Nitrofurantoin

Abbreviations: PR, partial response; SD, stable disease; PD, progressive disease. * % Patients with an evaluable assay. cAmplified: EGFR chromosome 7 centromere ratio of 2.0. bLoss: 30% of nuclei with definitive loss and 20-30% with indeterminate loss. x High, 1-4 + intensity in z25% of tumor cells; low, either no staining or 1-4 + intensity in 25% of tumor cells. Submitted by: Lois Haggard, PhD, Project Director Utah Department of Health PO Box 14201 Salt Lake City, UT 84111 Submitted to: Cynthia Irvin, PhD, State Liaison Privacy and Security Solutions for Interoperable Health Exchange Research Triangle Institute PO Box 12194 3040 Cornwallis Rd Research Traingle Park, NC Contract No. 290-05-0015. Objectives: Fosfomycin is a possible oral treatment for lower urinary tract infections caused by Escherichia coli with CTX-M extended-spectrum b-lactamases but is vulnerable to mutational resistance. Hypermutability among natural E. coli populations might facilitate the emergence of resistance to fosfomycin. We therefore examined the prevalence of mutators amongst urinary isolates of E. coli producing CTX-M b-lactamases. Methods: Urinary E. coli isolates with CTX-M b-lactamases n 220 ; were screened for resistance to both rifampicin and fosfomycin, as well as a mutator phenotype, by rifampicin and fosfomycin disc assays. Mutation frequencies for 10 isolates, identified as mutators by the initial disc screen, were determined in triplicate on agar with rifampicin or fosfomycin at 4 MIC and with fosfomycin or nitrofurantoin at 256 mg L. Results: The disc screen identified 10 likely mutators and quantitative tests indicated that 9 of these had mutation frequencies of 8.0 1061.5 104 for fosfomycin and 0.12.3 106 for rifampicin. These mutators were diverse in terms of PFGE type and 4 of the 10 were confirmed as strong mutators with rifampicin and fosfomycin. Only the strongest mutator isolate and hypermutable MutS control strain consistently gave single-step mutants resistant to 256 mg L fosfomycin. No nitrofurantoin-resistant mutants were selected from any isolate, although they could be selected from the hypermutable MutS control strain. Conclusions: Mutator phenotypes were found among E. coli expressing CTX-M b-lactamases and were independent of strain type. These had an increased propensity to fosfomycin resistance. Keywords: hypermutators, nitrofurantoin, UTIs. 50 copies ml ; to be 80% after at least a year of treatment 22, 23 ; . Further, therapies for HIV are becoming more compact, with fewer pills and once-daily dosing options available. HIV treatment is also increasingly well-tolerated. Therefore, dramatic suppression of viral replication permitting CD4 + cell count reconstitution can and should be expected of antiretroviral therapy that is not onerous and is usually well tolerated. Guidelines on the composition of initial HIV therapy are maintained by the U.S. Department of Health and Human Services DHHS ; and the International AIDS Society IAS ; and are useful documents worthy of careful reading 24, 25 ; . The U.S. guidelines recommend preferred and alternative regimens based on available data regarding efficacy and tolerability Table 1 ; . As new data become available, the guidelines are updated. This document is a must-read for anyone prescribing antiretroviral therapy and imodium.

Hormone deprivation with castration or drugs designed to lower testosterone levels results in bone mineral loss fracture rate increases in this setting and antivert.
Ington, D.C. The opinions expressed herein are those of the authors and do not necessarily reflect the views of USAID.
Redox dye-based aerobic assays Alamar Blue assay, tetrazoliumbased assay, resazurin reduction assay ; have been used to assess drug susceptibility of M. tuberculosis isolates.4, 5, 8, 12 Here we combined the in vitro model of dormancy with the resazurin reduction assay to develop robust whole cell assays to screen for anti-dormancy anti-tubercular compounds using H37Rv, BCG and M. smegmatis. Furthermore, all the nitrofurans showed substantial bactericidal activity in the aerobic REMA assay; these results were in agreement with previous observations, 3 in BCG by the cfu assay. MICs of streptomycin, ethambutol and ofloxacin against the fast-growing mycobacterium M. smegmatis matched with those obtained for H37Rv and BCG and also correlated well among the REMA and cfu assays. The MIC obtained by both REMA and cfu assays for rifampicin was higher than that obtained with H37Rv and BCG but similar to a previous finding in M. smegmatis.17 For isoniazid, ethionamide and p-aminosalicylic acid, higher MICs were obtained by the REMA assay. Since the MICs for these drugs by the cfu assay were comparable to those for slow-growing mycobacteria, the apparently discrepant REMA MICs may be ascribed to the rapid growth of M. smegmatis in the liquid medium with an associated overexpression of the target genes, 18, 19 and not due to inherent differences in the mechanism s ; of drug action between the species. Broadly speaking, the efficiency and the advantages of using M. smegmatis for the rapid and safe screening of anti-tubercular compounds outweigh the quantitative discrepancies in MICs that may be noted between H37Rv and the surrogate strain. Four drugs including metronidazole, nitrofurazone, furaltadone and nitrofurantoin, were used to develop the hypoxic HyRRA assay, as they were previously reported to exhibit anti-mycobacterial activity under anoxic conditions.2, 11 In the presence of metronidazole at 1711.6 mg L 10 mM ; the cultures remained blue post-resazurin addition and thereby confirmed bactericidal activity of metronidazole against dormant mycobacteria Figure S1 ; . Furthermore, isoniazid-treated H37Rv cultures remained pink even at test concentrations that were .10-fold higher than the MIC for aerobically cultured H37Rv Figure S1 this confirmed the dormant nature of hypoxia-adapted cultures in the HyRRA assay. At higher concentration of nitrofurans, a concordance in drug MICs was noted for HyRRA and cfu assays Figure 1a ; . However, at 10-fold lower drug concentrations, a disparity was noted for some of the drugs. For instance, by the cfu assay .99% loss of H37Rv viability was noted in the presence of 9.9 mg L 50 mM ; of nitrofurazone; however, by the HyRRA assay only 49% loss of viability was observed. Similarly, only 43% and 15% loss in viability was observed in the presence of 171.16 mg L 1 mM ; and 85.58 mg L 500 mM ; of metronidazole in contrast to 95% and 89% inhibition obtained with the cfu assay. On the other hand, a consensus in MIC was noted with nitrofurantoin by both the assays. The differences in MICs by the two assays might be explained by the fact that dormant cultures of H37Rv were unable to grow on solid medium plates but were maintained in viable form in broth cultures.20 Therefore, broth culture-based HyRRA assay truly reports the loss of viability in drug-treated dormant cultures and determines the MICs more accurately. Analogous drug assays were also established for BCG and M. smegmatis and MICs of test drugs were comparable to those obtained for H37Rv Figure 1b and c ; . In smegmatis MICs of nitrofurans were more than 10-fold higher !500 mM ; by the HyRRA assay in comparison with those determined by the cfu assay. A useful feature of the HyRRA assay is its ability to distinguish between the bactericidal or bacteriostatic effect of a drug. An overnight incubation of drug-treated dormant culture with resazurin reported bacterial viability by a change in colour of the redox dye Figure S1 ; . Prolonged incubation of these and colace.
REFERENCES 1. Browman GP, Levine MN, Mohide EA, Hayward RSA, Pritchard KI, Gafni A, et al. The practice guidelines development cycle: a conceptual tool for practice guidelines development and implementation. J Clin Oncol. 1995; 13: 502-12. Browman GP, Newman TE, Mohide EA, Graham ID, Levine MN, Pritchard KI, et al. Progress of clinical oncology guidelines development using the practice guidelines development cycle: the role of practitioner feedback. J Clin Oncol. 1998; 16 3 ; : 1226-31. 3. Bolderston A, Lloyd NS, Wong RKS, Holden L, Robb-Blenderman L, and the Supportive Care Guidelines Group of Cancer Care Ontario Program in Evidence-based Care. The Prevention and Management of Acute Skin Reactions Related to Radiation Therapy: A Systematic Review and Practice Guideline. Support Care Cancer. 2006; 14: 802-17.
Let he who will, snipe at the words of the eminent Dr. Swift! As for me, I do not egret for a moment robin from his essay! I would shrike my duty as an author if I failed to add that, since the submission of the original manuscript, I have encountered two individuals with chronic nitrofurantoin pulmonary reactions whose auscultatory findings were indistinguishable from those in and depakote.

MOL#10439 LEGENDS FOR FIGURES Fig. 1. Transepithelial transport of nitrofurantoin 10 M ; in MDCKII parent ; A ; , MDCKII-Bcrp1 B and C ; , MDCKII-BCRP D and E ; , MDCKII-MDR1 F ; and MDCKII-MRP2 G ; monolayers. The experiment was started with the addition of nitrofurantoin to one compartment basolateral or apical ; . After 2 and 4 hours, the percentage of drug appearing in the opposite compartment was measured by HPLC and plotted. BCRP inhibitor Ko143 C and E ; was present as indicated. Results are the means; error bars sometimes smaller than the symbols ; indicate the standard deviations n 3 ; . Closed circles: translocation from the basolateral to the apical compartment; open circles: translocation from the apical to the basolateral compartment. Thailand Beyrer C, Suwanvanichkij V, Mullany L, Richards AK, Franck N, Samuels A, Lee TJ, "Responding to AIDS, Tuberculosis, Malaria, and Emerging Infectious Diseases in Burma: Dilemmas of Policy and Practice." PLOS Med, October 2006, 3 10 ; : pp e-393. Tovanabutra S, Beyrer C, Sakkhachornphop S, et.al., "The Changing Molecular Epidemiology of HIV Type 1 among Northern Thai Drug Users, 1999 to 2002." AIDS Research and Human Retroviruses, 2004, 20 5 ; : pp 465-475 and imuran. DMD 11684 Moon JY, Lee DW and Park KH 1998 ; Inhibition of 7-ethoxycoumarin O-deethylase activity in rat liver microsomes by naturally occurring flavonoids: structure-activity relationships. Xenobiotica 28: 117-126. Paul MF, Paul HE, Bender RC, Kopko F, Harrington CM, Ells VR and Buzard JA 1960 ; Studies on the distribution and excretion of certain nitrofurans. Antibiot Chemother 10: 287-302. Pavek P, Merino G, Wagenaar E, Bolscher E, Novotna M, Jonker JW and Schinkel AH 2005 ; Human breast cancer resistance protein: interactions with steroid drugs, hormones, the dietary carcinogen 2-amino-1-methyl-6-phenylimidazo 4, 5-b ; pyridine, and transport of cimetidine. J Pharmacol Exp Ther 312: 144-152. Siess MH, Le Bon AM, Canivenc-Lavier MC, Amiot MJ, Sabatier S, Aubert SY and Suschetet M 1996 ; Flavonoids of honey and propolis: characterization and effects on hepatic drugmetabolizing enzymes and benzo[a]pyrene-DNA binding in rats. J Agric Food Chem 44: 2297-2301. Sparreboom A, Cox MC, Acharya MR and Figg WD 2004 ; Herbal remedies in the United States: potential adverse interactions with anticancer agents. J Clin Oncol 22: 2489-2503. Tanaka Y, Slitt AL, Leazer TM, Maher JM and Klaassen CD 2005 ; Tissue distribution and hormonal regulation of the breast cancer resistance protein Bcrp Abcg2 ; in rats and mice. Biochem Biophys Res Commun 326: 181-187. van Herwaarden AE, Jonker JW, Wagenaar E, Brinkhuis RF, Schellens JH, Beijnen JH and Schinkel AH 2003 ; The breast cancer resistance protein Bcrp1 Abcg2 ; restricts exposure to the dietary carcinogen 5-b]pyridine. Cancer Res 63: 6447-6452. van Herwaarden AE and Schinkel AH 2006 ; The function of breast cancer resistance protein in epithelial barriers, stem cells and milk secretion of drugs and xenotoxins. Trends Pharmacol Sci 27: 10-16. van Zanden JJ, Wortelboer HM, Bijlsma S, Punt A, Usta M, Bladeren PJ, Rietjens IM and Cnubben NH 2005 ; Quantitative structure activity relationship studies on the flavonoid mediated inhibition of multidrug resistance proteins 1 and 2. Biochem Pharmacol 69: 699-708. Veronese M, Salvaterra M, Barzaghi D and Setnikar I 1974 ; Urinary excretion in the rat of nifurpipone NP ; and of nitrofurantoin NTF ; administered by different routes. Arzneimittelforschung 24: 39-43. Walle T, Otake Y, Brubaker JA, Walle UK and Halushka PV 2001 ; Disposition and metabolism of the flavonoid chrysin in normal volunteers. Br J Clin Pharmacol 51: 143-146.
Reductase Fig. 3 ; and since mitochondria generatesignificant amounts of glutathione peroxidase substrates e.g. Refs. 51, 52 ; , theobserved oxidation of GSH is readily explained. The reason for the selective reduction states of NADH is less certain. Apparently, rhein further reduces the capacity for NAD P ; reduction. Since it inhibits NADH dehydrogenase at a site distinctfrom that of rotenone 44 ; , may further it reduce leakage-dependent production of NADH by reverse electron transport. In addition, the structure compound of the Fig. 1 ; shows that it is relatively lipophilic and a weak acid. Therefore, rheinshould be accumulated into the matrix space at the expense of the pH gradient and may reach intramitochondrialconcentrations which are high enough to allow inhibition of theotherNAD P ; -dependent dehydrogenase 44 ; . Sincethe compound also inhibitsenergy-dependent transhydrogenase 44 ; , NADPH becomes highly isolated from electron flow from either direction within the pathway shown in Fig. 8. Any remaining source of NADPH A'H2 in Fig. 8 ; could then readily maintain a reduced state of that nucleotide as seen in Fig. 5 or produce a specific rereduction of NADP as seen in Fig. 6. Alternatively, it is probable that the inhibitions of transhydrogenase and glutathione reductase by rhein are not complete. If the remaining activity transhydrogenof ase happens tobe greater than that glutathione reductase, of an accumulation of NADPH would be expected due to the energy-linked character of that reaction which shiftsthe equilibrium strongly towards NADPH 53-55 ; . Two little is known about the inhibitory actions of nitrofurantoin to discuss its sites of action in detail. However, it is clear from Table I1 that withrespect tothe production of selective reduction states it has activities analogous to those of rhein. The data in Fig. 7 do not support a direct role for pyridine nucleotide ratios in regulating the sensitivityof mitochondria to the permeability increase produced by Ca2 + .Regardless of whether both nucleotides are oxidized or reduced or differof entially oxidized and reduced at the time Ca2 + addition, the mitochondria become permeable upon accumulating the cation, providing that the content of GSH is low. The combinations of NAD P ; H and GSH levels shown in Fig. 7 are not Acknowledgment-We thankRandy J. Krebsbachfortechnical changed significantly by theaddition of Ca' + . The small assistance with portionsof his work. transient oxidation of NAD P ; H which is seen during Ca2 + REFERENCES uptake is reversed prior to the beginning of swelling data not 1. Fiskum, G., andLehninger, A. L. 1981 ; in Calcium and Cell shown ; . Thus, the combinations coenzyme levels shown in of Function Cheung, W . Y., ed ; Vol. 11, pp. 39-80, Academic Fig. 7 continue to exist while the mitochondria remain intact. Press, New York As swelling occurs, reduced nucleotides become oxidized due 2. Williamson, J. R., Cooper, R. H., and Hoek, J. B. 1981 ; Biochim. to collapse of the pH gradient see Ref. 9 ; and are perhaps Biophys. Acta 639, 243-295 degraded as described by Lotscher et al. 26 ; . This eventual : 3. Nicholls, D., andAkerman, K. 1982 ; Riochim.Biophys.Acta 683, 57-88 loss of reduced nucleotide thus occurs after the development and cytoxan. Metidine, nitrofurantoin, and probenecid did not overlap the range encompassing the 95% confidence intervals of 50 to 200% of the predicted M S values for each of these drugs. The respective M S observed values were 103, 9.3, and 4.7 times predicted for nitrofurantoin, cimetidine, and probenecid. However, the confidence intervals overlapped for the predicted and observed M S of p-aminohippurate. Table 1 provides the M S and Cls for the agents studied in the absence or presence of an inhibitor. Steady state was achieved in each infusion for each agent data not shown ; . Figures 1 and 2 provide steady-state plots of the serum and milk concentrations for a group of rats receiving cimetidine and nitrofurantoin. The M S for cimetidine was significantly decreased by coadministration of nitrofurantoin. Also, nitrofurantoin decreased cimetidine Cls. The coadministration of cimetidine did not significantly alter the M S of nitrofurantoin. However, cimetidine inhibited the Cls of nitrofurantoin. Probenecid increased the M S of cimetidine but did not alter cimetidine Cls. Probenecid did not significantly change either nitrofurantoin M S or Cls. The M S of PAH was not significantly changed by probenecid. Furthermore, it was not. While the choice of antibiotic discs can vary, gram positive organisms are generally tested using the following antibacterial agents: a-01 clindamycin 2-mcg a-02 lincomycin 2 mcg a-03 erythromycin 15 mcg a-04 penicillin g 10 units a-05 oxacillin 1-mcg or a-06 methicillin 5 mcg a-07 cephalothin 30 mcg a-08 tetracycline 30 mcg a-09 gentamicin 10 mcg likewise, gram negative organisms are generally tested using the following antibacterial agents: a-10 ampicillin 10 mcg a-07 cephalothin 30 mcg a-08 tetracycline 30 mcg a-09 gentamicin 10 mcg a-11 carbenicillin 100 mcg a-12 kanamycin 30 mcg a-13 tobramycin 10 mcg a-14 amikacin 30 mcg a-15 nitrofurantoin 300 mcg a-16 trimethoprim 5 mcg or a-17 sulfamethoxazole 25 mg price and ordering information a-18 laboratory handout and levothroid. Probably is adsorption of nitrofurantoin onto the surface of magnesium trisilicate. Uricosuric drugs, such as probenecid and sulfinpyrazone, can inhibit renal tubular secretion of nitrofurantoin. The resulting increase in nitrofurantoin serum levels may increase toxicity, and the decreased urinary levels could lessen its efficacy as a urinary tract antibacterial. Drug Laboratory Test Interactions: As a result of the presence of nitrofurantoin, a false-positive reaction for glucose in the urine may occur. This has been observed with Benedict's and Fehling's solutions but not with the glucose enzymatic test. Carcinogenesis, Mutagenesis, Impairment of Fertility: Nitrofkrantoin was not carcinogenic when fed to female Holtzman rats for 44.5 weeks or to female Sprague-Dawley rats for 75 weeks. Two chronic rodent bioassays utilizing male and female Sprague-Dawley rats and two chronic bioassays in Swiss mice and in BDF1 mice revealed no evidence of carcinogenicity. Ni6rofurantoin presented evidence of carcinogenic activity in female B6C3F1 mice as shown by increased incidences of tubular adenomas, benign mixed tumors, and granulosa cell tumors of the ovary. In male F344 N rats, there were increased incidences of uncommon kidney tubular cell neoplasms, osteosarcomas of the bone, and neoplasms of the subcutaneous tissue. In one study involving subcutaneous administration of 75 mg kg nitrofurantoin to pregnant female mice, lung papillary adenomas of unknown significance were observed in the F1 generation. Nitrofurantoih has been shown to induce point mutations in certain strains of Salmonella typhimurium and forward mutations in L5178Y mouse lymphoma cells. Nitrofurantin induced increased numbers of sister chromatid exchanges and chromosomal aberrations in Chinese hamster ovary cells but not in human cells in culture. Results of the sex-linked recessive lethal assay in Drosophila were negative after administration of nitrofurantoin by feeding or by injection. Njtrofurantoin did not induce heritable mutation in the rodent models examined. The significance of the carcinogenicity and mutagenicity findings relative to the therapeutic use of nitrofurantoin in humans is unknown. The administration of high doses of nitrofurantoin to rats causes temporary spermatogenic arrest; this is reversible on discontinuing the drug. Doses of 10 mg kg day or greater in healthy human males may, in certain unpredictable instances, produce a slight to moderate spermatogenic arrest with a decrease in sperm count. Pregnancy: Teratogenic effects: Pregnancy Category B. Several reproduction studies have been performed in rabbits and rats at doses up to six times the human dose and have revealed no evidence of impaired fertility or harm to the fetus due to nitrofurantoin. In a single published study conducted in mice at 68 times the human dose based on mg kg administered to the dam ; , growth retardation and a low incidence of minor and common malformations were observed. However, at 25 times the human dose, fetal malformations were not observed; the relevance of these findings to humans is uncertain. There are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed. Non-teratogenic effects: Nitrofurantoin has been shown in one published transplacental carcinogenicity study to induce lung papillary adenomas in the F1 generation mice at doses 19 times the human dose on a mg kg basis. The relationship of this finding to potential human carcinogenesis is presently unknown. Because of the uncertainty regarding the human implications of these animal data, this drug should be used during pregnancy only if clearly needed.

TABLE II Kinetic constants for the hydrolysis of the Phe8Xaa9 bond in Ang I and its analogs [Phe9]Ang I, [Arg10]Ang I, and [Phe9, Arg10]Ang I by the wild-type h-ACE C-domain and its mutants Y1096F, K1087A, and Y1096F K1087A Kinetic constants were determined in 50 mM HEPES buffer, pH 7.5, containing 50 mM NaCl and 10 mM ZnSO4 at 37 C. and kcat values were determined by nonlinear regression; values are means S.E. of three independent determinations for each peptide. Where individual kcat and Km values could not be determined independently indicated by a dash ; due to weak binding and limited solubility of substrates, kcat Km was determined from triplicate measurements of initial velocity v ; at low substrate concentration [S] Km ; , where v kcat Km ; [E]0[S]. Substrate Ang I [Phe9]Ang I [Arg10]Ang I [Phe9, Arg10]Ang I Ang I [Phe9]Ang I [Arg10]Ang I [Phe9, Arg10]Ang I Ang I [Phe9]Ang I [Arg10]Ang I [Phe9, Arg10]Ang I Ang I [Phe9]Ang I [Arg10]Ang I [Phe9, Arg10]Ang I Ang I [Phe9]Ang I [Arg10]Ang I [Phe9, Arg10]Ang I Enzyme Wild type Wild type Wild type Wild type Y1096F Y1096F Y1096F Y1096F K1087A K1087A K1087A K1087A Y1096F K1087A Y1096F K1087A Y1096F K1087A Y1096F K1087A R1098Q R1098Q R1098Q R1098Q Km M 52 0.18 32 -- 56 1.8 46 - - 25 0.06 - - 100 0.2 42 kcat s1 52 0.17 550 -- 110 1.3 57 - - 6.5 0.03 - - 60 0.3 1, kcat Km s1M1 1.0 0.004 17 and purinethol and Cheap nitrofurantoin.

462. Wininger DA, Fass RJ. Antibiotic-impregnated cement and beads for orthopedic infections. Antimicrob Chemother. 1996; 40: 26759. Mauerhan DR, Nelson CL, Smith DL et al. Prophylaxis against infection in total joint arthroplasty. J Bone Joint Surg. 1994; 76A: 3945. Liebergall M, Mosheiff R, Rand N et al. A double-blinded, randomized, controlled clinical trial to compare cefazolin and cefonicid for antimicrobial prophylaxis in clean orthopedic surgery. Israel J Med Sci. 1995; 31: 624. McQueen MM, Hughes SPF, May P et al. Cefuroxime in total joint arthroplasty. Intravenous or in bone cement. J Arthroplasty. 1990; 5: 16972. Josefsson G, Kolmert L. Prophylaxis with systematic antibiotics versus gentamicin bone cement in total hip arthroplasty. A ten-year survey of 1, 688 hips. Clin Orthop. 1993; 292: 2104. Nelson CL, Green TG, Porter RA et al. One day versus seven days of preventive antibiotic therapy in orthopedic surgery. Clin Orthop. 1983; 176: 25863. Gibbons RP, Stark RA, Gorrea RJ et al. The prophylactic use--or misuse--of antibiotics in transurethral prostatectomy. J Urol. 1978; 119: 3813. Ferrie B, Scott R. Prophylactic cefuroxime in transurethral resection. Urol Res. 1984; 12: 27981. Upton JD, Das S. Prophylactic antibiotics in transurethral resection of bladder tumors: are they necessary? Urology. 1986; 27: 4213. Houle AM, Mokhless I, Sarto N et al. Perioperative antibiotic prophylaxis for transurethral resection of the prostate: is it justified? J Urol. 1989; 142: 3179. Fair WR. Perioperative use of carbenicillin in transurethral resection of the prostate. Urology. 1986; 27 suppl 2 ; : 158. 473. Shah P, Williams G, Chaudary M et al. Short-term antibiotic prophylaxis and prostatectomy. Br J Urol. 1981; 53: 33943. Morris MJ, Golovsky D, Guinness MDG et al. The value of prophylactic antibiotics in transurethral prostatic resection: a controlled trial, with observations on the origin of postoperative infection. Br J Urol. 1976; 48: 47984. Gonzalez R, Wright R, Blackard CE. Prophylactic antibiotics in transurethral prostatectomy. J Urol. 1976; 116: 2035. Hills NH, Bultitude MI, Eykyn S. Co-trimoxazole in prevention of bacteriuria after prostatectomy. Br Med J. 1976; 2: 4989. Dorflinger T, Madsen PO. Antibiotics prophylaxis in transurethral surgery. Urology. 1984; 24: 6436. Matthew AD, Gonzales R, Jeffords D et al. Prevention of bacteriuria after transurethral prostatectomy with nitrofurantoin macrocrystals. J Urol. 1978; 120: 4423. Childs SJ, Wells WB, Mirelman S. Antibiotic prophylaxis for genitourinary surgery in community hospitals. J Urol. 1983; 130: 3058. Nielsen OS, Maigaard S, Frimdt-Mller N et al. Prophylactic antibiotics in transurethral prostatectomy. J Urol. 1981; 126: 602. Charton M, Vallancien G, Veillon B et al. Antibiotic prophylaxis or urinary tract infection after transurethral resection of the prostate: a randomized study. J Urol. 1987; 138: 879. Ramsey E, Sheth NK. Antibiotic prophylaxis in patients undergoing prostatectomy. Urology. 1983; 21: 3768.

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