diphenylhydantoin/inflammation

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Effect of non-steroidal anti-inflammatory drugs on the anticonvulsive activity of valproate and diphenylhydantoin against maximal electroshock-induced seizures in mice.

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Prostaglandins and their inhibitors may affect convulsive phenomena. Thus, the aim of this study was to examine possible interactions between non-steroidal anti-inflammatory drugs and two conventional antiepileptic drugs in terms of their anticonvulsive activity and side-effects. Also, the plasma

Non-steroidal anti-inflammatory drugs and the protective activity of valproate and diphenylhydantoin against maximal electroshock-induced seizures in mice--an interaction.

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Pharmacological studies of a new anti-inflammatory drug, 1-phenylsulfonyl-5,5-diphenylhydantoin (PC-796) in experimental animals. II. Toxicological and general pharmacological properties.

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Pharmacological studies of a new anti-inflammatory drug, 1-phenylsulfonyl-5,5-diphenylhydantoin (PC-796) in experimental animals. 3. Absorption, tissue distribution and metabolic fate.

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Pharmacological studies of a new anti-inflammatory drug, 1-phenylsulfonyl-5,5-diphenylhydantoin (PC-796) in experimental animals. I. Anti-inflammatory, analgesic and anti-pyretic activity.

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Relationship of drug metabolism and inflammation to the gingival response of rats treated with diphenylhydantoin.

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The role of inflammation in the pathogenesis of gingival enlargement during the administration of diphenylhydantoin sodium in cats.

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[Histopathological study on diphenylhydantoin gingival hyperplasia in rats, especially the role of gingival inflammation in diphenylhydantoin gingival hyperplasia].

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Diphenylhydantoin inhibits osteoclast differentiation and function through suppression of NFATc1 signaling.

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Diphenylhydantoin (DPH) is widely used as an anticonvulsant drug. We examined the effects of DPH on osteoclast differentiation and function using in vivo and in vitro assay systems. Transgenic mice overexpressing a soluble form of RANKL (RANKL Tg) exhibited increased osteoclastic bone resorption.

Cholestatic liver disease associated with diphenylhydantoin therapy. Possible pathogenic importance of altered bile salt metabolism.

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A ten-year-old boy persented with a prolonged cholestatic liver disease 5 weeks after starting diphenylhydantoin therapy. The initial phase of his illness was characterized by hepatocellular damage with swollen liver cells and centrilobular cholestasis. Severe hyperlipoproteinemia with eruptive

Diphenylhydantoin sodium promotes early and marked angiogenesis and results in increased collagen deposition and tensile strength in healing wounds.

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BACKGROUND Sodium diphenylhydantoin (DpH) (phenytoin) was first introduced as an antiepileptic in 1938. One of its side effects, gingival hyperplasia, prompted investigation into the possible application of this drug as a promoter of wound healing. Since the late 1950s phenytoin has been used in a

Diphenylhydantoin-induced gingival overgrowth in man: a clinico-pathological study.

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In a cross-sectional, epidemiological study of diphenylhydantoin-induced gingival overgrowth (DGO) in 60 epileptic patients, gingival lesion severity was statistically compared with other clinical, laboratory, and histopathological findings. Evident DGO was observed in 50% of patients, and positive

Gingival hyperplasia induced by diphenylhydantoin in a gorilla.

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An adult male lowland gorilla had been treated with diphenylhydantoin for 6 months following several acute convulsive episodes. The gorilla remained clinically normal during that period. Then, for no apparent reason, it refused its usual diet. Physical examination revealed acute inflammatory

Biopharmaceutical studies on hydantoin derivatives. V. Pharmacokinetics and pharmacodynamics of 5,5-diphenylhydantoin and 1-benzenesulfonyl-5,5-diphenylhydantoin.

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Disposition of 1-benzenesulfonyl-5,5-diphenylhydantoin (II) having a potent anti-inflammatory activity was compared with that of 5,5-diphenylhydantoin (I), an antiepileptic drug, in order to elucidate whether the pharmacodynamic difference between them can be explained by their physicochemical and

The effects of phenobarbital and diphenylhydantoin on liver function and morphology.

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Sixty-three children with seizure disorders receiving phenobarbital and/or diphenylhydantoin for more than 12 months had liver function tests evaluated. All 56 whose serum anticonvulsant concentrations were in the therapeutic range had elevations of their serum gamma glutamyl transpeptidase

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