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      Eficacia de la triple cura y su relación con el genotipo de Helicobacter Pylori Pacientes con dispepsia de la region centroccidental de Venezuela

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          Abstract

          Introducción: El Helicobacter pylori es una bacteria reconocida como agente causal de gastritis crónica, además de asociarse al desarrollo de úlcera gástrica, duodenal y está relacionada con el desarrollo de cáncer gástrico. Materiales y métodos: Se realizó un estudio de tipo experimental, incluyendo a los pacientes que acudieron a la consulta de Gastroenterología del Hospital "Dr. Antonio María Pineda" Barquisimeto en los meses de juniooctubre de 2009 presentando dispepsia, criterios de inclusión y exclusión; se les practicó endoscopia digestiva superior con biopsia de mucosa gástrica para test de ureasa rápida, estudio histológico y determinación de los genotipos de cagA y vacA H. pylori por Reacción en Cadena de la Polimerasa (PCR). Al confirmar la infección por la bacteria se indicó tratamiento con amoxicilina, claritromicina y pantoprazol durante 14 días consecutivos. A las 8 semanas de culminada la medicación, se practicó el segundo estudio endoscópico superior con toma de biopsias para test de ureasa rápida y estudio anatomopatológico. Resultados: Un total de 60 pacientes fueron incluidos, 76,7% mujeres y 23,3% hombres, edad promedio 38,3 años. La prevalencia de infección por H. pylori fue de 98,3% por test de ureasa y 86,67% por histología, el síntoma más frecuente asociado antes, durante y posterior a la medicación con triple cura fue la epigastralgía. Hubo un predominio de los genotipos cagA en 84,5% y las formas alélicas s1/m1 55,2%. El 56,3% de los pacientes que presentaban genotipo vacA s1/m1 respondió al tratamiento. Un 56,7% de los pacientes no respondió a la terapia triple, el 66,7% contaba con la forma alélica s2/m2 del vacA y 57,1% presentaba el genotipo cagA-positivo. Conclusión: La triple cura resulto ineficaz en el tratamiento para la infección por Helicobacter pylori en la población estudiada y presentar la forma alélica vacA s1/m1 es estadísticamente significativo para responder a esta terapia farmacológica. Mientras que presentar vacA s1/m2 es estadísticamente significativa para no responder a terapia triple.

          Translated abstract

          Introduction: Helicobacter pylori is a bacteria known as causal agent of chronic gastritis, as well as being associated to the development of gastric and duodenal ulcer and related to the development of gastric cancer. Goal: to establish the triple therapy based pharmacological treatment efficacy on patients with dyspepsia and proved H. pylori infection. Materials and methods: It was done an experimental type study, including patients that underwent evaluation on "Dr. Antonio Maria Pineda" University Hospital´s gastroenterology service, in Barquisimeto, between June - October 2009, who presented dyspepsia and fulfilled the inclusion exclusion criteria, they underwent a superior digestive endoscopy with gastric mucous membrane biopsy for fast urease test, histologic evaluation, and polymerase chain reaction (PCR) test aid establishment of cagA and vacA H. pylori genotype. When H. pylori infection was confirmed, a 14 continuous days amoxicillin, clarithromycin and pantoprazole based treatment was prescribed. 8 weeks later the ending of the pharmacological treatment a second superior digestive endoscopy including rapid urease test and histopathological assessment biopsy was performed. Results: 60 patients were included, 76,7% women and 23,4% men, average age 38,3 years old. The H. pylori’s prevalence were 98,3% by rapid urease test and 86,67 by histological assess, the most frequent related symptom before, through an after pharmacological triple therapy was epigastric pain. There was cagA genotype and s1/m1 allelic form predominance by 84, 5% and 55,2% respectively. 56,3% of vacA s1/m1 patients had a positive response to treatment. Triple therapy failed on 56,7% of patients, of them, 66,7% had the s2/m2 vacA´s allelic form and 57,1% had cagA genotype. Conclusion: Triple therapy was ineffective on Helicobacter pylori´s infection treatment for the studied population and having the vacA s1/m1 allelic form is statistically significant for responding to pharmacological triple therapy. Moreover having the vacA s1/m2 allelic form is statistically significant for pharmacological triple therapy failure.

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          Most cited references38

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          Effects of Helicobacter pylori infection on gastric acid secretion and serum gastrin levels in Mongolian gerbils.

          Body gastritis caused by Helicobacter pylori infection appears to inhibit gastric acid secretion. The aim of this study was to determine the effects of H pylori infection on gastric acid secretion and clarify its mechanisms with reference to interleukin 1beta (IL-1beta). (1) Mongolian gerbils were inoculated orally with H pylori. Before, six, and 12 weeks after inoculation, serum gastrin levels, gastric acid output, and IL-1beta mRNA levels in the gastric mucosa were determined. Pathological changes were also determined according to the updated Sydney system. (2) Effects of recombinant human IL-1 receptor antagonist (rhIL-1ra) on gastric acid output and serum gastrin levels were also determined. (1) Scores for activity and inflammation of gastritis and serum gastrin levels were significantly increased, and gastric acid output was significantly decreased six and 12 weeks after inoculation with H pylori. IL-1beta mRNA levels in the gastric mucosa were also elevated six and 12 weeks after inoculation with H pylori. (2) Acid output and serum gastrin levels in the infected groups returned to control levels after rhIL-1ra injection. Gastric acid secretion is decreased and serum gastrin levels are increased in Mongolian gerbils infected with H pylori. This change in gastric acid secretion appears to be mediated by IL-1beta induced by H pylori infection.
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            Virulence factor genotypes of Helicobacter pylori affect cure rates of eradication therapy.

            The cure rates of Helicobacter pylori infection by using a combination of a proton pump inhibitor (PPI) and antimicrobial agents are mainly influenced by bacterial susceptibility to antimicrobial agents and the magnitude of acid inhibition during the treatment. Currently used empirical triple therapies do not reliably produce a > or =80% cure rate on an intention-to-treat basis. Therefore, tailored regimens based on relevant microbiological findings and pharmacogenomics are recommended for attaining an acceptable > or =95% cure rate. Recently, virulence factors of H. pylori, such as cagA and vacA, are reported to be major factors determining the cure rates. Individuals infected with strains with cagA-negative and vacA s2 genotypes have significantly increased risk of eradication failure of H. pylori infection. These virulence factors enhance gastric mucosal inflammation and are associated with the development of peptic ulcer and gastric cancer. H. pylori virulence factors induce proinflammatory cytokines, such as interleukin (IL)-1, IL-8, and tumor necrosis factor (TNF)- which influence mucosal inflammation and/or gastric acid secretion. When physicians select an H. pylori eradication regimen with an acceptable cure rate, they might need to consider H. pylori virulence factors, especially cagA and vacA.
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              Effect of Helicobacter pylori eradication on gastritis in relation to cagA: a prospective 1-year follow-up study.

              Whether Helicobacter pylori eradication resolves intestinal metaplasia and atrophy and whether infection with cagA+ H. pylori is related to a specific clinical outcome are not known. The aim of this study was to investigate the role of H. pylori eradication on the course of intestinal metaplasia (IM) and atrophy in relation to cagA. In a large prospective study, the cagA status of H. pylori isolated from consecutive dyspeptic patients was related to clinical outcome before and 1 year after successful eradication of H. pylori. At pretreatment and 4-6 weeks and on average 1 year after eradication therapy, the degree of gastritis and the status of H. pylori were assessed by culture and histopathology. Specimens of cagA+ H. pylori were recovered from 122 of 155 (79%) patients infected with H. pylori. Pretreatment degrees of gastritis activity, superficial epithelial damage, IM, and atrophy were significantly greater in patients infected with cagA+ H. pylori (P < 0.001). After successful eradication of H. pylori, a significant improvement of activity of gastritis and superficial epithelial damage occurred (P < 0.001), but the degree of IM and atrophy did not change, irrespective of the cagA status. The usefulness of H. pylori eradication to revert precancerous lesions such as IM and atrophy after 1-year follow-up is questionable.
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                Author and article information

                Contributors
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                Journal
                gen
                Gen
                Gen
                Sociedad Venezolana de Gastroentereología (Caracas )
                0016-3503
                December 2011
                : 65
                : 4
                : 341-348
                Affiliations
                [1 ] Hospital Central Universitario Dr. Antonio María Pineda Venezuela
                Article
                S0016-35032011000400010
                ec8095ad-9eb4-4187-a6d6-e8f26affcb91

                http://creativecommons.org/licenses/by/4.0/

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                SciELO Venezuela

                Self URI (journal page): http://www.scielo.org.ve/scielo.php?script=sci_serial&pid=0016-3503&lng=en

                Helicobacter pylori´s,H. pylori genotype,vacA,cagA,Dyspepsia,Triple therapy,Helicobacter pylori,Genotipo de H. pylori,Dispepsia,Triple cura

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