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      Tratamiento del Helicobacter Pylori con Omeprazol, Amoxilina y Claritromicina en esquemas de 7 y 10 días


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          OBJETIVO: La terapia de un inhibidor de la bomba de protones más dos antibióticos es el tratamiento más aceptado para la infección por el Helicobacter pylori. Sin embargo, no hay consenso sobre su duración. El objetivo fue comparar los porcentajes de erradicación del esquema de omeprazol+claritromicina+amoxicilina administrados durante 7 vs 10 días. METODOLOGÍA: Seleccionamos pacientes del Hospital Militar Central y Policlínico Peruano-Japonés con síntomas del tracto gastrointestinal superior y Helicobacter pylori. Excluimos aquéllos con úlcera péptica. Para el diagnóstico se tomaron biopsias para la prueba de la ureasa, PCR, cultivo y coloración con plata. Empleamos omeprazol+claritromicina+ amoxicilina, durante 7 días versus 10 días. Realizamos endoscopía control al mes de terminado el tratamiento, y utilizamos técnicas de biología molecular para diferenciar las recurrencias de las reinfecciones. Evaluamos la susceptibilidad a claritromicina. RESULTADOS: Incluimos 36 pacientes en cada grupo. En ambos la erradicación fue igual: 86.1% (31/36). En varios pacientes en que persistió la bacteria se identificó la misma cepa que la inicial. El 91.18% de nuestras muestras fueron sensibles a claritromicina. CONCLUSIONES: En el Perú la combinación de omeprazol+claritromicina+amoxicilina para erradicar la infección por el Helicobacter pylori da resultados superiores al 80%. El esquema de 7 y 10 días erradicó a la bacteria en el 86% de nuestros pacientes.

          Translated abstract

          AIM: The most accepted treatment for infection by Helicobacter pylori is the proton pump inhibitor based therapy with two antibiotics. However, there is no consensus regarding the duration. The purpose here was to compare eradication percentages in the omeprazole + amoxicillin + clarithromycin regimen administered during 7 days versus 10 days and confront the results with a previous 14-day* experience in Peru. METHOD: Patients from the Central Military Hospital and Peruvian-Japanese Hospital evidencing chronic upper gastrointestinal tract symptoms were recruited. We excluded patients with peptic ulcer. Biopsies were taken for diagnosis, for urease and PCR tests, culture and coloring with silver. Omeprazole + clarithromycin + amoxicillin was used during 7 days versus 10 days. Control endoscopy was performed one month after treatment had been completed and molecular biology techniques were used to differentiate recurrences from new infections. Susceptibility to clarithromycin was assessed. RESULTS: 36 patients were included in each group. Eradication was the same in both groups: 86.1% (31/36). In several patients in whom the bacteria persisted, the same initial nucleus was found. In a previous study* using this same regimen during 14 days, a 93% eradication was obtained. 91.18% of our samples were susceptible to clarithromycin. CONCLUSIONS: In Peru, the omeprazole + clarithromycin + amoxicillin combination gives results higher than 80% in the eradication of infection by Helicobacter pylori. The 7 and 10 days regimens eradicated the bacteria in 86% of our patients.

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          DNA diversity among clinical isolates of Helicobacter pylori detected by PCR-based RAPD fingerprinting.

          The RAPD (or AP-PCR) DNA fingerprinting method was used to distinguish among clinical isolates of Helicobacter pylori, a bacterium whose long term carriage is associated with gastritis, peptic ulcers and gastric carcinomas. This method uses arbitrarily chosen oligonucleotides to prime DNA synthesis from genomic sites to which they are fortuitously matched, or almost matched. Most 10-nt primers with > or = 60% G + C yielded strain-specific arrays of up to 15 prominent fragments, as did most longer (> or = 17-nt) primers, whereas most 10-nt primers with 50% G+C did not. Each of 64 independent H. pylori isolates, 60 of which were from patients in the same hospital, was distinguishable with a single RAPD primer, which suggests a high level of DNA sequence diversity within this species. In contrast, isolates from initial and followup biopsies were indistinguishable in each of three cases tested.
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            cagA Status and eradication treatment outcome of anti-Helicobacter pylori triple therapies in patients with nonulcer dyspepsia.

            The differences in eradication rates reported in clinical trials aiming to cure Helicobacter pylori infection cannot be entirely explained by the type of regimen, bacterial resistance, or lack of compliance. Using data from a clinical trial, a logistic regression model was constructed to determine whether cagA status, assessed by PCR, affects the outcome of eradication. Resistance to clarithromycin (10% of the strains) predicted failure perfectly. In the model (n = 156), a cagA-lacking strain (odds ratio [OR] = 2.2; 95% confidence interval [CI], (1.1 to 4.7), tobacco smoking OR = 3.1; 95% CI, 1.3 to 7.0), and a double dose of proton pump inhibitor in the treatment regimen (OR = 0.3; 95% CI, 0.2 to 0.7) were associated with the treatment outcome. The exact role of cagA in the outcome of H. pylori eradication therapy has not been explored. However, the type of histological lesions which it causes in the gastric mucosa may be implicated. Regardless of the mechanism involved, cagA status is a good predictive marker of eradication outcome.
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              Sequential inactivation of rdxA (HP0954) and frxA (HP0642) nitroreductase genes causes moderate and high-level metronidazole resistance in Helicobacter pylori.

              Helicobacter pylori is a human-pathogenic bacterial species that is subdivided geographically, with different genotypes predominating in different parts of the world. Here we test and extend an earlier conclusion that metronidazole (Mtz) resistance is due to mutation in rdxA (HP0954), which encodes a nitroreductase that converts Mtz from prodrug to bactericidal agent. We found that (i) rdxA genes PCR amplified from 50 representative Mtz(r) strains from previously unstudied populations in Asia, South Africa, Europe, and the Americas could, in each case, transform Mtz(s) H. pylori to Mtz(r); (ii) Mtz(r) mutant derivatives of a cultured Mtz(s) strain resulted from mutation in rdxA; and (iii) transformation of Mtz(s) strains with rdxA-null alleles usually resulted in moderate level Mtz resistance (16 microg/ml). However, resistance to higher Mtz levels was common among clinical isolates, a result that implicates at least one additional gene. Expression in Escherichia coli of frxA (HP0642; flavin oxidoreductase), an rdxA paralog, made this normally resistant species Mtz(s), and frxA inactivation enhanced Mtz resistance in rdxA-deficient cells but had little effect on the Mtz susceptibility of rdxA(+) cells. Strains carrying frxA-null and rdxA-null alleles could mutate to even higher resistance, a result implicating one or more additional genes in residual Mtz susceptibility and hyperresistance. We conclude that most Mtz resistance in H. pylori depends on rdxA inactivation, that mutations in frxA can enhance resistance, and that genes that confer Mtz resistance without rdxA inactivation are rare or nonexistent in H. pylori populations.

                Author and article information

                Revista de Gastroenterología del Perú
                Rev. gastroenterol. Perú
                Sociedad de Gastroenterología del Perú (Lima, , Peru )
                July 2003
                : 23
                : 3
                : 177-183
                [06] Chicago Illinois orgnameCook County Hospital orgdiv1Dpto. de Medicina
                [03] orgnameUniversidad Peruana Cayetano Heredia
                [01] orgnameHospital Militar Central orgdiv1Dpto. de Gastroenterología
                [04] orgnameUniversidad Peruana Cayetano Heredia y Universidad John Hopkins orgdiv1Grupo de Fisiología Gastrointestinal
                [05] orgnameUniversidad Peruana Cayetano Heredia Policlínico Peruano-Japonés
                [02] orgnameMEDCO orgdiv1Departamento Médico
                S1022-51292003000300003 S1022-5129(03)02300303

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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                Trabajos originales

                Helicobacter pylori,tratamiento,ensayo clínico,treatment,clinical trial


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