906 resultados para Helicobacter pylori genotypes


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Background Compared to the general population, Helicobacter pylori infection is more common among adults with intellectual disability (ID) and is associated with greater levels of disability, maladaptive behaviour, and institutionalization. Little information exists about the effects of eradication therapy in this group, so we aimed to evaluate: (1) success of a standard H. pylori eradication protocol; (2) frequency of side-effects; and (3) impact of eradication on level of functional ability and maladaptive behaviour. Method A cohort of adults with ID underwent assessment of their levels of function and maladaptive behaviour, medical history, physical examination, and H. pylori testing using serology and faecal antigen tests. Some received standard H. pylori eradication therapy. Twelve months later, participants underwent repeat assessment, were grouped by change in H. pylori status and compared. Results Of 168 participants, 117 (70%) were currently infected with H. pylori at baseline, and 96 (82%) of the 117 were given standard H. pylori eradication therapy. The overall eradication rate was 61% but 31% reported side-effects. Institutional status of the participants, their level of behaviour or function, and number of comorbid medical conditions were not associated with failure of eradication. There were no statistically significant differences in level of behaviour or function, ferritin, or weight between the groups in whom H. pylori was eradicated or stayed positive. Conclusion Adults with ID have lower H. pylori eradication and higher side-effect rates than the general population. Levels of maladaptive behaviour and disability did not improve with eradication and thus greater levels of maladaptive behaviour or disability appear to be risk factors for, rather than consequences of, H. pylori infection.

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Helicobacter pylori is one of the most common pathogenic bacterial infections, colonising an estimated half of all humans. It is associated with the development of serious gastroduodenal disease - including peptic ulcers, gastric lymphoma and acute chronic gastritis. Current recommended regimes are not wholly effective and patient compliance, side-effects and bacterial resistance can be problematic. Drug delivery to the site of residence in the gastric mucosa may improve efficacy of the current and emerging treatments. Gastric retentive delivery systems potentially allow increased penetration of the mucus layer and therefore increased drug concentration at the site of action. Proposed gastric retentive systems for the enhancement of local drug delivery include floating systems, expandable or swellable systems and bioadhesive systems. Generally, problems with these formulations are lack of specificity, limited to mucus turnover or failure to persist in the stomach. Gastric mucoadhesive systems are hailed as a promising technology to address this issue, penetrating the mucus layer and prolonging activity at the mucus-epithelial interface. This review appraises gastroretentive delivery strategies specifically with regard to their application as a delivery system to target Helicobacter. As drug-resistant strains emerge, the development of a vaccine to eradicate and prevent reinfection is an attractive proposition. Proposed prophylactic and therapeutic vaccines have been delivered using a number of mucosal routes using viral and non-viral vectors. The delivery form, inclusion of adjuvants, and delivery regime will influence the immune response generated. © 2005 Bentham Science Publishers Ltd.

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Non-steroidal anti-inflammatory drugs (NSAIDs) cause peptic ulcer disease, but whether they interact with Helicobacter pylori to promote damage is controversial. Moreover, the reported induction of apoptosis in gastric cells by H. pylori lipopolysaccharide (LPS) (10-9 g /ml) contrasts with studies showing low immunological potency of this LPS. Therefore, the effects of LPS from H. pylori NCTC 11637 and Escherichia coli 0111:B4 on apoptosis in a primary culture of guinea-pig gastric mucous cells were investigated in the presence and absence of the NSAID, ibuprofen. Cell loss was estimated by a crystal violet assay, and apoptosis determined from caspase activity and from condensation and fragmentation of nuclei. Exposure to E. coli LPS for 24 h caused cell loss and enhanced apoptotic activity at concentrations ≥ 10-9 g/ml, but similar effects were only obtained with H. pylori LPS at concentrations ≥10-6 g/ml. Although ibuprofen (250 μM) caused cell loss and apoptosis, addition of either E. coli or H. pylori LPSs further enhanced these effects. In conclusion, LPS and ibuprofen interact to enhance gastric cell loss and apoptosis. In such interactions, E. coli LPS is more potent than that of H. pylori. The low potency of H. pylori LPS may contribute to a chronic low-grade gastritis that can be enhanced by the use of NSAIDs. © W. S. Maney & Son Ltd.

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Historically, abdominal complaints have been generally dealt with palliatively. Seldom were underlying causes given consideration. However, in 1982 (Warren & Marshall, 1983), the identification of the bacterial agent Helicobacter pylori (known hereafter in this paper as H. pylori) as a potential link between gastrointestinal complaints such as gastric and duodenal ulcers, Crohn's Disease, and some forms of gastric cancer has given rise for concern. In 1994, the National Institute for Health recommended that patients with complaints of dyspepsia be studied for the occurrence of H. pylori. This study proposes to study the occurrence of H. pylori in patients who complain with dyspepsia with a relatively non invasive screening technique to be done in an office setting. The study findings were considered signifcant if p $\le$.05. This study indicated that 49% of patients with complaints of dyspepsia were postive for H. pylori infection with p =.000. ^

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Helicobacter pylori is a spiral, Gram negative, mobile, and microaerophilic bacteria recognized as a major cause of gastritis, ulcer, gastric cancer, and gastric low grade, B cell, mucosa – associated lymphoid tissue (MALT) lymphoma, constituting an important microorganism in medical microbiology. Its importance comes from the difficulty of treatment because the requirement of multiple drugs use, besides the increasing emergence of resistant and multiresistant strains to antibiotics used in th e clinic. In order to expand safe and effective therapeutic options , chemical studies on medicinal plants by obtaining extracts, fractions, isolated compounds or essential oils with some biological activity has been intensified . Given the above, the objective was to evaluate the inhi bitory activity of organic extracts derived from Syzygium cumini and Encholirium spectabile, with antiulcer history, and the essential oil, obtained from S. cumini, against H. pylori (ATCC 43504) by the disk diffusion method, for qualitative evaluation, an d determination of minimum inhibitory concentration (MIC) using the broth microdilution method, for quantitative analysis. Also was evaluated the extracts in vitro toxicity by a hemolytic assay using sheep red blood cells, and VERO and HeLa cells using the MTT assay to analyze cell viability. The extracts of both plant used in antimicrobial assays did not inhibit bacterial growth, however the essential oil of S. cumini (SCFO) proved effective, showing MIC value of 205 μg/mL (0.024 % dilution of the original oil). In the hemolytic assay, the same oil shows moderate toxicity, by promote 25% hemolysis at 1000 μg/mL. Regarding the cytotoxicity in cell culture, the SCFO, at 260 μg/mL, affected the cell viability around 80% of HeLa and 50% of VERO cells. So the oi l obtained from S. cumini leaves has antimicrobial activity against H. pylori and cytotoxicity potential, suggesting a source of new molecule drug candidates, since new stages of toxicity in vitro and in vivo, as well, chemical characterization be evaluate d. Moreover, the development of a prospective drug delivery system can result in a prototype to be used in preclinical tests.

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There is substantial evidence that infection with Helicobacter pylori plays a role in the development of gastric cancer and that it is rarely found in gastric biopsy of atrophic gastritis and gastric cancer. On advanced gastric tumors, the bacteria can be lost from the stomach. Aims - To analyze the hypothesis that the prevalence of H.pylori in operated advanced gastric carcinomas and adjacent non-tumor tissues is high, comparing intestinal and diffuse tumors according to Lauren’s classifi cation. Methods - A prospective controlled study enrolled 56 patients from “Hospital Universitário”, Federal University of Rio Grande do Norte, Natal, RN, Brazil, with advanced gastric cancer, treated from February 2000 to March 2003. Immediately after partial gastrectomy, the resected stomach was opened and several mucosal biopsy samples were taken from the gastric tumor and from the adjacent mucosa within 4 cm distance from the tumor margin. Tissue sections were stained with hematoxylin and eosin. Lauren‘s classifi cation for gastric cancer was used, to analyse the prevalence of H. pylori in intestinal or diffuse carcinomas assessed by the urease rapid test, IgG by ELISA and Giemsa staining. H. pylori infected patients were treated with omeprazole, clarithromycin and amoxicillin for 7 days. Follow-up endoscopy and serology were performed 6 months after treatment to determine successful eradication of H. pylori in non-tumor tissue. Thereafter, follow-up endoscopies were scheduled annually. Chi-square and MacNemar tests with 0.05 signifi cance were used. Results - Thirty-four tumors (60.7%) were intestinal-type and 22 (39.3%) diffuse type carcinomas. In adjacent non-tumor gastric mucosa, chronic gastritis were found in 53 cases (94.6%) and atrophic mucosa in 36 patients (64.3%). All the patients with atrophic mucosa were H. pylori positive. When examined by Giemsa and urease test, H. pylori positive rate in tumor tissue of intestinal type carcinomas was higher than that in diffuse carcinomas. In tumor tissues, 34 (60.7%) H. pylori-positive in gastric carcinomas were detected by Giemsa method. H. pylori was observed in 30 of 56 cases (53.5%) in tissues 4 cm adjacent to tumors. This difference was not signifi cant. Eradication of H. pylori in non-tumor tissue of gastric remnant led to a complete negativity on the 12th postoperative month. Conclusions - The data confi rmed the hypothesis of a high prevalence of H. pylori in tumor tissue of gastric advanced carcinomas and in adjacent non-tumor mucosa of operated stomachs. The presence of H. pylori was predominant in the intestinal-type carcinoma

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Cette thèse présente la découverte de nouveaux inhibiteurs de l’amidotransférase ARNt-dépendante (AdT), et résume les connaissances récentes sur la biosynthèse du Gln-ARNtGln et de l’Asn-ARNtAsn par la voie indirecte chez la bactérie Helicobacter pylori. Dans le cytoplasme des eucaryotes, vingt acides aminés sont liés à leur ARNt correspondant par vingt aminoacyl-ARNt synthétases (aaRSs). Ces enzymes sont très spécifiques, et leur fonction est importante pour le décodage correct du code génétique. Cependant, la plupart des bactéries, dont H. pylori, sont dépourvues d’asparaginyl-ARNt synthétase et/ou de glutaminyl-ARNt synthétase. Pour former le Gln-ARNtGln, H. pylori utilise une GluRS noncanonique nommée GluRS2 qui glutamyle spécifiquement l’ARNtGln ; ensuite, une AdT trimérique, la GatCAB corrige le Glu-ARNtGln mésapparié en le transamidant pour former le Gln-ARNtGln, qui lira correctement les codons glutamine pendant la biosynthèse des protéines sur les ribosomes. La formation de l’Asn-ARNtAsn est similaire à celle du Gln-ARNtGln, et utilise la même GatCAB et une AspRS non-discriminatrice. Depuis des années 2000, la GatCAB est considérée comme une cible prometteuse pour le développement de nouveaux antibiotiques, puisqu’elle est absente du cytoplasme de l’être humain, et qu’elle est encodée dans le génome de plusieurs bactéries pathogènes. Dans le chapitre 3, nous présentons la découverte par la technique du « phage display » de peptides cycliques riches en tryptophane et en proline, et qui inhibent l’activité de la GatCAB de H. pylori. Les peptides P10 (CMPVWKPDC) et P9 (CSAHNWPNC) inhibent cette enzyme de façon compétitive par rapport au substrat Glu-ARNtGln. Leur constante d’inhibition (Ki) est 126 μM pour P10, et 392 μM pour P9. Des modèles moléculaires ont montré qu’ils lient le site actif de la réaction de transmidation catalysée par la GatCAB, grâce à la formation d’une interaction π-π entre le résidu Trp de ces peptides et le résidu Tyr81 de la sous-unité GatB, comme fait le A76 3’-terminal de l’ARNt. Dans une autre étude concernant des petits composés contenant un groupe sulfone, et qui mimiquent l’intermédiaire de la réaction de transamidation, nous avons identifié des composés qui inhibent la GatCAB de H. pylori de façon compétitive par rapport au substrat Glu-ARNtGln. Cinq fois plus petits que les peptides cycliques mentionnés plus haut, ces composés inhibent l’activité de la GatCAB avec des Ki de 139 μM pour le composé 7, et de 214 μM pour le composé 4. Ces inhibiteurs de GatCAB pourraient être utiles pour des études mécanistiques, et pourraient être des molécules de base pour le développement de nouvelles classes d’antibiotiques contre des infections causées par H. pylori.

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El estudio tiene el objetivo de determinar la prevalencia de Helicobacter Pylori y factores de riesgo asociados en niños en edad escolar del área urbana del cantón Cuenca. Resultados: la prevalencia de Helicobacter Pylori en escolares del área urbana del cantón Cuenca fue de 14.3: los factores de riesgo asociados a la infección que reflejaron significancia estadística fueron edad RP 1.79. (IC 1.10-2.87, P o.41); anafalbetismo de los padres RP 2.49, (ICI. 23-5. 03. P 0.017); no practicar el lavado de manos RP 63.40, (IC 15.71-255.84, P 0.000); no lavar los alimentos RP 9.88, (IC 5,43-17.97, P 0.000); compartir la cama RP 2.23, (IC 1,33-3.73, P 0.00); no disponer de servicio higiénico RP 5.11, (IC 3.01-8.66, P 0.000) y no consumir agua potable RP 4.79, (IC 2.96-7.74, P 0.000). También se encontró asociación con dolor abdominal recurrente RP 3.48, (IC 2.03-5.96, P 0.0000) Los factores de riesgo que no se asociaron a infección fueron género RP 1.36, (IC 0.82-2.24, P 0.224) y ocupación manual de los padres RP 1.21, (IC 0.54-2.68, P 0.626). Los signos y síntomas que no estuvieron asociados con la presencia de Helicobacter Pylori fueron naúsea y vómito RP 0.87, (IC 0.13-5.56, P 0.886); sensación de llenura RP 1.70, (IC 0.87-3.30, P 0.127) y pirosis RP 2.24, (IC 0.95-5.27, P 0.083). Conclusiones: 1. La prevalencia de Helicobacter Pylori en escolares del área urbana del cantón Cuenca 2003-2004 fue 14.3. 2. La prevalencia de Helicobacter Pylori es directamente proporcional con la edad. 3. La falta de aplicación de las normas básicas de higiene incrementa el riesgo de infección. 4. Las condiciones sanitarias desfavorables son un determinante para la mayor prevalencia de infección. 5. En la mayoría de escolares, la infección no cursó con sintomatología clínica. 6. Dolor abdominal recurrente fue la manifestación clínica más importante en niños sintomáticos infectados

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Estudio clínico descriptivo con una muestra de 100 pacientes con síntomas digestvos y sometidos a endoscopía, para obtener muestras de biopsia gástrica y realizar cultivo de Helico-bacter Pylori, prueba de la ureasa y tinción de Gram, 59 pacientes resultaron H. Pylori positivo al cultivo, siendo asignados al azar en dos grupos de tratamiento. El primer grupo recibió cimetidina a una dosis de 800 mgs. tres veces al día por un período acortado de 7 días (grupo tratado). El segundo grupo (grupo control) recibió cimetidina a la dosis de 800 mgs. diarios durante un mes. A las 4 semanas posteriores al tratamiento se realizó control endoscópico e histopatológico excluyéndose del estudio 23 pacientes que no se sometieron al control. De los 36 pacientes objeto del estudio se obtuvo los siguients resultados: se erradicó el H. Pylori en el 71.43del grupo tratado y en el 40del grupo control p 0.05. Los síntomas en los dos grupos no presentaron diferencias significativas. Hubo mejoría endoscópica e histopatológica en el grupo tratado con diferencia significativa (p menor que 0.001) en comparación con el grupo control. Se realiza comparaciones con series citadas en la literatura y se realizan las recomendaciones pertinentes

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El conocimiento de la prevalencia del helicobacter en la población y los factores de riesgo para controlar la enfermedad son importantes, para su control y erradicación. Conocer la prevalencia de la bacteria en la población, urbana y rural de la ciudad de Cuenca; y determinar si hay factores de riesgo que favorezcan la propagación de la infección. La prevalencia del Helicobacter en la ciudad de Cuenca - Ecuador, es de 44.9 por ciento, no hay diferencia estadísticamente significativas entre los habitantes del sector urbano 48.3 por ciento y rural 41.6 por ciento, las variables: residencia, [RP; 0.86] género, actividad manual, [RP; 0.98 IC: 0.82-1.24] ingesta de agua potable, [RP; 0.99 IC: 0.68-1.48], no se relacionan con la presencia del antígeno de Helicobacter en materia fecal, por lo que no constituyen un factor de riesgo para contraer la infección, la viariable edad, correlaciona positivamente con la prevalencia de la infección. 1.- La prevalencia del Helicobacter Pylori en el cantón Cuenca-Ecuador, en el año 2003, es del 44.9 por ciento que le ubica como una zona de prevalencia intermedia, menor a la esperada en un país en vías de desarrollo. 2.- No hay diferencias entre habitar en zona urbana y rural para prevalencia del Helicobacter Pylori 4.- La mayor parte de infección por Helicobacter Pylori, se adquiere en la infancia 5.- Las variables género, ingesta de agua potable, ocupación manual, no son factores de riesgo para contraer la infección

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El conocimiento de la prevalencia del helicobacter en la población y los factores de riesgo para contraer la enfermedad son importantes, para su control y erradicación. El objetivo es conocer la pravalencia de la bacteria en la población urbana y rural de la ciudad de Cuenca, utilizando una prueba de alta sensibilidad y especificidad como es el Antígeno de Helicobacter Pylori fecal; y determinar si hay factores que favorezcan la propagación de la infección. Los resultados fueron la prevalencia de helicobacter en la Ciudad de Cuenca, Ecuador, es del 44.9 por ciento, no hay diferencias estadísticamente significativa entre los habitantes del sector urbano 48.3 por ciento y rural 41.6 por ciento, las variables: residencia, [OR: 1.31 IC:1. 0-1.6 género, [OR: 0.75 IC 0.5-1.0] actividad profesional, [OR: 1.-0 IC: 0.7-1.4] ingesta de alcohol, [OR: 1.2, IC: 0.8-1.7] ingesta de agua potable, [OR: 1.00, IC:0.6-1.4], no se relacionan con la presencia del antígeno de helicobacter en material fecal, variable edad, correlaciona positivamente con la prevalencia de la infección. Conclusión. 1.- La prevalencia del helicobacter en la ciudad de Cuenca le ubica como una zona de riesgo intermedio para contraer la infección 2.- No hay diferencia entre habitar en zona rural o urbana. 3.- La edad es un factor de riesgo, a mayor edad mayor probabilidad de contaminación. 4.- Las variables género ingesta de alcohol, ingesta de agua no potable, no son factores exclusivos de riesgo para contraer la infección

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There is substantial evidence that infection with Helicobacter pylori plays a role in the development of gastric cancer and that it is rarely found in gastric biopsy of atrophic gastritis and gastric cancer. On advanced gastric tumors, the bacteria can be lost from the stomach. Aims - To analyze the hypothesis that the prevalence of H.pylori in operated advanced gastric carcinomas and adjacent non-tumor tissues is high, comparing intestinal and diffuse tumors according to Lauren’s classifi cation. Methods - A prospective controlled study enrolled 56 patients from “Hospital Universitário”, Federal University of Rio Grande do Norte, Natal, RN, Brazil, with advanced gastric cancer, treated from February 2000 to March 2003. Immediately after partial gastrectomy, the resected stomach was opened and several mucosal biopsy samples were taken from the gastric tumor and from the adjacent mucosa within 4 cm distance from the tumor margin. Tissue sections were stained with hematoxylin and eosin. Lauren‘s classifi cation for gastric cancer was used, to analyse the prevalence of H. pylori in intestinal or diffuse carcinomas assessed by the urease rapid test, IgG by ELISA and Giemsa staining. H. pylori infected patients were treated with omeprazole, clarithromycin and amoxicillin for 7 days. Follow-up endoscopy and serology were performed 6 months after treatment to determine successful eradication of H. pylori in non-tumor tissue. Thereafter, follow-up endoscopies were scheduled annually. Chi-square and MacNemar tests with 0.05 signifi cance were used. Results - Thirty-four tumors (60.7%) were intestinal-type and 22 (39.3%) diffuse type carcinomas. In adjacent non-tumor gastric mucosa, chronic gastritis were found in 53 cases (94.6%) and atrophic mucosa in 36 patients (64.3%). All the patients with atrophic mucosa were H. pylori positive. When examined by Giemsa and urease test, H. pylori positive rate in tumor tissue of intestinal type carcinomas was higher than that in diffuse carcinomas. In tumor tissues, 34 (60.7%) H. pylori-positive in gastric carcinomas were detected by Giemsa method. H. pylori was observed in 30 of 56 cases (53.5%) in tissues 4 cm adjacent to tumors. This difference was not signifi cant. Eradication of H. pylori in non-tumor tissue of gastric remnant led to a complete negativity on the 12th postoperative month. Conclusions - The data confi rmed the hypothesis of a high prevalence of H. pylori in tumor tissue of gastric advanced carcinomas and in adjacent non-tumor mucosa of operated stomachs. The presence of H. pylori was predominant in the intestinal-type carcinoma

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This study consisted in the comparison of the prevalence of Helicobacter pylori (H. pylori) present in the stomach and in saliva of a sample of Portuguese adolescents and the assessment of the association between H. pylori infection with socio-demographic variables and prevalence of dental caries.