Abstract:Eighty-one clinical isolates of Helicobacter pylorishowed no resistance to rifampin (MIC range, 0.032 to 2 μg/ml; MIC at which 50% of isolates are inhibited [MIC50], 0.25 μg/ml). The MIC50 of rifabutin was 0.008 μg/ml (n = 16). All resistant laboratory mutants of H. pylori ATCC 43504 showed amino acid exchanges in codons 524 to 545 or codon 585 of the rpoB gene, corresponding to the gene sequences from Mycobacterium tuberculosis andEscherichia coli.
“…There is a low prevalence of H. pylori resistance to rifampicin and rifabutin. Heep et al found no resistance to rifampicin in 81 clinical isolates of H. pylori in Germany (19). Similarly, Fujimura et al from Japan detected no rifampicin resistance among 52 H. pylori isolates.…”
In vitro activity of rifampicin has been shown against H. pylori. It has also been reported that the prevalence of H. pylori is low in patients with tuberculosis treated with rifampicin. Clinical trials are required to establish the efficacy of rifampicin as a salvage therapy for eradication of H. pylori. We aimed to evaluate the efficacy of rifampicin-based salvage therapy for eradication of H. pylori in patients with peptic ulcer disease. Twenty-eight patients with peptic ulcer disease who either had failed eradication of H. pylori or had a recurrence of H. pylori following successful eradication were included in the prospective study. The inclusion criteria included one or more failed attempts at eradication and presence of H. pylori infection as evidenced by positivity of at least two of three tests: rapid urease test (RUT), 14C urea breath test (UBT), and histology. The subjects were treated with a 10-day regimen consisting of rifampicin, 450 mg od, tetracycline, 1 g bd, and esomeprazole, 40 mg bd. Four weeks after completion of therapy, H. pylori status was assessed by RUT, 14C, UBT, and histology. Liver function tests were done before and at the end of therapy. The study subjects included 25 males and 3 females with a mean age of 33.7+/-8.92 years (range: 22-65 years). The median duration of symptoms was 42 months, with a range of 1-180 months. The median number of eradication attempts was two, with one prior attempt in 6 (21.4%), two attempts in 19 (67.9%), and three attempts in 3 (10.7%) patients. Successful H. pylori eradication as defined by concomitant negativity of RUT, UBT, and histology with special stains was achieved in 32.1% (9/28) of patients by intention-to-treat and 33.3% (9/27) of patients by per-protocol analysis. This pilot study suggests that rifampicin-based regimes have no role as salvage eradication therapy in refractory cases of H. pylori infection with peptic ulcer disease.
“…There is a low prevalence of H. pylori resistance to rifampicin and rifabutin. Heep et al found no resistance to rifampicin in 81 clinical isolates of H. pylori in Germany (19). Similarly, Fujimura et al from Japan detected no rifampicin resistance among 52 H. pylori isolates.…”
In vitro activity of rifampicin has been shown against H. pylori. It has also been reported that the prevalence of H. pylori is low in patients with tuberculosis treated with rifampicin. Clinical trials are required to establish the efficacy of rifampicin as a salvage therapy for eradication of H. pylori. We aimed to evaluate the efficacy of rifampicin-based salvage therapy for eradication of H. pylori in patients with peptic ulcer disease. Twenty-eight patients with peptic ulcer disease who either had failed eradication of H. pylori or had a recurrence of H. pylori following successful eradication were included in the prospective study. The inclusion criteria included one or more failed attempts at eradication and presence of H. pylori infection as evidenced by positivity of at least two of three tests: rapid urease test (RUT), 14C urea breath test (UBT), and histology. The subjects were treated with a 10-day regimen consisting of rifampicin, 450 mg od, tetracycline, 1 g bd, and esomeprazole, 40 mg bd. Four weeks after completion of therapy, H. pylori status was assessed by RUT, 14C, UBT, and histology. Liver function tests were done before and at the end of therapy. The study subjects included 25 males and 3 females with a mean age of 33.7+/-8.92 years (range: 22-65 years). The median duration of symptoms was 42 months, with a range of 1-180 months. The median number of eradication attempts was two, with one prior attempt in 6 (21.4%), two attempts in 19 (67.9%), and three attempts in 3 (10.7%) patients. Successful H. pylori eradication as defined by concomitant negativity of RUT, UBT, and histology with special stains was achieved in 32.1% (9/28) of patients by intention-to-treat and 33.3% (9/27) of patients by per-protocol analysis. This pilot study suggests that rifampicin-based regimes have no role as salvage eradication therapy in refractory cases of H. pylori infection with peptic ulcer disease.
“…12,14 Thus, the rate of H. pylori infection in patients with NTM who have been treated with a combination of clarithromycin and rifampicin is of great interest. In the present study, the rate of H. pylori infection in patients with NTM who had been administered antimicrobial agents, including clarithromycin, longterm, was found to be significantly lower (33.3%; P = 0.0006) than the general prevalence of H. pylori infection in Japanese adults over 40 years old who had had routine upper gastrointestinal endoscopy and no H. pylori eradication (77.5%; 145 of 187 patients).…”
“…Furthermore, selection of resistant H. pylori strains has been low in experimental conditions. Thus, until now, no rifabutin-resistant strain has been isolated from patients who were or were not treated for H. pylori infection [31]. • Perri et al [33,34] used a 1-week regimen of pantoprazole, amoxicillin, and rifabutin in patients who were still infected with H. pylori after two or more courses of 1-week triple therapies, with an eradication rate of 71% by intention-to-treat analysis.…”
“…In this respect, rifabutin-based rescue therapies represent an encouraging strategy for eradication failures. H. pylori has been proved to be highly susceptible in vitro to rifabutin, a rifamycin derivative of the established tuberculostatic drug [30][31][32]. Furthermore, selection of resistant H. pylori strains has been low in experimental conditions.…”
Even with the current most effective treatment regimens, about 10% to 20% of patients will fail to eradicate Helicobacter pylori infection. Therefore, in designing a treatment strategy, we should not focus on the results of primary therapy alone but also on the final (overall) eradication rate. The choice of a second-line treatment depends on which treatment was used initially, because retreatment with the same regimen is not recommended. Therefore, it seems that performing culture after a first eradication failure is not necessary and assessing H. pylori sensitivity to antibiotics only after failure of the second treatment is suggested in clinical practice. Different possibilities of empirical treatment are suggested. After failure of proton pump inhibitor (PPI)-amoxicillin-clarithromycin, quadruple therapy has been generally used. More recently, replacing the PPI and the bismuth compound by ranitidine bismuth citrate has also achieved good results. After PPI-amoxicillin-nitroimidazole failure, retreatment with PPI-amoxicillin-clarithromycin has proved to be effective. Finally, the first therapy should not combine clarithromycin and metronidazole in the same regimen because of the problem of resistance against both antibiotics. Recently, rifabutin-based rescue therapies have been shown to constitute an encouraging strategy for eradication failures because they are effective for H. pylori strains resistant to antibiotics.
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