e., total daily dose 240 mg), failed to achieve an intragastric milieu consistent
with dual PPI plus amoxicillin therapy being an effective anti-H. pylori regimen. “
“Levofloxacin has been proposed to replace clarithromycin for Helicobacter pylori treatment. Seven- and 10-day fluoroquinolone triple therapies have generally failed to achieve cure rates of ≥90%, whereas 14-day therapy has achieved 95% success. The aim was to assess the efficacy and effect of fluoroquinolone resistance on 14-day levofloxacin-containing triple therapy with or without the addition of bismuth. Helicobacter pylori-positive patients with functional Selleckchem CP-690550 dyspepsia or healed peptic ulcers were randomized to receive lansoprazole 30 mg b.i.d., amoxicillin 1000 mg b.i.d., and levofloxacin 500 mg daily with (B-LAL) or without (LAL) bismuth potassium citrate 220 mg b.i.d. for 14 days. Eradication was assessed by 13C-urea breath testing 4 weeks after completing treatment. Antimicrobial susceptibility was by the agar dilution method. Success was defined as PP success ≥90%. A total of 152 of 161 patients (81 LAL and 80 B-LAL) enrolled completed treatment. The PP rates were 94.6% (70/74; 95% CI, 86.9–97.9%)
with B-LAL and 85.9% (95% CI, 76.5–91.9%) with LAL (p = .07); the ITT eradication rates were 87.5% (95% CI, 78.5–93.1%) with B-LAL and 82.7% (95% CI, 73–89.4%) with LAL (p = .39). Levofloxacin resistance was present in 30.3%. Treatment success was excellent with susceptible strains (97.5%) versus resistant strains (70.6%) for B-LAL and 97.3% versus 37.5% for LAL, respectively. Fourteen-day
fluoroquinolone therapy was highly effective when fluoroquinolone resistance rates are <12%. The selleck inhibitor addition Progesterone of bismuth maintained effectiveness with fluoroquinolone resistance as high as 25%. “
“Background: Helicobacter pylori produces γ-glutamyltranspeptidase (GGT), a potential virulence factor involved in induction of host cell apoptosis. Regulation of the production of this protein is not known. Methods: The transcription start sites were determined by primer extension analysis. Transcription level of the GGT gene was examined by measuring the mRNA by RT-PCR and expression level of GGT protein was examined by Western blot analysis under different conditions. Results: Two transcription start sites were identified; thymine at 78-bp upstream and adenine at 79-bp upstream from the ATG codon of the GGT gene. There was a possible -10 consensus promoter sequence (ATTAAT), but no apparent -35 consensus sequence was found. The transcription of the mRNA and the expression of the protein were at almost constant level during the course of culture. The mRNA level increased by exposure to low pH; however, the actual protein expression level remained almost constant. Addition of glutamine or glutamate did not affect the mRNA level and the protein expression level to a remarkable degree, nor did co-culture with AGS cells affect the GGT activity level. Conclusion: It was suggested that H.