Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eruptive herpes zoster infection (VZV) and its primary and secondary diseases are reported in 28 patients aged between 25 and 85 years. In 2 cases, malignant primary diseases were found. In 16 patients, a disorder of glucose utilization was diagnosed, 8 of them accompanied by a disorder of fat metabolism and 5 by a hyperuricemia. In one case a severe encephalomyelitis was observed. In 2 patients the activation of the VZV infection was related to the cytostatic or immunosuppressive therapy of a generalized Hodgkin's disease and a multiple sclerosis. Once a liver abscess as a sequel to amebic dysentery was diagnosed and once a megaloplastic anemia with symptoms of a funicular myelopathy following a vitamin B12 deficiency syndrome. In VZV infection the search for basal metabolic disorders is of particular importance.
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PMID:[Significance of diabetes mellitus in the activation of the varicella zoster virus (author's transl)]. 19 45

Uric acid, the naturally occurring product of purine metabolism, is a strong peroxynitrite scavenger, as demonstrated by the capacity to bind peroxynitrite but not nitric oxide (NO) produced by lipopolysaccharide-stimulated cells of a mouse monocyte line. In this study, we used uric acid to treat experimental allergic encephalomyelitis (EAE) in the PLSJL strain of mice, which develop a chronic form of the disease with remissions and exacerbations. Uric acid administration was found to have strong therapeutic effects in a dose-dependent fashion. A regimen of four daily doses of 500 mg/kg uric acid was required to promote long-term survival regardless of whether treatment was initiated before or after the clinical symptoms of EAE had appeared. The requirement for multiple doses is likely to be caused by the rapid clearance of uric acid in mice which, unlike humans, metabolize uric acid a step further to allantoin. Uric acid treatment also was found to diminish clinical signs of a disease resembling EAE in interferon-gamma receptor knockout mice. A possible association between multiple sclerosis (MS), the disease on which EAE is modeled, and uric acid is supported by the finding that patients with MS have significantly lower levels of serum uric acid than controls. In addition, statistical evaluation of more than 20 million patient records for the incidence of MS and gout (hyperuricemic) revealed that the two diseases are almost mutually exclusive, raising the possibility that hyperuricemia may protect against MS.
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PMID:Uric acid, a natural scavenger of peroxynitrite, in experimental allergic encephalomyelitis and multiple sclerosis. 943 51

Uric acid, the naturally occurring product of purine metabolism, is widely used as a diagnostic parameter in different diseases. The concentration of uric acid may vary between broad ranges without causing symptoms, like idiopathic hyperuricemia, which behind metabolic disorders were always suggested. Recently the uric acid has been shown as a strong scavenger of oxidative stress molecules or radicals. Uric acid was successfully used to treat experimental allergic encephalomyelitis, the mouse model of multiple sclerosis (M. S.). It was shown, that patients with multiple sclerosis had significantly lower levels of serum uric acid than the control persons. In addition, statistical evaluation of more than 20 million patient records for the incidence of MS and hyperuricemic gout revealed, that the hyperuricemia may protect against MS.
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PMID:[Uric acid as a scavenger in oxidative stress]. 1007 5

Uric acid (UA) is a purine metabolite that selectively inhibits peroxynitrite-mediated reactions implicated in the pathogenesis of multiple sclerosis (MS) and other neurodegenerative diseases. Serum UA levels are inversely associated with the incidence of MS in humans because MS patients have low serum UA levels and individuals with hyperuricemia (gout) rarely develop the disease. Moreover, the administration of UA is therapeutic in experimental allergic encephalomyelitis (EAE), an animal model of MS. Thus, raising serum UA levels in MS patients, by oral administration of a UA precursor such as inosine, may have therapeutic value. We have assessed the effects of inosine, as well as inosinic acid, on parameters relevant to the chemical reactivity of peroxynitrite and the pathogenesis of EAE. Both had no effect on chemical reactions associated with peroxynitrite, such as tyrosine nitration, or on the activation of inflammatory cells in vitro. Moreover, when mice treated with the urate oxidase inhibitor potassium oxonate were fed inosine or inosinic acid, serum UA levels were elevated markedly for a period of hours, whereas only a minor, transient increase in serum inosine was detected. Administration of inosinic acid suppressed the appearance of clinical signs of EAE and promoted recovery from ongoing disease. The therapeutic effect on animals with active EAE was associated with increased UA, but not inosine, levels in CNS tissue. We, therefore, conclude that the mode of action of inosine and inosinic acid in EAE is via their metabolism to UA.
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PMID:Therapeutic intervention in experimental allergic encephalomyelitis by administration of uric acid precursors. 1245 Nov 83