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)

The purpose of this paper is to show several diseases that manifest symmetrical hyperintense lesions on the middle cerebellar peduncles, the largest connecting peduncles between the brainstem and the cerebellum, in conventional magnetic resonance (MR) images. We retrospectively reviewed cranial MR images obtained with 0.3-, 0.5-, 1.0-, and 1.5-Tesla scanners. We found symmetrical middle cerebellar peduncular lesions in patients with Wilson's disease; hepatic encephalopathy; extrapontine myelinolysis; acute disseminated encephalomyelitis; wallerian degeneration of the pontocerebellar tracts after either pontine infarction, pontine hemorrhage, or central pontine myelinolysis; leukodystrophy; olivopontocerebellar atrophy; and toluene abuse. Definitive diagnosis of these diseases can be made relatively easily on the basis of clinical data; however, examination of associated brainstem or supratentorial lesions in MR images is also important.
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PMID:Symmetrical lesions of the middle cerebellar peduncle: MR imaging and differential diagnosis. 1609 30

Tetrathiomolybdate (TM) is a potent anticopper drug developed for Wilson's disease. We have found multiple efficacious results from decreasing copper levels with TM in mouse models of disease, using serum Cp as a surrogate marker of copper status and targeting Cp values of 20% to 50% of baseline. We have found efficacious results of TM therapy in mouse models of fibrosis; inflammation; damage from exogenous agents, such as acetaminophen and doxorubicin; and immune-modulated diseases, such as concanavalin A hepatitis, collagen II-induced arthritis, and the non-obese diabetic (NOD) mouse model of type I diabetes. In the current study, we examine TM efficacy in the EAE mouse model of multiple sclerosis (MS). We find that clinical scores of neurologic damage are significantly inhibited by TM therapy, whether therapy is started before MS-inducing antigen administration or after symptoms from antigen administration develop. Furthermore, we find that experimental autoimmune encephalomyelitis (EAE) treatment produces a marked increase of oxidant damage, as measured by urine isoprostane levels, and TM suppresses these isoprostane increases strongly and significantly. Finally, we find marked increases of inflammatory and immune-related cytokines in this model, and we find that TM strongly and significantly suppresses these increases.
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PMID:Efficacy of tetrathiomolybdate in a mouse model of multiple sclerosis. 1901 Feb 95

A female patient receiving pantoprazole during a corticosteroid therapy for encephalomyelitis disseminata developed severe acute hepatitis one month after initiation of pantoprazole treatment. Other causes of hepatic dysfunction including viral hepatitis, autoimmune hepatitis, primary sclerosing cholangitis, primary biliary cirrhosis, haemochromatosis or Wilson's disease were excluded. Liver biopsy showed severe hepatic lesions with extensive necroses of the parenchyma. One week after discontinuation of pantoprazole the liver function began to improve and gradually the patient fully recovered. One year earlier the patient had been treated with pantoprazole before and had developed a milder form of hepatitis then. This case argues for an idiosyncratic hepatocellular damage caused by pantoprazole.
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PMID:Pantoprazole induces severe acute hepatitis. 2129 7