Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuromyasthenia (benign myalgic encephalomyelitis) is a term used to describe a protracted and incomplete recovery phase following viral-like illnesses. There are few significant physical findings or abnormal laboratory determinations. Although depressive symptoms have been observed in individuals with neuromyasthenia, systematic psychological investigations based on a standardized interview technique have not been reported. This study was designed to investigate the prevalence of psychiatric disorders and psychiatric symptoms in a group of patients presenting with neuromyasthenia. The study consisted of three parts: a structured psychiatric interview (The National Institute of Mental Health Diagnostic Interview Schedule), a self-report measure (The Beck Depression Inventory) and Dexamethasone Suppression Test. Results indicated that relative to a matched comparison group of non-clinical volunteers, a significant percentage (67%) of neuromyasthenic patients met criteria for major depression. Even more striking was the observation that 50 percent of the sample had a major depressive episode prior to the development of neuromyasthenia. These findings suggest that sporadic neuromyasthenia may be the result of an organic illness in psychologically susceptible individuals.
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PMID:Depression in patients with neuromyasthenia (benign myalgic encephalomyelitis). 358 62

The present study was designed to investigate the interaction between neuroendocrine mediators and the immune system in chronic fatigue syndrome (CFS). We examined the sensitivity of the immune system to the glucocorticoid agonist dexamethasone and the beta2-adrenergic agonist terbutaline in 15 adolescent girls with CFS and 14 age- and sex-matched controls. Dexamethasone inhibits T-cell proliferation in healthy controls and in CFS patients. However, the maximal effect of dexamethasone on T-cell proliferation is significantly reduced in CFS patients as compared with controls. The beta2-adrenergic receptor agonist terbutaline inhibits tumor necrosis factor-alpha production and enhances interleukin-10 production by monocytes. Our data demonstrate that the capacity of a beta2-adrenergic agonist to regulate the production of these two cytokines is also reduced in CFS patients. We did not observe differences in baseline or CRH-induced cortisol and ACTH between CFS patients and controls. Baseline noradrenaline was similar in CFS and controls, whereas baseline adrenaline levels were significantly higher in CFS patients. We conclude that CFS is accompanied by a relative resistance of the immune system to regulation by the neuroendocrine system. Based on these data, we suggest CFS should be viewed as a disease of deficient neuroendocrine-immune communication.
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PMID:Disturbed neuroendocrine-immune interactions in chronic fatigue syndrome. 1069 Aug 78