Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

H2-antagonists such as cimetidine and ranitidine are metabolized by cytochrome P-450. In this way they may interfere with theophylline metabolism. Cimetidine is known to have this effect and frequently to induce a theophylline toxic effect, while data concerning ranitidine are more uncertain. In this paper, we report the case of a 67-year-old woman with non-insulin dependent diabetes. She was taking aminophylline for respiratory failure and after ranitidine infusion exhibited generalized convulsions. Theophylline values which were monitored within the therapeutic range, increased toxic levels after ranitidine therapy and epileptic episodes. The increase in theophylline levels was associated with a further reduction in the clearance rate of the bronchodilator. We think that ranitidine may combine with other clinical factors known to reduce theophylline metabolism mainly in the elderly and severely ill patients. Theophylline-induced seizures may occur when theophylline serum levels are slightly above the therapeutic range, as in our case report.
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PMID:Seizures during concomitant treatment with theophylline and ranitidine: a case report. 209 63

In awake rats, ranitidine was more effective than cimetidine in elevating blood pressure following intracerebroventricular (i.c.v.) injection, yet neither drug affected the hypotensive response to subsequent injections of muscimol (8.8 nmol i.c.v.). Bicuculline (0.01 nmol) microinjected into the inferior colliculus of rats caused clonic seizures whereas cimetidine (100 nmol) had no effect. The antihistamines did not prevent GABAB receptor-mediated inhibition of twitch responses in transmurally stimulated guinea-pig ileum. Ranitidine potentiated rather than inhibited GABAA receptor-mediated contractions of ileum longitudinal muscle. Cimetidine had no effect on these responses except at high concentrations (3 X 10(-4) M) which caused a slight dextral shift in the contractile response curve for GABA that may be attributed to antimuscarinic actions of cimetidine. Taken together, these data do not support the concept that the centrally mediated pressor effects of H2 antagonists are caused by GABA receptor blockade.
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PMID:Pressor responses to central injection of H2 antagonists not caused by GABA blockade. 287 34

Cimetidine-related neurotoxicity may be characterized by signs of affective dysfunction, toxic delusional state and/or delirium, confusion and/or amnestic signs, coma, epileptic phenomena and focal neurological signs. EEG features are rarely mentioned in the literature. They are discussed here in a patient presenting with cimetidine-related mental impairment and epileptic seizures. Some of the clinical signs are related to our incomplete understanding of the neurotransmitter function of histamine in the brain. It is suggested that transient functional deafferentiation of the cortex may occur with chemical histamine receptor blockade at brain stem level. EEG monitoring may be helpful in patients at risk.
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PMID:Cimetidine neurotoxicity. EEG and behaviour aspects. 648 91

A 92-year-old woman with a normal serum calcium level received cimetidine postoperatively. She became severely hypocalcemic and exhibited tetany, seizures, and impaired mental status. Her condition responded to intravenous diazepam, phenytoin sodium, and gluconate calcium. Normal serum calcium levels were maintained by calcium infusions until the cimetidine treatment was stopped. Cimetidine may have been responsible for the observed complications due to its effect on serum parathyroid hormone level.
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PMID:Effect of cimetidine on serum calcium levels in an elderly patient. 725 16

The effects of muscimol, aminooxyacetic acid (AOAA), diamino-n-butyric acid (DABA), baclofen, bicuculline, picrotoxin, strychnine, diazepam, phenobarbitone and phenytoin on cimetidine-induced seizures were studied in mice. Cimetidine (400-1000 mg/kg, i.p.) induced dose-dependent tonic convulsion. Muscimol, AOAA and DABA effectively protected mice against cimetidine-induced seizures. Bicuculline and picrotoxin significantly potentiated the seizures induced by cimetidine and effectively antagonized the protective effects of muscimol, AOAA and DABA against the seizures. Diazepam and phenobarbitone significantly protected the mice against cimetidine-induced seizures while phenytoin and strychnine did not significantly alter the seizures. These results indicate that the attenuation of central gamma-aminobutyric acid neurotransmission may underlie cimetidine-induced seizures in mice.
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PMID:Cimetidine-induced seizures in mice. Antagonism by some GABAergic agents. 827 50

Cimetidine and phenytoin are useful medications often used together in patients with seizure disorders secondary to brain masses or metabolic abnormalities. We describe a case of thrombocytopenia in the setting of concurrent phenytoin, dexamethasone and cimetidine administration, and compare it with previously described cases of thrombocytopenia induced by concurrent use of phenytoin, cimetidine, and glucocorticoids. The similarities between these cases suggest mechanisms by which these agents may induce thrombocytopenia, specifically through potential downregulation of epoxide hydrolase by glucocorticoids.
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PMID:Thrombocytopenia following administration of phenytoin, dexamethasone and cimetidine: a case report and a potential mechanism. 832 96

The aim of this study was to evaluate the effects of acute (1 day) and chronic (7 days) administrations of cimetidine, an H2 histamine receptor antagonist, on the protective activity of conventional antiepileptic drugs (AEDs) against pentetrazole (PTZ)-induced seizures in mice. Cimetidine (up to 100 mg/kg), given alone either acutely or chronically, did not alter significantly PTZ-induced seizures in mice. However, the drug (at 20 mg/kg, administered acutely) potentiated the anticonvulsant activity of ethosuximide (ETX) by reducing its ED50 from 134 to 103 mg/kg (p < 0.05). This effect was associated with a 74% elevation of plasma ETX level (p < 0.01). In contrast, chronic (7 days) administration of cimetidine (20 mg/kg) did not affect the anticonvulsant activity of ETX in the PTZ test and its plasma levels. On the other hand, cimetidine (20 mg/kg), given either acutely or chronically, when co-administered with valproate, clonazepam, and phenobarbital had no significant impact on the anticonvulsant properties of these AEDs against PTZ-induced seizures and their plasma levels in mice. The results indicate that there may be no risk in prescribing cimetidine for other than epilepsy reasons in patients treated with valproate, clonazepam or phenobarbital.
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PMID:Influence of cimetidine on the anticonvulsant activity of conventional antiepileptic drugs against pentetrazole-induced seizures in mice. 1653 41