are not significantly different from these of the healthy controls. The cortisol differences between in and outpatients were still present after considering the influences of age, sex, body mass index, severity or endogeneity of illness, unipolar/bipolar subclassification, or specific symptoms such as suicidal thoughts, insomnia, psychomotor disorders, psychoticism, weight loss or anxiety. The results indicate that hypercortisolism as measured by basal morning plasma levels is not a feature of major depression per se, but rather of an interaction between the illness and hospitalization.
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PMID:The relevance of the in- versus outpatient status for studies on HPA-axis in depression: spontaneous hypercortisolism is a feature of major depressed inpatients and not of major depression per se. 807 85

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