Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cyclosporine is a potent immunosuppressant that is more and more widely used, particularly after organ transplantations. Many neurological side effects, including convulsions, that could be related to this drug, have been previously observed, most often with high blood concentrations. We report, for the first time, a case of prolonged confusion where a non convulsive status epilepticus may be discussed. It occurred in a 64-year-old woman, 17 days after a liver transplantation. The whole blood cyclosporine value was 230 micrograms/l (normal range: 100-200 micrograms/l) at the beginning of the status epilepticus. The cyclosporine imputability and the part of other factors that could have facilite are discussed.
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PMID:[Prolonged confusion syndrome in the course of cyclosporine treatment: a state of confusion?]. 223 52

Acute neurodegeneration in man is encountered during and following stroke, transient cardiac arrest, brain trauma, insulin-induced hypoglycemia and status epilepticus. All these severe clinical conditions are characterized by neuronal calcium overload, aberrant cell signaling, generation of free radicals and elevation of cellular free fatty acids, conditions that favor activation of the mitochondrial permeability transition pore (mtPTP). Cyclosporin A (CsA) and its analog N-methyl-valine-4-cyclosporin A (MeValCsA) are potent blockers of the mtPTP and protect against neuronal death following excitotoxicity and oxygen glucose deprivation. Also, CsA and MeValCsA diminish cell death following cerebral ischemia, trauma, and hypoglycemia. Here we present data that strongly imply the mtPT in acute neurodegeneration in vivo. Compounds that readily pass the blood-brain-barrier (BBB) and block the mtPT may be neuroprotective in stroke.
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PMID:Mitochondrial permeability transition in acute neurodegeneration. 1202 55

Cyclosporin A is an essential drug for graft versus host disease (GvHD) prophylaxis in allogeneic hematopoietic stem cell transplantation. Cyclosporin A-associated neurotoxicity is common but poorly understood. The authors herein report on 3 patients receiving transplants for thalassemia. GvHD prophylaxis included cyclosporin A, prednisolone, and methotrexate. All patients developed a status epilepticus with cortical signal alterations located mainly in occipital regions on T2-weighted magnetic resonance imaging. Complete disappearance of the neurologic symptoms and radiographic findings was observed without discontinuing cyclosporin A therapy. Especially, pediatric thalassemics receiving busulfan/cyclophosphamide as preparative regimen seem to be significantly prone to cyclosporin A-associated seizures.
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PMID:Cyclosporin A-associated status epilepticus related to hematopoietic stem cell transplantation for thalassemia. 1463 24

Leptomycin B (LMB), originally developed as an anti-fungal agent, has potent neuroprotective properties against status epilepticus (SE, a prolonged seizure activity). However, the pharmacological profiles and mechanisms of LMB for neuroprotection remain elusive. In the present study, we found that LMB increased phosphorylation levels of protein kinase A (PKA) catalytic subunits, protein phosphatase 2B (PP2B, calcineurin) and extracellular signal-regulated kinase 1/2 (ERK1/2) under normal condition, and abolished SE-induced neuronal death. Co-treatment of H-89 (a PKA inhibitor) with LMB could not affect the seizure latency and its severity in response to pilocarpine. However, H-89 co-treatment abrogated the protective effect of LMB on SE-induced neuronal damage. Cyclosporin A (CsA, a PP2B inhibitor) co-treatment effectively prevented SE-induced neuronal death without altered seizure susceptibility in response to pilocarpine more than LMB alone. H-89 co-treatment inhibited LMB-mediated ERK1/2 phosphorylation, but CsA enhanced it. U0126 (an ERK1/2 inhibitor) co-treatment abolished the protective effect of LMB on SE-induced neuronal death without alterations in PKA and PP2B phosphorylations. To the best of our knowledge, the present data demonstrate a previously unreported potential neuroprotective role of LMB against SE via PKA- and PP2B-mediated ERK1/2 activation.
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PMID:Leptomycin B attenuates neuronal death via PKA- and PP2B-mediated ERK1/2 activation in the rat hippocampus following status epilepticus. 2860 33