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PubMed2000

Furazolidone combination therapies for Helicobacter pylori infection in the United States.

BACKGROUND: Antibiotic resistance has begun to impair the ability to cure Helicobacter pylori infection. AIM: To evaluate furazolidone as a component of combination therapies for treatment of H. pylori infection in the United States. METHODS: Patients with active H. pylori infection received furazolidone combination therapy for 14 days (furazolidone 100 mg and tetracycline 500 mg t.d.s.; omeprazole 20 mg o.d. in the morning and, depending on the pre-treatment antimicrobial susceptibility pattern, 500 mg of metronidazole or clarithromycin t.d.s.). RESULTS: A total of 27 patients received the metronidazole containing combination (cure rate 100%) and seven received the clarithromycin combination (cure rate 86%). Overall the cure rates for intention-to-treat was 97% (95% CI: 85% to 100%). The single failure took the clarithromycin containing combination for only 2 days (per protocol cure rate = 100%). Side-effects were common and led to discontinuation of therapy in 26% of patients. An attempt to eliminate metronidazole and clarithromycin and use furazolidone, tetracycline, and lansoprazole b.d. produced an unsatisfactory cure rate of 72%. CONCLUSION: Furazolidone combination therapy appears to be effective. Additional studies with different antimicrobial combinations and duration of therapy are warranted.

Anti-Ulcer Agents↗

PubMed2003

Effect of different doses of furazolidone with amoxicillin and omeprazole on eradication of Helicobacter pylori.

BACKGROUND: Resistance to metronidazole is one of the most common reasons for Helicobacter pylori treatment failure with classic triple therapy. In contrast, the clarithromycin-based regimen is not cost-effective for developing countries. Furazolidone is a very good substitute for metronidazole and clarithromycin, but its many side-effects limit widespread use. The aim of the present study was to assess the efficacy of two different doses of furazolidone in combination with amoxycillin and omeprazole. METHODS: A total of 123 patients with duodenal ulcer were randomized and received the following medications for two weeks. Group A: furazolidone 2 x 200 mg + amoxycillin 2 x 1 g + omeprazole 2 x 20 mg/day. Group B: furazolidone 2 x 50 mg + amoxycillin 2 x 1 g + omeprazole 2 x 20 mg/day. Control endoscopy was performed after 6 weeks and two biopsy specimens from the antrum and two from the corpus were taken for a urease test and histology. Eradication was concluded if all tests were negative for H. pylori. RESULTS: In total, 110 patients completed the study. Four patients in group A did not tolerate the regimen on day 8 of therapy and were excluded from the study. Serious complications such as fever, and fatigue and dizziness, which occurred in the beginning of the second week of treatment (days 8-10), were more common in group A than in group B (19%, 15.9% and 14.3%, respectively, in group A vs 0% in group B). The eradication rate by per protocol analysis was significantly higher in group A than in group B (88.9%vs 67.9%, respectively, P = 0.008). However, this difference was low and not statistically significant by intention-to-treat analysis (76.2% in group A and 62.3% in group B, P = 0.09). CONCLUSION: The regimen with a non-reduced dose of furazolidone in combination with amoxycillin and omeprazole was effective when the patients tolerated the drugs and completed the study.

Adult↗

PubMed1988

The absorption of a new sustained release furazolidone formulation from the digestive tract of piglets and calves.

Chyme concentrations and total recoveries of furazolidone (5 mg/kg body-weight) were determined by a HPLC-method, after oral administration of two different furazolidone formulations to piglets (n = 6) and pre-ruminant calves (n = 8), provided with an ileal re-entrant canula. Additional blood samples were taken from the calves to measure the time dependent plasma levels of furazolidone. In the case of the normal crystalline preparation, the results indicate an almost complete absorption of the drug from the upper parts of the digestive tract. In both species, 96-99% of the dose had been absorbed by the time it reached the end of the ileum. The mean ileal recovery of the newly developed furazolidone formulation in calves and piglets was 14% and 38%, respectively. In calves the observed maximum plasma concentrations of furazolidone after oral application of the sustained release formulation were 14 times lower than with the normal crystalline preparation.

Administration, Oral↗

PubMed1988

Some effects of furazolidone on the testis and plasma levels of testosterone, luteinizing hormone and prolactin in mature male turkeys.

Adult male turkeys were treated orally with furazolidone at doses of 1, 2.5, 5 or 20 mg/kg for 14 days and their plasma analysed for luteinizing hormone (LH), testosterone and prolactin (PRL) concentrations before, during and after treatment. At 20 mg/kg the drug produced a significant decrease in the plasma levels of LH and testosterone at the end of treatment, whereas at 5 mg/kg the drug had no significant effect. Prolactin concentrations were unaffected by any of the drug doses used. Intramuscular injection of luteinizing hormone releasing hormone (LHRH) at a dose of 5 micrograms/kg produced after 30 min a significant rise in plasma levels of LH, an effect that was decreased significantly by treatment with 20 mg/kg furazolidone. Incubation of normal turkey semen with graded doses of furazolidone or nitrofurazone for up to 30 min resulted in a dose- and time-dependent decrease in sperm motility. At a concentration of 20 mg/ml a complete absence of sperm motility was observed after incubation with either drug, although, on the whole, nitrofurazone seemed more potent than furazolidone as a sperm-immobilizing agent. Histological changes occurred in the 20 mg/kg group and consisted of a decrease in spermatocyte production, corrugation of sperm cell nuclear envelopes and distention of the endoplasmic reticulum of elongate spermatids. It is concluded that furazolidone depresses pituitary LH output but may, in addition, directly affect spermatogenesis and sperm motility.

Animals↗

PubMed2001

Furazolidone- and nitrofurantoin-resistant Helicobacter pylori: prevalence and role of genes involved in metronidazole resistance.

The prevalence of furazolidone, nitrofurantoin, and metronidazole resistance among Helicobacter pylori strains was assessed with 431 clinical isolates. Fifty-two percent were metronidazole resistant, compared to 2% (7 of 431) with resistance to furazolidone and nitrofurantoin. All seven furazolidone- and nitrofurantoin-resistant isolates were also metronidazole resistant. rdxA, frxA, and fdxB knockouts did not result in furazolidone or nitrofurantoin resistance. These data suggest that furazolidone and nitrofurantoin may be good alternatives to metronidazole for treating H. pylori infection.

Anti-Infective Agents, Urinary↗

PubMed1989

Furazolidone and chloramphenicol for treatment of typhoid fever.

Seventy-one adults who were hospitalized between March 1985 and March 1987 were entered into a randomized, double-blind study to compare the efficacy and safety of furazolidone and chloramphenicol in therapy for typhoid fever. Patients received chloramphenicol capsules (total daily dosage, 2 g) plus placebo tablets for furazolidone tablets (total daily dosage, 800 mg) plus placebo capsules for 14 days. Seven patients were excluded from the analysis of efficacy because blood, bile, or bone marrow cultures at admission failed to demonstrate the presence of Salmonella typhi. Four additional patients were excluded because of intercurrent illness or failure to return for follow-up visits. Cure was achieved in 31 (97%) of 32 chloramphenicol recipients and 24 (86%) of 28 furazolidone recipients. In the chloramphenicol group, one patient experienced moderate sideroblastic anemia, and another experienced moderate neutropenia. Both adverse reactions resolved spontaneously within 7 days. Mild gastritis was reported by two patients who received furazolidone and one who received chloramphenicol. This study has demonstrated that furazolidone is an effective and safe alternative to chloramphenicol for the treatment of typhoid fever in adults.

Adult↗

PubMed1979

Effects of furazolidone in the early chick embryo.

Effects of furazolidone in early chick embryos were investigated in order to determine the feasibility of using this biological system as a model for studying the mechanism(s) of furazolidone toxicity. Double and triple injections of varying dosages of furazolidone were administered via the yolk sac at early stages of incubation. Toxic levels of the drug affecting both growth and levels of glycogen were dosage-dependent and time-dependent. Double injections of furazolidone at a dose as little as 60 microgram/egg administered at 40 and 72 hr of incubation significantly retarded growth (P less than .001) and increased glycogen levels (P less than .05) in the embryo and yolk sac. Mortality was high in embryos receiving toxic levels of furazolidone, but no gross abnormalities were observed.

Animals↗

PubMed1992

[In vitro studies of intestinal absorption and biotransformation of furazolidone].

The intestinal biotransformation and absorption of the nitrofuran furazolidone were investigated in isolated gut cells and in the isolated perfused gut. In case of inhibiting furazolidone metabolism by high oxygen tension almost equal concentrations of the parent compound were measured on the mucosal and serosal side of the perfused gut segments. Lowering oxygen supply in order to adjust it to physiological conditions caused a complete degradation of furazolidone in isolated gut cells. Accordingly, hardly any unchanged furazolidone was detected on the serosal side of the isolated perfused gut. An open-chain cyanometabolite was formed in both systems indicating a reductive metabolic process which induces highly reactive intermediates. This metabolite also reached the serosal side of the gut representing the systemic circuit. Thus, the low systemic bioavailability is due to the considerable intestinal metabolism rather than a limited absorption. Unknown metabolites will reach the systemic circuit, the toxic potential of which is still obscure. Independent of its metabolic degradation, thus probably due to its redox cycle furazolidone inhibited intestinal functions as e. g. the flow of water and the transport of sodium.

Animals↗

PubMed1978

Furazolidone-induced cardiomyopathy in turkeys. Association with a relative alpha1-antitrypsin deficiency.

A naturally occurring cardiomyopathy (round heart disease) which is potentiated by inbreeding and a cardiomyopathy produced by furazolidone, a nitrofuran derivative, were studied for an associated alpha1-antitrypsin deficiency in two flocks of turkeys (one inbred for round heart disease and a commercial flock). At 4 weeks of age, the furazolidone-fed birds of both flocks demonstrated a marked increase in mortality and cardiac dilatation associated with disordered hepatic metabolism when compared with controls. Although PAS-positive, diastase-resistant globules were observed in the livers of both strains of turkeys fed furazolidone, these globules were present in lysosomes and not in the rough endoplasmic reticulum as in alpha1-antitrypsin deficiency. The control inbred birds with round heart disease did not demonstrate histologic or biochemical evidence of an alpha1-antitrypsin deficiency. It is proposed that furazolidone in the turkey produces primary hepatic damage that is reflected in lowered total serum proteins, including trypsin inhibitory capacity, and that the alterations produced by furazolidone are superimposed on round heart disease in the inbred flock.

Animals↗

PubMedDate not supplied

Matrix solid phase dispersion (MSPD) isolation and liquid chromatographic determination of furazolidone in pork muscle tissue.

A method for the isolation and liquid chromatographic (LC) determination of furazolidone in pork muscle tissue is presented. Blank or furazolidone-fortified pork muscle tissue samples (0.5 g) were blended with octadecylsilyl (C18, 18% load, endcapped, 2 g) derivatized silica. A column made from C18/pork matrix was first washed with hexane (8 mL), followed by elution of furazolidone with ethyl acetate. The ethyl acetate extract was then passed through an activated alumina column. The eluate contained furazolidone that was free from interfering compounds when analyzed by LC with UV detection (photodiode array, 365 nm). Detector response with increasing concentrations of furazolidone isolated from fortified samples was linear (r = 0.998 +/- 0.002) with an average percentage recovery of 89.5 +/- 8.1% for the concentration range (7.8-250 ng/g) examined and resulted in a minimum detectable limit of 390 pg on column, and a detector response of more than 5 times baseline noise. The inter-assay variability was 9.9 +/- 5.4% with an intra-assay variability of 1.5%.

Animals↗

PubMed1989

[Effects of furazolidone on brain monoamines in the treatment of peptic ulcer].

The purpose of this study was to investigate the protective role of furazolidone against the formation of duodenal ulcer induced by cysteamine and the effect of furazolidone on NE, DA and 5-HT concentrations in various brain regions (telencephalon, diencephalon and brainstem). The results indicated that one dose of cysteamine (280 mg/kg) produced 90-92% ulceration with no mortality within the first 24 hours, whereas cysteamine plus furazolidone significantly decreased the duodenal ulceration from 90% to 0. Using a sensitive spectrofluorimetric method, we found that cysteamine markedly diminished the NE levels in all regions but the DA level only in telencephalon. Meanwhile, cysteamine plus furazolidone increased the DA level in the same region. This suggested that the protective role of furazolidone against the formation of duodenal ulcer induced by cysteamine in rat may be related to increased DA level in telencephalon.

Animals↗

PubMed1994

Stability-indicating first-derivative spectrophotometric determination of furazolidone.

A first derivative (1D) spectrophotometric method is described for the determination of furazolidone in the presence of its degradation product (5-nitrofuraldehyde). The method was based on the direct measurement at the maximum of the first derivative curve for furazolidone at 390 nm, which is the zero crossing point of 5-nitrofuraldehyde thus avoiding interference from the degradation product. 5-Nitrofuraldehyde was determined after thin-layer chromatographic separation using silica gel G254 as the coating substance, and mixture of toluene and 1.4-dioxan (95:5) as the developing system. After separation, furazolidone content and its degradation product, 5-nitrofuraldehyde, could be determined separately by first-derivative spectrophotometry at 390 and 290 nm, respectively. 2.5-25 micrograms ml-1 of furazolidone and 5-nitrofuraldehyde could be determined by this method with good accuracy. The proposed method was successfully applied to determine furazolidone in its tablets and 5-nitrofuraldehyde in expired tablets. The results obtained were in good agreement with those obtained by the official method.

Drug Stability↗

PubMed1976

[The effect of furazolidone or carbadox in the starter mixture for early-weaned piglets].

For a period of 14 days, piglets from six litters, weaned between the 25th and 28th day of age, were fed the COS 2 starter containing either a premix with furazolidone or carboadox of Czechoslovak origin. Bentonite hydrosilicate was used as a carrier in both cases. Furazolidone administered in the dose of 200 mg per 1 kg of feed prevented diarrhoea, insignificantly increased body weight gain, and decreased the consumption of feed per 1 kg of gain from 5.6 kg in the control to 4.0 kg in the test animals. Carbadox administered in the dose of 50 mg per 1 kg of feed suppressed the signs of enteritis in comparison with the control piglets, significantly increased body weight gains, and reduced feed consumption to 1.9 kg per 1 kg of gain. No differences were recorded in the concentration of blood glucose, total protein, and total cholesterol in plasma. The control piglets showed increased parameters of the adrenocortical function. The proportion (percentage) of haemolytic E. coli in rectum was affected neither by carbadox nor by furazolidone; furazolidone suppressed the occurrence of lactoso-negative strains. An insignificant drop of the number of haemolytic E. coki in the duodenum and jejunum of the furazolidone-and carbadox-treated piglets was observed after 14 days. With their clinical effects, the two substances tested manifest themselves as suitable for the reduction of losses in weaned piglets.

Adrenal Cortex↗

PubMed1991

Attenuating effect of the monoamine oxidase inhibitor furazolidone on the anti-carcinogenetic effect of cysteamine on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of furazolidone on inhibition by cysteamine of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in inbred Wistar rats. After oral treatment with MNNG for 25 weeks, rats received cysteamine, furazolidone, or both compounds. In week 52, rats treated with cysteamine had a significantly decreased incidence of gastric cancers. Concomitant treatment with furazolidone significantly attenuated the inhibitory effect of cysteamine on gastric carcinogenesis. Administration of furazolidone alone significantly increased the number, but not the incidence, of gastric cancers. The norepinephrine concentration of the antral portion of the gastric wall and the labelling index of the antral mucosa were significantly reduced in rats treated with cysteamine, and significantly higher in rats treated with both compounds than in those treated with cysteamine alone. These findings indicate that the cysteamine-induced inhibition of gastric carcinogenesis is mediated by catecholamines.

Adenocarcinoma↗

PubMedDate not supplied

An adaptive response of Vibrio cholerae strain OGAWA 154 to furazolidone.

Since furazolidone is an antimicrobial drug, any possibility of its evoking an adaptive response appears to be very important. This response was studied in Vibrio cholerae cells as a model system. In order to determine this response, a dose-response relation of these cells to furazolidone and the kinetics of inactivation of the drug were studied. The study of the adaptive response of these cells to furazolidone reveals that cells treated with a low concentration of furazolidone for a particular period were 100% more resistant to the lethal effects of a subsequent challenging dose than control cultures. Variation of the challenging dose level showed better survival of adapted cells than control cells. A time-dependent response study reveals a maximum response at 15-30 min, and a gradual fall thereafter.

Acclimatization↗

PubMed1991

The use of pig hepatocytes to study the nature of protein-bound metabolites of furazolidone: a new analytical method for their detection.

The biotransformation of furazolidone, both in vivo and in vitro, results in the formation of so-called bound metabolites. Following the incubation of pig hepatocytes with [14C]furazolidone, a dose- and time-related increase in the formation of bound metabolites was observed. After withdrawal of the drug from the medium, levels decreased gradually to about 50% within 36 hr. Using a newly developed method, it was shown that in the case of cells and liver microsomes at least 70% of the bound residues still contained the 3-amino-2-oxazolidinone (AOZ) side chain of furazolidone. For liver samples of piglets that had been treated orally with the drug for 10 days, followed by withdrawal periods of 2 hr or 14 days, fractions of releasable AOZ were 23 and 14%, respectively, equivalent to levels of 3.8 and 0.3 micrograms furazolidone/g of tissue, respectively. The release of the AOZ side chain of furazolidone from at least part of the bound metabolites shows their drug-related nature and highlights the requirement for both adequate withdrawal periods and the need for appropriate control methods. The relative simplicity of the newly developed method may be helpful in further establishing and controlling adequate withdrawal periods.

Animals↗

PubMed1984

The effect of furazolidone on fertility of male chickens.

In mature chickens, furazolidone (0.4% w/w, 10 days) decreased the weight of the testes, but did not affect significantly the concentrations of testosterone in testes and plasma, nor the concentrations of ascorbic acid, protein or cholesterol in the testes. Feeding furazolidone at a concentration of 0.08% w/w for 10 days decreased significantly the weights of the testes, wattles and combs. Treatment also produced significant reductions in the concentration of testosterone in plasma and testes, and some reductions in ascorbic acid, protein and cholesterol concentrations in the testes. Administration of furazolidone by crop tube at doses of 40 or 80 mg/kg for five days caused significant decreases in the concentrations of testicular and plasma testosterone, and reductions in ascorbic acid, protein and cholesterol concentrations in the testes. The sizes of the testes, wattles and combs were also significantly reduced. Monoamine oxidase activity in the testes was significantly inhibited by furazolidone. In all the treated birds testicular concentrations of 5-hydroxy-tryptamine were significantly raised, except in those fed the drug at a dose of 0.04% w/w for 10 days.

Animals↗

PubMed1991

Morphological changes associated with furazolidone-induced cardiomyopathy: effects of digoxin and propranolol.

The purpose of the present study was to examine light microscopic data qualitatively as well as quantitatively from an animal model of dilated cardiomyopathy in the turkey. A previous study reported the gross cardioprotective effect of propranolol and the lack of cardioprotection with digoxin in furazolidone-induced cardiomyopathy. It was therefore important to define whether the response of the myocardium to therapeutic interventions differed from the structural responses seen in their absence. In furazolidone-treated birds with resultant cardiac dilation there was myocyte hypertrophy, enlargement of nuclei and reorientation of subepicardial myocardial fibres. Similar changes were noted in birds receiving both furazolidone and digoxin. However, birds receiving propranolol, a non-selective beta-receptor antagonist, and furazolidone did not demonstrate a hypertrophic response or reorientation of fibres. These data indicate that propranolol maintained myocardial morphology and morphometry and thus prevented the structural sequelae of the disease, which is a better achievement of therapy than simple arrest of the progress. A role for intracellular calcium is implied. The cardioprotective effect seen with beta blockade suggests that membrane related events may lead to the contractile dysfunction that results in dilation and cardiac hypertrophy.

Animals↗