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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The multiple organic failure syndrome (MOFS or MOF) is the result of a hyperergic and chaotic activation of the unspecific immune (inflammatory) system. It may be elicited, either as a consequence of hypodynamic shock phenomena with initial tissular lesions caused by a diseased peripheral vascular bed, characteristic of states of shock, or as the result of an inflammatory aseptic or septic focus occurring in the process of transformation of tissular territories diseased under the action of various factors (traumatic, thermic, immune etc.). The local inflammatory process sets in motion a series of elements of the immune apparatus, such as: polynuclear neutrophilic leucocytes, macrophages, complement, which lead, when they begin to exert an hyperergic action, to the cascade activation of these elements also outside the focus of lesion, generating disseminated lesions at the level of organs and systems of organs. The lesions have an aleatory character and affect variously organs and territories, leading finally to insufficiency phenomena with clinical expression: renal failure, pulmonary failure, encephalopathy, shock digestive tract, intravascular disseminated coagulation, state of shock initially hyperdynamic and afterwards hypodynamic, metabolic disturbances etc. The specific manifestations, the symptomatology, the therapy and the prognosis of the syndrome are described.
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PMID:[The multiple organ failure syndrome (MOFS) and septic states]. 168 7

From the middle of 1990's, there repeated in winter season an outbreak of encephalopathy in Japan that appeared to be associated with influenza. A national survey was conducted, and a total of 507 patients was diagnosed as having influenza-associated encephalopathy during 1998-2002 on the basis of virologic analysis. Type A influenza was more pathogenic than type B, and A: H3 type was more invasive than A: H1 type. Encephalitis developed mainly in children below 5 years of age, either on the day that influenza signs appeared or on the next day. We hypothesized that the replicated viruses at nasopharyngeal epithelium disrupt the olfactory mucosa. Via olfactory nerve system, the stimuli may be transmitted to the brain eventually to activate glial cells, and to induce the production of pro-inflammatory cytokines. The cytokine storm results in neural cell damage as well as apoptosis of glial cells due to TNF-induced mitochondrial respiratory failure. The disruption of blood-brain barrier progresses to the systemic cytokine storm, resulting in DIC and MOF.
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PMID:[Influenza-associated encephalopathy--pathophysiology and disease mechanisms]. 1461 37

Patients with a new type of influenza-associated encephalopathy with high mortality are increasing in Japan and the United States. We present three patients treated with methyprednisolone pulse treatment and plasma exchange to remove cytokines, and all three patients recovered without severe sequela. IL-6 decreased dramatically after the start of the plasma exchange and methyprednisolone. Therefore when influenza-associated encephalopathy is actually diagnosed, steroid pulse therapy should be started at an early stage, and when signs of DIC and/or MOF appear, plasma exchange is recommended to remove the cytokines and NOx.
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PMID:Efficacy of plasma exchange and methylprednisolone pulse therapy on influenza-associated encephalopathy. 1603 52