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protoporphyrin/epileptischer anfall
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Seite 1 von 18 Ergebnisse
[Effect of endogenous heme oxygenase-carbon monoxide on brain damage induced by recurrent febrile seizures].
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OBJECTIVE
Febrile seizures (FS) are the most common seizure disorders in children. Approximately one third of children with a febrile seizure have recurrent events. Although most FS may not represent a serious health problem, those that are more prolonged and recurrent may cause hippocampal damage
Endogenous heme oxygenase prevents impairment of cerebral vascular functions caused by seizures.
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In newborn pigs, the mechanism of seizure-induced cerebral hyperemia involves carbon monoxide (CO), the vasodilator product of heme catabolism by heme oxygenase (HO). We hypothesized that seizures cause cerebral vascular dysfunction when HO activity is inhibited. With the use of cranial window
Epileptic seizures increase circulating endothelial cells in peripheral blood as early indicators of cerebral vascular damage.
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Circulating endothelial cells (CECs) are nonhematopoetic mononuclear cells in peripheral blood that are dislodged from injured vessels during cardiovascular disease, systemic vascular disease, and inflammation. Their occurrence during cerebrovascular insults has not been previously described.
Carbon monoxide regulates cerebral blood flow in epileptic seizures but not in hypercapnia.
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Carbon monoxide (CO) is an endogenously produced gas sharing many properties with nitric oxide (NO), notably activating soluble guanylate cyclase and relaxing blood vessels. The brain can generate high quantities of CO from a constitutive enzyme, haem oxygenase (HO-2). To determine whether CO is
Cerebrovasodilatory contribution of endogenous carbon monoxide during seizures in newborn pigs.
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Carbon monoxide (CO) and the excitatory amino acid glutamate both dilate cerebral arterioles in newborn pigs. The key enzyme in CO synthesis is heme oxygenase, which is highly expressed in neurons with glutamatergic receptor activity as well as cerebral microvessels. During seizures the
Epileptic seizures cause extended postictal cerebral vascular dysfunction that is prevented by HO-1 overexpression.
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The extended postictal state is characterized by neurological problems in patients. Inadequate blood supply to the brain and impaired cerebral autoregulation may contribute to seizure-induced neuronal damage. Recent evidence in newborn pigs indicates that activation of the antioxidative enzyme heme
Does iron deficiency raise the seizure threshold?
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To determine the effect of iron status on the seizure threshold, measures of iron sufficiency were prospectively evaluated in 51 children presenting to a pediatric emergency department with a febrile illness with (26) or without (25) an associated febrile seizure. A higher proportion of children
Antioxidant roles of heme oxygenase, carbon monoxide, and bilirubin in cerebral circulation during seizures.
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Postictal cerebrovascular dysfunction is an adverse effect of seizures in newborn piglets. The brain heme oxygenase (HO) provides protection against cerebrovascular dysfunction. We investigated the contribution of reactive oxygen species (ROS) to seizure-induced vascular damage and the mechanism of
Phenytoin reduces 5-aminolevulinic acid-induced protoporphyrin IX accumulation in malignant glioma cells.
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Epileptic seizures are among the presenting clinical signs of malignant glioma patients, frequently necessitating treatment with antiepileptic drugs (AEDs). The efficacy of 5-aminolevulinic acid (5-ALA)-based intraoperative fluorescence-guided surgery and photodynamic therapy (PDT) in glioblastoma
Heme oxygenase inhibition reduces neuronal activation evoked by bicuculline in newborn pigs.
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Carbon monoxide (CO) is a product of heme degradation by heme oxygenase (HO) that is highly expressed in the brain. The present study addresses the hypothesis that CO can be involved in brain neuronal function. The effects of the HO inhibitor, tin protoporphyrin (SnPP), on brain electrical activity
[Hereditary coproporphyria (Hepatic coproporphyria), Erythropoietic coproporphyria].
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Hereditary coproporphyria (Hepatic coproporphyria: HCP); HCP is the rarest and least recognized among hepatic porphyrias and is characterised by an excess of faecal and urinary excretion of coproporphyrin (mainly isomer III). The deficiency is in coproporphyrinogen oxidase. HCP was first described
Iron-induced lipid peroxidation and brain injury responses.
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Head trauma with cerebral contusion causes extravasation of red blood cells, followed by hemolysis and deposition of iron-containing blood products within the neuropil. Liberation of heme compounds is associated with deposition of hemosiderin, and with gliosis, neuronal loss and occasionally the
[Porphyria variegata--a case report].
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In a man aged 28 years abdominal pains with constipation appeared, and were followed after 2 weeks by generalized maximal epileptic seizures, gradually progressing signs of proximal polyneuropathy, numerous brownish patches on the face and trunk, and hepatomegaly. In the urine raised levels were
Lead toxicosis in cats-a review.
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Although the incidence of lead toxicosis in small animals continues to decrease, it remains a significant malady. We have reviewed the literature of the past 45 years, which revealed 70 cases involving cats. Sources, signs, diagnosis, pathology and treatment of feline lead toxicosis are reviewed. In
Effects of new anticonvulsant medications on porphyrin synthesis in cultured liver cells: potential implications for patients with acute porphyria.
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Some patients with acute hereditary porphyrias have seizures and require anticonvulsant therapy, but many anticonvulsants induce exacerbations of the hepatic porphyrias. Recently, several new anticonvulsants have become available. Among these are gabapentin, vigabatrin, felbamate, lamotrigine, and
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