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Although hypoglycemia is known to be associated with levofloxacin, patients are continually being hospitalized because of this adverse event. Here we have reported two further cases of severe hypoglycemia and discussed the possibility that the hypoglycemia is the result of interactions between levofloxacin and certain drugs, in order to alert physicians to be aware that geriatric patients, particularly those with Type 2 diabetes and in polytherapy, are at risk of showing this adverse reaction. CASES SUMMARY: A 91-year-old woman with Type 2 diabetes on metformin and glibenclamide, also under treatment with oral antihypertensive drugs, platelet antiaggregant, low-molecular- weight heparin and buprenorphine, was prescribed levofloxacin for a bacterial infection. Liver function and renal function parameters were within normal limits. After repeated administration of levofloxacin, her serum glycemic levels had decreased to 47 mg/dl and the patient was in a coma. After stopping levofloxacin her glycemia level returned to the normal value. A 61 year-old male, affected by tonsillar squamous cell carcinoma, with Type 2 diabetes on metformin and glibenclamide, under treatment with low-molecular-weight heparin for deep venous thrombosis, hydromorphone and undergoing nutritional support, was treated with levofloxacin for a bacterial infection. After 72 h the patient was unresponsive and his blood glucose levels were 38 mg/dl. After discontinuation of levofloxacin administration the patient was treated with glucose infusion and his glycemic values gradually returned to the normal range.
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To evaluate the efficacy of prulifloxacin versus levofloxacin therapy in severe COPD patients with exacerbations of chronic bronchitis.
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One hundred and forty patients aged 45 to 70 years old, with a PSA level between 2.5 and 10 ng/mL and normal digital rectal examinations (DRE), were included in this study between June 2009 and November 2010. The patients were randomly assigned into two groups. The first group received oral levofloxacin 500 mg 1*1 for 21 days; the second, the control group, was given no treatment. Initially, total PSA, free PSA, a DRE, urinary ultrasonography (including prostate volume, postvoiding residual urine), uroflowmetry, International Prostate Symptom Score, National Institutes of Health Chronic Prostatitis Symptom Index, and International Index of Erectile Function tests were performed. All of these were repeated at the end of 3 weeks of antibiotic treatment. An additional PSA measurement was also performed at day 10 of the treatment. All patients underwent transrectal ultrasonography (TRUS) guided prostate biopsy at day 21, just the day after the final (third) PSA sampling.
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Acinetobacter baumannii, an aerobic, non-motile, gram-negative bacterium is an important nosocomial pathogen which shows resistance to the most antibiotics. Carbapenems are the most commonly used antibiotics for the treatment of infections caused by this pathogen. However the emergence of resistance against carbapenems in an increasing rate generates serious problems for antimicrobial therapy. The aims of this study were to detect the antibiotic susceptibility, and the presence of blaOXA resistance genes of clinical A.baumannii isolates and to determine the clonal relationship between these isolates. A total of 79 A.baumannii strains isolated from various clinical specimens (37 respiratory tract samples, 11 wound, 10 blood, 8 catheters, 6 tissue, 5 urine, 2 abscess) of the patients admitted to Mersin University Medical School Hospital between May 2012-January 2013, were included in the study. The isolates were identified by conventional methods and Vitek®2 Compact automated system. Antibiotic susceptibilities of the isolates were determined by Kirby-Bauer disk diffusion method and evaluated according to CLSI criteria. The presence of blaOXA-51, blaOXA-23, blaOXA-24, blaOXA-48 and blaOXA-58 genes were detected by an in-house polymerase chain reaction (PCR), and the clonal relationship between the isolates were identified by pulsed-field gel electroforesis (PFGE) using the ApaI restriction enzyme. In our study, all of the isolates were susceptible to colistin, while the resistance rates against piperacillin-tazobactam, ciprofloxacin, imipenem, meropenem, cefoperazone/sulbactam, trimethoprim-sulfamethoxazole, ceftazidime, levofloxacin, gentamicin, tetracycline, ampicillin-sulbactam, amikacin, netilmicin and tigecycline were 97.5%, 96.2%, 94.9%, 94.9%, 93.6%, 91.1%, 88.6%, 86%, 83.6%, 77.2%, 69.6%, 55.7%, 27.8% and 3.8%, respectively. All the isolates were identified as A.baumannii with the OXA-specific PCR and OXA16S rDNA sequence analysis. All of the isolates (100%) harboured blaOXA-51 and 71 (89.9%) harboured blaOXA-23 gene, however they were all negative for blaOXA-24, blaOXA-48 and blaOXA-58 genes. According to PFGE results 10 pulsotypes were identified, of these eight pulsotypes formed 77 (97.5%) similar strains with indistinguishable PFGE profiles ranging between 3-30 [A (n= 30), B (n= 20), C (n= 9), D (n= 5), E (n= 4), F (n= 3), G (n= 3), H (n= 3)]. When compared with the other clones, clones A and B were dominant among the samples and they have exhibited high level of antibiotic resistance. The rest two pulsotypes [I (n= 1), J (n= 1)] were in close relation with the main cluster. No common outbreak isolate was detected, but the relationship between the majority of the strains pointed out that there was a cross contamination problem in our hospital. In conclusion blaOXA-51 and blaOXA-23 were detected as predominant genes responsible from carbapenem resistance in our clinical A.baumannii strains, and it was considered that the high prevalence of clones A and B may constitute a threat in terms of hospitalized patients.
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To compare the effectiveness and security of levofloxacin treatment in front betalactamic therapy in patient with community-acquired pneumonia that require hospitalization (CAPH).
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From 777 patients, 119 were positive for H. pylori where a total of 187 strains were isolated. The resistance rates were noted to be 37.4% (metronidazole), 2.1% (clarithromycin), 1% (levofloxacin and ciprofloxacin), and 0% (amoxicillin and tetracycline). Different resistance profiles were observed among isolates from the antrum and corpus of 13 patients. Resistance to one type of antibiotic was observed in 36.4% of the strains where mono-resistance to metronidazole was the most common. Resistance to ≥2 antibiotics was noted in 3.3% of isolates. High metronidazole MICs of ≥256 μg/mL were observed among the resistant strains.
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The in vivo efficacy of the novel quinolone gemifloxacin (SB-265805) was examined in a rat respiratory tract infection (RTI) model against four strains of Streptococcus pneumoniae and two strains of Haemophilus influenzae with varying susceptibilities to standard antimicrobial agents. Animals were infected intrabronchially to produce pneumonia and therapy with oral gemifloxacin, amoxycillin-clavulanate, ciprofloxacin, cefuroxime, azithromycin, trovafloxacin, grepafloxacin or levofloxacin was started 24 h after infection. The doses administered were chosen to approximate in the rat the serum or tissue concentrations measured in humans following therapeutic dosing. Therapy continued once- or twice-daily for 3 days, and approximately 17 h after the end of therapy the lungs were excised for bacterial enumeration. Following infection with strains of S. pneumoniae, gemifloxacin produced a 3-5 log reduction in bacterial numbers compared with untreated animals. Gemifloxacin was as effective as amoxycillin- clavulanate, and was as potent or more potent than all other comparators. Notably, the quinolone agents trovafloxacin, ciprofloxacin, grepafloxacin and levofloxacin were significantly less effective (P < 0.01) than gemifloxacin: these agents reduced bacterial numbers by < or =3 log compared with untreated animals. Gemifloxacin produced a marked response against H. influenzae infection, reducing bacterial numbers significantly (P < 0.01) compared with untreated controls. Gemifloxacin was significantly more potent than cefuroxime and azithromycin. None of the other comparator agents was more potent than gemifloxacin. The excellent efficacy seen in these experimental models of RTI with S. pneumoniae and H. influenzae confirms the in vitro activity of gemifloxacin against these organisms. This indicates that gemifloxacin may be of significant benefit in the treatment of RTI.
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Levofloxacin is not inferior to cefuroxime with regard to clinical efficacy in treating AECOPD.