Disease relevance of Furantoin

• During trimethoprim-sulfamehtoxazole prophylaxis, 8.5% of monthly vaginal and 27% of monthly fecal cultures grew Escherichia coli, as compared to 36 and 96%, respectively for nitrofurantoin macrocrystals [1].
• Persistence of bacteriuria was associated with amoxicillin-resistant strains in the amoxicillin group but nitrofurantoin-susceptible strains in the nitrofurantoin group [2].
• In the presence of a mouse hepatic microsomal drug-activating system, however, nitrofurantoin metabolites produced dose dependent toxicity to the lymphocytes [3].
• Urine samples from 12 humans receiving oral therapeutic doses of nitrofurantoin were mutagenic for Salmonella typhimurium strain TA 100 and nonmutagenic for strain TA 100-FR1 [4].
• The simultaneous occurrence of pulmonary fibrosis and chronic active hepatitis in a patient undergoing long-term nitrofurantoin therapy is reported [5].

Psychiatry related information on Furantoin

• The above differences between population controls and cases may be connected with recall bias, because the case-control pair analysis did not indicate a teratogenic potential of nitrofurantoin use during the second and the third months of gestation, i.e. in the critical period for major congenital abnormalities [6].

High impact information on Furantoin

• They were mucoid, and sensitive to ultraviolet light and the radiomimetic agent nitrofurantoin, which are characteristics of lon mutants [7].
• In contrast, the prevalence of resistance to nitrofurantoin, gentamicin, and ciprofloxacin hydrochloride was 0% to 2% among E coli and less than 10% among all isolates combined, and did not change significantly during the 5-year period [8].
• Nitrofurantoin, a commonly used urinary tract antiseptic, has been associated with idiosyncratic pulmonary and hepatic damage [3].
• The findings suggest that glutathione plays a major role in protecting cells from nitrofurantoin-induced damage, and that studies of lymphocyte toxicity and glutathione metabolism in patients experiencing idiosyncratic reactions to nitrofurantoin may lead to elucidation of the biochemical and genetic basis of drug susceptibility [3].
• Cells from a patient with glutathione synthetase deficiency showed markedly enhanced nitrofurantoin toxicity [3].

Chemical compound and disease context of Furantoin

• Results were available for 38,835 urinary isolates of E. coli that had been tested against ampicillin, cephalothin, ciprofloxacin, nitrofurantoin, and trimethoprim-sulfamethoxazole [9].
• The prevalence of furazolidone, nitrofurantoin, and metronidazole resistance among Helicobacter pylori strains was assessed with 431 clinical isolates [10].
• The main objectives of this study were to determine whether the nitroreductase enzyme encoded by the rdxA gene of Helicobacter pylori was responsible for reductive activation of nitrofurantoin and whether a triple-therapy regimen with nitrofurantoin was able to eradicate metronidazole-sensitive and -resistant H. pylori infections from mice [11].
• Ciprofloxacin-resistant Escherichia coli isolates (n = 1,858) from outpatient midstream urine specimens at 40 North American clinical laboratories in 2004 to 2005 were frequently resistant to ampicillin (79.8% of isolates) and trimethoprim-sulfamethoxazole (66.5%); concurrent resistance to cefdinir (9.0%) or nitrofurantoin (4.0%) was less common [12].
• Whilst the cure rate for Escherichia coli infection was similar, 81.5% cured with nitrofurantoin MR, 82.5% with co-trimoxazole and 78.4% by trimethoprim, for non-E. coli pathogens nitrofurantoin MR was equivalent to co-trimoxazole with 86.7% cure but higher than trimethoprim at 72.0% [13].

Biological context of Furantoin

• Alternative first-line agents include the fluoroquinolones, nitrofurantoin, and fosfomycin.Factors to be considered in the selection of appropriate antimicrobial therapy include pharmacokinetics, spectrum of activity of the antimicrobial agent, resistance prevalence for the community, potential for adverse effects, and duration of therapy [14].
• Two patients with diffuse interstitial lung disease after long-term nitrofurantoin therapy were characterized clinically by exertional dyspnea and basilar rales, roentgenographically by diffuse interstitial infiltrate and physiologically by a restrictive lung defect [15].
• The influence of food on nitrofurantoin bioavailability [16].
• The kinetics of the aerobic reduction of nitrofurantoin by NADPH-cytochrome P-450 Ic) reductase [17].
• The molecular components of nitrofurantoin critical to its inhibitory effect upon platelet aggregation [18].

Anatomical context of Furantoin

• The conclusion is proffered that nitrofurantoin-induced jaundice is not always due to cholestatic hepatitis, but can result from obstruction of the common bile duct due to edema of the pancreatic head secondary to nitrofurantoin pancreatitis [19].
• The ability of nitrofurantoin to interact with HbO2 and cause superoxide formation may represent one mechanism by which it produces red cell toxicity and suggests that generation of superoxide in erythrocytes may occur via a different mechanism than that which occurs in microsomes [20].
• Bovine chromaffin granules which synthesize and store catecholamines produced the nitrofurantoin anion radical when intact granules were treated with nitrofurantoin [21].
• Concentrations of rhein and nitrofurantoin in the micromolar range induce Ca2+ release and the development of increased inner membrane permeability in liver mitochondria [22].
• The formation of nitrofurantoin radical, semiquinone radicals of catecholamines, and oxygen-derived radicals by chromaffin granules is proposed to cause damage to adrenal medulla, and this process may lead to neurotoxicity [21].

Associations of Furantoin with other chemical compounds

• Nifurtimox and nitrofurantoin are reduced by intact rat liver mitochondria to nitro anion radicals whose autoxidation generates superoxide anion as detected by direct electron spin resonance spectroscopy and by spin-trapping experiments, respectively [23].
• In in vitro studies, nitrofurantoin therapy failed to induce lymphoblast transformation or histamine release [15].
• These drugs include chloral hydrate, hyaluronidase, nalidixic acid, nitrofurantoin, p-aminosalicylic acid, phenazopyridine, probenecid, and X-ray contrast media [24].
• In therapeutic trials, trimethoprim 200 to 400mg daily has been shown to be comparable in efficacy with co-trimoxazole, ampicillin 2g, cephalexin 2g, oxolinic acid 1.5g and nitrofurantoin 200mg daily in the treatment of acute urinary tract infection [25].
• The efficacy and tolerance of ofloxacin were compared with those of co-trimoxazole in upper urinary tract infections (UTIs) and nitrofurantoin in lower UTIs in a prospective, controlled, randomised, observer-blind study [26].

Gene context of Furantoin

• Further characterisation of pHL1 revealed that resistance to nitrofurantoin was due to the overexpression of the hslV-hslU operon which encodes an ATP-dependent protease complex in E. coli [27].
• Effects of the Flavonoid Chrysin on Nitrofurantoin Pharmacokinetics in Rats: Potential Involvement of ABCG2 [28].
• The SOS response was induced with nitrofurantoin, SOS induction of the gene sulA was determined on the basis of the amount of beta-galactosidase synthesized, i.e. by the SOS chromotest (Quillardet et al., 1982a) [29].
• Repair-deficient and repair-proficient strains of E. coli K12 were sensitive to nitrofurantoin treatment to varying degrees with the double mutant strain (uvrA 6, recA 13) being most sensitive [30].
• This model, using genetically defined target cell populations, clearly demonstrates the importance of endogenous catalase in protecting against nitrofurantoin-induced cytotoxicity, suggesting that H2O2 is a critical intermediary in the direct cell injury mediated by the drug [31].

Analytical, diagnostic and therapeutic context of Furantoin

• Side effects after treatment with nitrofurantoin [32].
• CONCLUSIONS: Ambulatory care physicians are increasing their use of fluoroquinolones and nitrofurantoin, even though they are not highly recommended and not the most cost-effective [33].
• Surgical site infections, STIs, and abscesses could be managed by surgical debridement and drainage without specific antimicrobial agents against VRE and UTIs could be resolved with nitrofurantoin or removal of Foley catheters [34].
• Nitrofurantoin (50 mg) was administered in a three-way random crossover design to six healthy men [35].
• After oral administration of the antibiotic nitrofurantoin, the area under the plasma concentration-time curve in wild-type female mice was approximately 2-fold higher than in wild-type male mice [36].

References