Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF) have been implicated in the pathogenesis of human immunodeficiency virus (HIV)-associated encephalopathy. The effects of pentoxifylline on brain PAF levels were examined in mice infected with the LP-BM5 murine leukemia virus (MuLV). Seven weeks after viral inoculation, significant increases in serum TNF-alpha and brain PAF levels were observed. One week of treatment with pentoxifylline initiated 6 weeks postinfection significantly reduced both serum TNF-alpha and brain PAF levels. A significant positive correlation was observed between the levels of these substances (r = 0.62; P < 0.01). This study demonstrates that pentoxifylline treatment was effective in decreasing the levels of TNF-alpha in the serum and PAF levels in the brain of mice infected with the LP-BM5 MuLV.
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PMID:Pentoxifylline decreases brain levels of platelet activating factor in murine AIDS. 915 42

Liver transplantation is the only effective treatment for potentially fatal cases of fulminant hepatic failure. However, it is very difficult to predict which cases will be fatal. The mortality may depend on alternative medical therapies. According to a nationwide survey of patients with fulminant hepatic failure presenting with encephalopathy of a coma grade greater than II within 8 weeks from the first symptoms of illness with a prothrombin time less than 40% of normal value, there were 93 patients in 311 hospitals between January and December 1998 in Japan. During this period, there were 11 patients with late-onset hepatic failure. The etiology was HAV infection in 4%, HBV infection in 44%, and nonA-nonB in 41%. Specific therapies were intensively used in all patients. The mean survival rate was 41%, with differences depending on the etiology. Six patients underwent liver transplantation, and 5 survived. In animal experiments, sinusoidal fibrin deposition caused massive liver necrosis. Activation of Kupffer cells and hepatic macrophages was a major contributing factor of this development. There were different mechanisms of such fibrin deposition. Tumor necrosis factor-alpha and superoxide anions released from hepatic macrophages after endotoxin administration destroyed endothelial cells, and then coagulopathy occurred in the sinusoids in rats given Propionibacteriom acnes, while a tissue factor from Kupffer cells played that role in rats undergoing partial hepatectomy. The prognosis of fulminant hepatic failure may depend on the etiology. The indication for liver transplantation for this disease must be carefully decided by analyzing the etiology, pathological conditions, and response to therapies in each case.
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PMID:Indications and criteria for liver transplantation for fulminant hepatic failure. 1210 71

The calcineurin inhibitors cyclosporine and tacrolimus are used for their immunosuppressive effects. Neurotoxic side effects include tremor, paresthesia, and headache. Rarer neurotoxicities include seizure, posterior reversible encephalopathy syndrome, and encephalopathy. Tacrolimus tends to be more neurotoxic than cyclosporine. Management of toxicities associated with calcineurin inhibitors includes dose reduction, switching between calcineurin inhibitors, or switching to a calcineurin-free regimen. Tumor necrosis factor (TNF) inhibitors are used in autoimmune diseases. Management of demyelinating conditions among patients treated with anti-TNF should follow standard of care and withdrawal of the anti-TNF. This drug class should be avoided in patients with a history of demyelinating conditions.
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PMID:Neurologic Toxicities Associated with Tumor Necrosis Factor Inhibitors and Calcineurin Inhibitors. 3304 Aug 70