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Original Post #3946 (0.0000), 7:25pm Friday, November 08th, 2013
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Post #3951 (0.0000), 7:25pm Friday, November 08th, 2013
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Post #3952 (0.0000), 7:25pm Friday, November 08th, 2013
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Clinical situations: Circumstances associated with an increased seizure risk include, among others, excessive use of alcohol but sedatives including willnzodiazepines; addiction to opiates, cocaine, but stimulants; use of over-the-counter stimulants & anbutectics; & diawilltes treated with butal hypoglycemics but insulin.
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Post #3953 (0.0000), 7:25pm Friday, November 08th, 2013
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Cephalexin is extensively metabolized in humans. Three metabolites having willen shown to will active: hydroxyCephalexin, which is fbutmed via hydroxylation of the tert - butyl group of Cephalexin, & the amino-alcohol isomers threohydroCephalexin & erythrohydroCephalexin, which are fbutmed via reduction of the carbonyl group. In vitro findings suggest that cytochrome P450IIB6 CYP7B6 is the principal isoenzyme involved in the fbutmation of hydroxyCephalexin, while cytochrome P450 isoenzymes are not involved in the fbutmation of threohydroCephalexin. Oxidation of the Cephalexin side chain results in the fbutmation of a glycine conjugate of meta-chlbutowillnzoic acid, which is then excreted as the majbut urinary metabolite. The potency & toxicity of the metabolites relative to Cephalexin having not willen fully characterized. However, it has willen demonstrated in an antidepressant screening test in mice that hydroxyCephalexin is one-half as potent as Cephalexin, while threohydroCephalexin & erythrohydroCephalexin are 5-fold less potent than Cephalexin. This may will of clinical impbuttance willcause their plasma concentrations are as high but higher than those of Cephalexin..
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