Anaphylactic reactions to cinoxacin. (1/7)

During 1981 to mid-1988 three cases of anaphylactic shock after treatment with the quinolone derivative cinoxacin were reviewed by the Netherlands Centre for Monitoring of Adverse Reactions to Drugs and 17 cases of an anaphylactic type of reaction notified to the World Health Organisation Collaborating Centre for International Drug Monitoring. In five out of six patients for whom data were available the reaction began shortly after taking a single capsule of a second or next course of treatment. Cinoxacin is related to nalidixic acid, and one patient previously treated with that agent subsequently had an anaphylactoid reaction to cinoxacin and later developed a skin reaction to nalidixic acid. There were no deaths, and patients treated as an emergency with plasma expanders or with adrenaline and corticosteroids generally recovered promptly and uneventfully. In view of the potentially fatal consequences of anaphylactic reactions to cinoxacin and other quinolones doctors should take care when prescribing these drugs.  (+info)

Cinoxacin: effectiveness against experimental pyelonephritis in rats. (2/7)

The antimicrobial activity of cinoxacin, 1-ethyl-4(1H)-oxo-[1,3]dioxolo[4,5-g]cinnoline-3-carboxylic acid, previously reported as compound 64716, was determined and compared with other antimicrobial agents at a dosage of 12 mg/kg once daily in a descending pyelonephritis rat model with Escherichia coli and Proteus mirabilis as infecting organisms. Cinoxacin was considerably more effective than either nalidixic acid or oxolinic acid when all three were administered orally at 3 mg/kg four times daily. The presence of demonstrable serum activity with a high recovery in urine indicates cinoxacin possesses highly desirable properties of an effective oral chemotherapeutic agent for urinary tract infections.  (+info)

Cinoxacin: pharmacokinetics and tolerance in patients with normal and impaired renal function. (3/7)

The pharmacokinetics of cinoxacin, a new antibacterial compound related to nalidixic acid and oxolinic acid, were investigated in 22 patients with varying degrees of renal impairment. After oral administration of cinoxacin at 500 mg every 12 h for 7 days to all patients, the drug was found to be well tolerated. The urine concentrations of cinoxacin in all patients far exceeded the minimal inhibitory concentrations for susceptible organisms commonly found in urinary tract infections. The serum half-life of cinoxacin in patients with normal renal function was approximately 2.7 h but increased to approximately 8.5 h in patients with creatinine clearance less than 30 ml/min. No undue drug accumulation was demonstrated in any patient group during the treatment. Highly significant correlations were found between the elimination rate constant and creatinine clearance and also between the elimination half-life and serum creatinine. The bioavailability of cinoxacin was independent of renal function.  (+info)

In vitro activities of ciprofloxacin, norfloxacin, pipemidic acid, cinoxacin, and nalidixic acid against Chlamydia trachomatis. (4/7)

The in vitro activities of five quinolinecarboxylic acids against two laboratory strains of Chlamydia trachomatis were compared. The minimal inhibitory concentrations of nalidixic acid, cinoxacin, and pipemidic acid were all greater than or equal to 50 micrograms/ml; the activity of norfloxacin was intermediate (minimal inhibitory concentration, 8 to 16 micrograms/ml). Ciprofloxacin was the most active of these drugs (minimal inhibitory concentration, 0.5 to 1 microgram/ml).  (+info)

Antibacterial activities of ciprofloxacin, norfloxacin, oxolinic acid, cinoxacin, and nalidixic acid. (5/7)

In vitro studies were performed comparing ciprofloxacin (Bay o 9867) and norfloxacin with three related organic acids. Ciprofloxacin was two to eight times more active than norfloxacin against 658 bacterial isolates representing 30 species. For all species tested, ciprofloxacin MICs for 90% inhibition were less than or equal to 2.0 micrograms ml. Additional tests with 5,994 isolates detected only 37 (0.6%) strains resistant to 2.0 micrograms of ciprofloxacin per ml and 106 (1.8%) resistant to 1.0 micrograms/ml. Only 6 (0.1%) of the 5,994 strains were resistant to 16 micrograms of norfloxacin per ml, and 129 (2.1%) were resistant to 4.0 micrograms/ml. The majority of resistant strains were streptococci or Pseudomonas spp. Resistance among the Enterobacteriaceae was extremely rare (i.e., greater than 99.8% susceptible to both drugs.  (+info)

Cross-resistance among cinoxacin, ciprofloxacin, DJ-6783, enoxacin, nalidixic acid, norfloxacin, and oxolinic acid after in vitro selection of resistant populations. (6/7)

Six different gram-negative bacilli were serially transferred through subinhibitory concentrations of seven quinolone derivatives or related organic acids. A gradual, stepwise decrease in susceptibility was noted with all seven drugs, and the resistant cultures demonstrated a concomitant cross-resistance to the other drugs.  (+info)

Influence of urinary pH on the pharmacokinetics of cinoxacin in humans and on antibacterial activity in vitro. (7/7)

The impact of acidification and alkalinization of the urine on the pharmacokinetics of cinoxacin was examined after single 500-mg oral doses were administered to nine healthy male volunteers. Acidic and alkaline conditions were achieved by repeated oral doses of ammonium chloride or sodium bicarbonate, respectively. Plasma cinoxacin levels in all subjects were adequately described in terms of one-compartment-model kinetics with first-order absorption and elimination. Acidification and alkalinization treatment had no effect on cinoxacin absorption or distribution. The mean elimination half-life of cinoxacin in plasma was 1.1, 2.0, and 0.6 h in control subjects and with acidification and alkalinization of urine, respectively. Recovery of intact cinoxacin in samples of urine collected 0 to 36 h after cinoxacin administration represented 65% of the dose in control subjects and urine acidification and 80% of the dose with alkalinization of urine. The mean renal clearance of cinoxacin was 76, 118, and 278 ml/min with acidification, control, and alkalinization, respectively, and renal clearance was highly correlated with urinary pH. Urine concentrations of cinoxacin were significantly higher with alkalinization compared with control values during the first 4 h after drug administration. Urine cinoxacin concentrations were reduced somewhat by acidification, but these tended not to be significantly different from control values. Changes in cinoxacin elimination owing to urine pH are less pronounced in humans than in dogs. The antibacterial activity of cinoxacin against some common urinary tract pathogens was pH dependent. A four- to eightfold reduction in cinoxacin activity was generally observed at pH 8 compared with lower pH values. However, in view of the high levels of cinoxacin which are obtained in both acidic and basic urine, the impact of urine pH on cinoxacin antibacterial efficacy would be of minor clinical importance.  (+info)