Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A short review is given of the pharmacokinetic characteristics and side effects of the nitroimidazoles: metronidazole, tinidazole and ornidazole. The drugs are well absorbed from the gastrointestinal tract, maximum plasma levels generally being obtained 1 to 4 h after oral intake. Metronidazole has been shown to be absorbed after rectal administration; vaginal absorption is documented for all three drugs. The nitroimidazoles are widely distributed in the body, cross the placenta and appear in breast milk. Therapeutically effective concentrations of e.g. metronidazole have been demonstrated in e.g. the central nervous system, middle ear discharges, bile, peritoneal fluid, and fluids and tissues of the female genital tract. The binding to plasma proteins is less than 20%. Available data suggest that the elimination half-lives of these drugs differ, being 7-8 h for metronidazole, about 12 h for tinidazole and 14-15 h for ornidazole. Both metronidazole and ornidazole, but not tinidazole, seem to be extensively metabolized before elimination. The nature and frequency of adverse reactions to this drug include encephalopathy in a few patients treated with doses between 5 and 10 g daily as an adjunct to radiotherapy, and peripheral neuropathy observed in patients treated for prolonged periods with high doses. Among the common side effects of the nitroimidazoles are symptoms from the gastrointestinal tract such as nausea, anorexia, vomiting and metallic or bitter taste. Dizziness, ataxia and headache have been reported. When given together with alcohol, a disulfiram-like intolerance reaction can be obtained.
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PMID:Pharmacokinetics of nitroimidazoles. Spectrum of adverse reactions. 694 57

Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.
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PMID:Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice. 975 38

Tritrichomonas foetus, a microscopic single-celled flagellated protozoan parasite, traditionally identified as a cause of reproductive disease in cattle, has been demonstrated as an important cause of diarrhea in cats. Until recently, an effective antimicrobial treatment for feline Tritrichomonas foetus had not been idnetified. Since recommended dosages of antimicrobial drugs have failed in cats infected with Tritrichomonas foetus and in vitro studies have revealed multiple drug resistance, investigations continue in the effort to find an effective treatment. One particular study by Dr.Jody Gookin noted no clinicopathological abnormalities or adverse effects with the use of ronidazole, and the research concluded that ronidazole administered at 30 to 50 mg/kg orally twice daily for 2 weeks was capable of resolving diarrhea and eradicating infections of Tritrichomonas foetus in cats. Clinical use of ronidazole has revealed a reversible, possibly dose-related, neurotoxicity. Cats receiving ronidazole should be monitored for signs of nystagmus, ataxia, or behavior change, and ronidazole should be discontinued immediately if any of these signs are observed. Many compounding pharmacists have begun stocking pure ronidazole powder to prepare veterinarian prescriptions for the treatnment of Tritrichomonas foetus. Doses of ronidazole are usually prepared as capsules, the most desirable dosage form because (1)the capsules mask the extremely bitter taste of ronidazole, (2)exact dosing reduces the risk of neurotoxicity that has been reported at higher doses, and (3)the owner can be assured that the entire dose is ingested by the cat after administration of a capsule.
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PMID:Ronidazole in the treatment of trichomonad infections in cats. 2397 16