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Data regarding the effectiveness of second-line treatment of Helicobacter pylori infection are limited, especially if microbiological studies are considered.
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Antibiotic treatment of Helicobacter pylori infection in active peptic ulcer disease has been demonstrated to speed ulcer healing, reduce the risk of rebleeding, and prevent long-term recurrence. The objective of this study was to determine whether Medicare patients with peptic ulcer disease who are admitted to acute care hospitals are being tested or treated for H pylori infection as recommended by a National Institutes of Health consensus panel.
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Empirical cefoperazone-sulbactam monotherapy could be a useful adjunct to surgical intervention for intra-abdominal infections.
N. subflava, Pr. nigrescens Po. gingivalis and E. coli were highly susceptible to triclosan (MIC range 0.1-3.9 mg/L), whereas the lactobacillus and S. mutans were less susceptible (MIC range 15.6-20.8 mg/L). Triclosan exposure resulted in a highly significant ( approximately 400-fold) reduction in triclosan susceptibility (P < 0.01) for the positive control E. coli, although its MICs towards chlorhexidine, metronidazole and tetracycline were not significantly altered. Minor ( approximately two-fold) decreases in triclosan susceptibility (MIC) occurred for Pr. nigrescens and in S. sanguis and S. oralis (MBC). Mean changes in susceptibilities (MIC and MBC) of the oral species to chlorhexidine, metronidazole and tetracycline did not exceed two-fold, although chlorhexidine MBCs for S. sanguis were markedly, but transiently, increased.
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Combinations of gentamicin/metronidazole/cefuroxime and gentamicin/cefuroxime were adequate for gastrointestinal and extra-gastrointestinal neonatal operations, respectively, in these sub-Saharan African settings, which may be useful in similar regions.
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Antibiotic exposure is not associated with preterm birth and does not worsen Nugent score among women with normal vaginal flora and positive fetal fibronectin.
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Randomized, dose-ranging pilot study conducted in 2 phases consisting of 20 participants in each phase. In the first phase, participants were randomized to the vaginal suppository (metronidazole 750 mg/miconazole nitrate 200 mg) twice a day for 7 days versus oral metronidazole 2 g single dose. In the second phase, participants randomized to suppository used it once a day for 7 days. Women were reevaluated on days 12 to 15 and 30 to 35. Treatment failures were defined as persistence of trichomonas by wet prep and/or culture.
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This case series reports the outcomes of 8 patients (ages 9-14 years) who presented with 9 immature permanent teeth with pulpal necrosis and apical periodontitis. During treatment, 5 of the teeth were found to have at least some residual vital tissue remaining in the root canal systems. After NaOCl irrigation and medication with ciprofloxacin, metronidazole, and minocycline, these teeth were sealed with mineral trioxide aggregate and restored. The other group of 4 teeth had no evidence of any residual vital pulp tissue. This second group of teeth was treated with NaOCl irrigation and medicated with ciprofloxacin, metronidazole, and minocycline followed by a revascularization procedure adopted from the trauma literature (bleeding evoked to form an intracanal blood clot). In both groups of patients, there was evidence of satisfactory postoperative clinical outcomes (1-5 years); the patients were asymptomatic, no sinus tracts were evident, apical periodontitis was resolved, and there was radiographic evidence of continuing thickness of dentinal walls, apical closure, or increased root length.
The authors identified 13 articles and included 6 of them. Investigators in all studies reported greater reductions in probing depth or in loss of clinical attachment level after adjunct systemic antibiotic therapy when compared with mechanical debridement alone. Antibiotics tested included metronidazole, clindamycin, tetracycline hydrochloride, amoxicillin, and amoxicillin and potassium clavulanate. Five studies presented a high risk of bias, and 1 study presented an unclear risk.
Eighty and four strains of H. pylori determined by PCR method. Of the isolated strains, 49 (58.33%) were resistant, 7 (8.33%) were semi-sensitive to metronidazole and 200bp deletion in rdxA gene was observed in 2 strains.
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Background. The decline of Helicobacter pylori (H. pylori) eradication rates with standard triple therapy resulted in a search for novel therapies for first-line therapy of H. pylori infection. Aim. The aim of the study is to compare the efficacy of concomitant therapy with sequential therapy as the first-line therapy of H. pylori eradication. Methods. We reviewed medical records of patients who were confirmed to have H. pylori infection and received eradication treatment from September 2012 to March 2015. The concomitant group was treated with rabeprazole, amoxicillin, clarithromycin, and metronidazole for 7 days. The sequential group was treated with rabeprazole and amoxicillin for 5 days and then rabeprazole, clarithromycin, and metronidazole for an additional 5 days. Six weeks after the treatment period, patients in both groups underwent 13C-Urea breath test (UBT) to confirm H. pylori eradication. Results. The eradication rate was 90.3% in the concomitant group and 85.5% in the sequential group. However, the eradication rates between the two groups showed no statistical difference (P = 0.343). Conclusion. No statistical difference was found in eradication rates between the two groups. However, in areas where antibiotic resistance is high, concomitant therapy may be more effective than sequential therapy for H. pylori eradication.
We describe a patient with metronidazole-induced encephalopathy involving reversible lesions in the anterior commissure, basal ganglia, and cerebellar white matter, which have not been reported previously. We observed inferior olivary hypertrophy, believed to be the result of lesions in the midbrain and cerebellar white matter rather than the result of lesions induced by metronidazole therapy. By using diffusion-weighted imaging and apparent diffusion coefficient maps, we found that metronidazole-induced encephalopathy might be caused by cytotoxic edema.