ABSTRACT The increase of H. pylori resistance to clarithromycin is a concern. This study evaluated the prevalence of H. pylori’s primary resistance to clarithromycin and its association with virulence factors in adult dyspeptic patients and asymptomatic children. The gastric mucosa from patients (153 gastritis, 24 gastric cancer, 21 peptic ulcer) and gastric juice obtained by string test from 24 H. pylori and 23S rRNA positive asymptomatic children were included. The clarithromycin resistance was assessed by TaqMan RT-PCR 23S rRNA point mutations, A2142G and/or A2143G, and H. pylori virulence markers by PCR. Overall, the clarithromycin resistance was 14.4% (32/222), 14.2% in adults, and 12% in children, whereas origin, gender, and disease were not distinctive factors. The most prevalent point mutation was A2143G (62.5%). The point mutation was significantly less frequent in cagA-positive (11.4%) than in cagA-negative (23.6%) strains (p=0.03 OR = 0.4 95%CI = 0.19 - 0.91) as well as in cagE-positive (10.2%), cagE-negative (21.2%) (p=0.03 OR: 0.4 I.C:0.20-0.91). No difference was found in iceA or vacA alleles genotypes. Primary resistance to clarithromycin was lower than that reported in Southeast Brazil. The cagA and cagE positive H. pylori samples have few point mutations suggesting that individuals infected with virulent strains may be more susceptible to anti-H. pylori treatment.

RESUMO Objetivo. Identificar tendências temporais e padrões espaciais de mortalidade relacionada ao câncer gástrico em todo o Brasil. Métodos. Realizou-se um estudo ecológico a partir de declarações de óbito registradas de 2000 a 2019 em que o câncer gástrico foi indicado como qualquer causa de morte (causa básica ou associada). As tendências ao longo do tempo foram avaliadas a partir de modelos de regressão por pontos de inflexão (joinpoint). Os aglomerados espaciais e espaço-temporais foram identificados por estatística de varredura espaço-temporal de Kulldorff para detectar áreas de alto risco. Resultados. O câncer gástrico foi registrado como qualquer causa de morte em 276.897/22.663.091 (1,22%) declarações de óbito. A mortalidade relacionada ao câncer gástrico ajustada por idade aumentou significativamente ao longo do tempo [variação percentual anual (VPA): 0,7, intervalo de confiança (IC) de 95%: 0,5 a 0,8]. O aumento da mortalidade foi mais acentuado no Norte e Nordeste, regiões menos desenvolvidas (região Norte, VPA: 3,1, IC 95%: 2,7 a 3,5; região Nordeste, VPA: 3,1, IC 95%: 2,5 a 3,7). Identificaram-se oito aglomerados de alto risco de mortalidade relacionada ao câncer gástrico em associação espaço-temporal nas regiões Norte, Sul, Nordeste e Centro-Oeste, além de um grande aglomerado que abrangia uma larga faixa geográfica nas regiões Sul e Sudeste do Brasil durante os primeiros anos do período de estudo (2000 a 2009). Conclusões. Mais recentemente, no período de 2010 a 2019, identificaram-se aglomerados de câncer gástrico na região Nordeste. O aumento da mortalidade em todo o país nesta análise de dados relativos a 20 anos evidencia a persistência da alta carga de câncer gástrico no Brasil, sobretudo em regiões desfavorecidas do ponto de vista socioeconômico. A identificação dessas áreas em que a população corre alto risco de morte relacionada ao câncer gástrico enfatiza a necessidade de desenvolver medidas de controle efetivas e intersetoriais.

ABSTRACT Objective. To identify nationwide temporal trends and spatial patterns of gastric cancer–related mortality in Brazil. Methods. An ecological study was performed using death certificates registered from 2000 to 2019 in which gastric cancer was recorded as any cause of death (an underlying or associated cause). Trends over time were assessed using joinpoint regression models. Spatial and spatiotemporal clusters were identified by Kulldorff’s space–time scan statistics to identify high-risk areas. Results. In 276 897/22 663 091 (1.22%) death certificates gastric cancer was recorded as any cause of death. Age-adjusted gastric cancer–related mortality increased significantly over time (annual percentage change [APC]: 0.7, 95% confidence interval [CI]: 0.5 to 0.8). The increase in mortality was more pronounced in the less-developed North and Northeast Regions (North Region, APC: 3.1, 95% CI: 2.7 to 3.5; Northeast Region, APC: 3.1, 95% CI: 2.5 to 3.7). Eight spatiotemporally associated high-risk clusters of gastric cancer–related mortality were identified in the North, South, Northeast and Central–West Regions, as well as a major cluster covering a wide geographical range in the South and Southeast Regions of Brazil during the first years of the study period (2000 to 2009). Conclusions. More recently, during 2010 to 2019, clusters of gastric cancer have been identified in the Northeast Region. The nationwide increase in mortality in this analysis of 20 years of data highlights the persistently high burden of gastric cancer in Brazil, especially in socioeconomically disadvantaged regions. The identification of these areas where the population is at high risk for gastric cancer–related mortality emphasizes the need to develop effective and intersectoral control measures.

RESUMEN Objetivo. Identificar las tendencias temporales y los patrones espaciales de la mortalidad relacionada con el cáncer gástrico a nivel nacional en Brasil. Métodos. Se realizó un estudio ecológico, empleando certificados de defunción registrados entre los años 2000 y 2019 en los que se notificó cáncer gástrico como cualquier causa de muerte (subyacente o asociada). Se evaluaron las tendencias con el transcurso del tiempo mediante modelos de regresión de punto de inflexión (joinpoint). Se identificaron los conglomerados espaciales y espaciotemporales mediante la técnica estadística de exploración espaciotemporal de Kulldorff para determinar cuáles eran las áreas de alto riesgo. Resultados. En 276 897 de 22 663 091 certificados de defunción (1,22%), se registró cáncer gástrico como cualquier causa de muerte. La mortalidad relacionada con el cáncer gástrico ajustada por edad aumentó significativamente con el tiempo (cambio porcentual anual: 0,7; intervalo de confianza [IC] del 95%: 0,5 a 0,8). El aumento de la mortalidad fue más acusado en la regiones Norte y Noreste, menos desarrolladas, (región Norte, cambio porcentual anual: 3,1, IC del 95%: 2,7 a 3,5; región Noreste, cambio porcentual anual: 3,1, IC del 95%: 2,5 a 3,7). Durante los primeros años del período de estudio (del 2000 al 2009), se identificaron ocho conglomerados de alto riesgo de mortalidad relacionada con el cáncer gástrico y con asociación espacial y temporal en las regiones Norte, Sur, Noreste y Centro-Oeste, así como un conglomerado importante que cubría un amplio rango geográfico en las regiones Sur y Sureste de Brasil. Conclusiones. Más recientemente, del 2010 al 2019, se han identificado conglomerados de cáncer gástrico en la región noreste. El aumento nacional de la mortalidad en este análisis de veinte años de datos destaca la carga persistentemente alta del cáncer gástrico en Brasil, especialmente en las regiones socioeconómicamente desfavorecidas. La identificación de estas áreas en que la población presenta un alto riesgo de mortalidad relacionada con el cáncer gástrico subraya la necesidad de elaborar medidas de control intersectoriales y efectivas.

ABSTRACT Trypanosoma cruzi and Helicobacter pylori (HP) are pathogens that cause chronic diseases and have been associated with hypergastrinemia. The aim of this study was to evaluate the fasting gastrin levels in patients with different clinical forms of Chagas disease (CD), coinfected or not by HP. The enrolled individuals were outpatients attending at the university hospital. HP infection was assessed by serology and 13 C-urea breath test. Fasting serum gastrin concentration was measured by chemiluminescence assay. Gastric endoscopic and histological features were also evaluated. Associations between CD and serum gastrin level were evaluated in a logistical model, adjusting for age, gender and HP status. A total of 113 patients were evaluated (45 with Chagas disease and 68 controls). In the multivariate analysis, increasing serum gastrin levels (OR= 1.02; 95% CI= 1.01-1.12), increasing age (OR= 1.05; 95% CI= 1.02 - 1.09) and HP-positive status (OR = 2.88; 95% CI = 1.10 - 7.51) remained independently associated with CD. The serum gastrin levels were significantly higher in the group of patients with the cardiodigestive form ( P = 0.03) as well as with digestive form ( P = <0.001) of Chagas disease than in the controls. In conclusion, patients with cardiodigestive and digestive clinical forms of CD have increased basal serum gastrin levels in comparison with controls. Moreover, we also demonstrated that H. pylori coinfection contributes to the hypergastrinemia shown in CD.

Introduction Most studies that have evaluated the stomachs of patients with Chagas disease were performed before the discovery of Helicobacter pylori and used no control groups. This study compared the gastric features of chagasic and non-chagasic patients and assessed whether gastritis could be associated with Chagas disease. Methods Gastric biopsy samples were taken from patients who underwent endoscopy for histological analysis according to the Updated Sydney System. H. pylori infection was assessed by histology, 16S ribosomal ribonucleic acid (rRNA) polymerase chain reaction (PCR), serology and the 13C-urea breath test. Patients were considered H. pylori-negative when all of these diagnostic tests were negative. Clinical and socio-demographic data were obtained by reviewing medical records and using a questionnaire. Results The prevalence of H. pylori infection (70.3% versus 71.7%) and chronic gastritis (92.2% versus 85%) was similar in the chagasic and non-chagasic groups, respectively; such as peptic ulcer, atrophy and intestinal metaplasia. Gastritis was associated with H. pylori infection independent of Chagas disease in a log-binomial regression model. However, the chagasic H. pylori-negative patients showed a significantly higher grade of mononuclear (in the corpus) and polymorphonuclear (PMN) (in the antrum) cell infiltration. Additionally, the patients with the digestive form of Chagas disease showed a significantly lower prevalence of corpus atrophy than those with other clinical forms. Conclusions The prevalence of H. pylori infection and of gastric histological and endoscopic features was similar among the chagasic and non-chagasic patients. Additionally, this is the first controlled study to demonstrate that H. pylori is the major cause of gastritis in patients with Chagas disease.

Helicobacter pylori infection is one of the most common infections worldwide and is associated with gastric diseases. Virulence factors such as VacA and CagA have been shown to increase the risk of these diseases. Studies have suggested a causal role of CagA EPIYA-C in gastric carcinogenesis and this factor has been shown to be geographically diverse. We investigated the number of CagA EPIYA motifs and the vacA i genotypes in H. pylori strains from asymptomatic children. We included samples from 40 infected children (18 females and 22 males), extracted DNA directly from the gastric mucus/juice (obtained using the string procedure) and analysed the DNA using polymerase chain reaction and DNA sequencing. The vacA i1 genotype was present in 30 (75%) samples, the i2 allele was present in nine (22.5%) samples and both alleles were present in one (2.5%) sample. The cagA-positive samples showed distinct patterns in the 3&#8217; variable region of cagA and 18 of the 30 (60%) strains contained 1 EPIYA-C motif, whereas 12 (40%) strains contained two EPIYA-C motifs. We confirmed that the studied population was colonised early by the most virulent H. pylori strains, as demonstrated by the high frequency of the vacA i1 allele and the high number of EPIYA-C motifs. Therefore, asymptomatic children from an urban community in Fortaleza in northeastern Brazil are frequently colonised with the most virulent H. pylori strains.

Helicobacter pylori causes chronic gastric inflammation and significantly increases the risk of duodenal and gastric ulcer disease and distal gastric carcinoma. In this study, we evaluated the Helicobacter pylori vacA and cagA genotypes in patients from a Brazilian region where there is a high prevalence of gastric cancer. Polymerase chain reaction (PCR) was used to investigate vacA mosaicism and cagA status in the gastric mucosa of 134 H. pylori-positive patients, including 76 with gastritis: 28 with peptic ulcer disease and 30 with gastric cancer. The s1m1 variant was the predominant vacA genotype observed, whereas the s1 allele was more frequently observed in patients with more severe diseases associated with H. pylori infection [p = 0.03, odds ratio (OR) = 5.72, 95% confidence interval (CI) = 1.15-38.60]. Furthermore, all of the s1 alleles were s1b. Mixed vacA m1/m2 strains were found more frequently in patients with gastric cancer and a cagA-positive status was significantly associated with gastric cancer (p = 0.016, OR = 10.36, 95% CI = 1.35-217.31). Patients with gastric cancer (21/21, 100%, p = 0.006) or peptic ulcers (20/21, 95%, p = 0.02) were more frequently colonised by more virulent H. pylori strains compared to gastritis patients (41/61, 67.2%). In conclusion, in the northeastern of Brazil, which is one of the regions with the highest prevalence of gastric cancer in the country, infection with the most virulent H. pylori strains, carrying the cagA gene and s1m1 vacA alleles, predominates and is correlated with more severe H. pylori-associated diseases.

INTRODUÇÃO: No presente estudo, foi comparada a soroprevalência da infecção por Helicobacter pylori entre os indivíduos chagásicos e não-chagásicos, bem como entre subgrupos de chagásicos com as formas clínicas indeterminada, cardíaca, digestiva e cardiodigestiva. MÉTODOS: Os indivíduos avaliados eram provenientes da região do Triângulo Mineiro, Minas Gerais, Brasil. Foram realizados testes sorológicos convencionais para diagnóstico da infecção pelo T. cruzi e os chagásicos foram classificados de acordo com a forma clínica. O diagnóstico de infecção por H. pylori foi estabelecido pela detecção de anticorpos IgG específicos utilizando-se um kit comercial de ELISA. RESULTADOS: A prevalência da infecção por H. pylorifoi 77,1% (239/310) no grupo de pacientes chagásicos e 69,1% (168/243) no grupo de não-chagásicos. Esta diferença foi estatisticamente significativa mesmo após ajuste para idade e sexo (OR = 1,57; 95% CI, 1,02-2,42; p = 0,04) na análise multivariada. A prevalência da infecção aumentou de acordo com a idade no grupo não-chagásicos (p = 0,007, χ2 for trend) mas este aumento não foi observado no grupo dos chagásicos (p = 0,15, χ2 for trend). Não houve associação da infecção por H. pylori com a forma digestiva ou com qualquer outra forma clínica da doença de Chagas (p = 0,27). CONCLUSÕES: Foi demonstrado que pacientes chagásicos apresentam maior prevalência da infecção por H. pylori quando comparados com não-chagásicos, independente da forma clínica da doença. Os fatores que contribuem para a frequente co-infecção Helicobacter pylori e Trypanosoma cruzi, bem como seus efeitos na evolução clínica das doenças associadas devem ser melhor estudados.

INTRODUCTION: In this study, we evaluated the seroprevalence of Helicobacter pylori infection among chagasic and non-chagasic subjects as well as among the subgroups of chagasic patients with the indeterminate, cardiac, digestive, and cardiodigestive clinical forms. METHODS: The evaluated subjects were from the Triângulo Mineiro region, Minas Gerais, Brazil. Chagasic patients showed positive reactions to the conventional serological tests used and were classified according to the clinical form of their disease. Immunoglobulin G antibodies specific to H. pylori were measured using a commercial enzyme-linked immunosorbent assay kit. RESULTS: The overall H. pylori prevalence was 77.1% (239/310) in chagasic and 69.1% (168/243) in non-chagasic patients. This difference was statistically significant even after adjustment for age and sex (odds ratio = 1.57; 95% confidence interval, 1.02-2.42; p = 0.04) in multivariate analysis. The prevalence of infection increased with age in the non-chagasic group (p = 0.007, χ2 for trend), but not in the chagasic group (p = 0.15, χ2 for trend). H. pylori infection was not associated with digestive or other clinical forms of Chagas disease (p = 0.27). CONCLUSIONS: Our findings demonstrate that chagasic patients have a higher prevalence of H. pylori compared to non-chagasic subjects; a similar prevalence was found among the diverse clinical forms of the disease. The factors contributing to the frequent co-infection with H. pylori and Trypanosoma cruzi as well as its effects on the clinical outcome deserve further study.

The hypothesis that Helicobactermight be a risk factor for human liver diseases has arisen after the detection of Helicobacter DNA in hepatic tissue of patients with hepatobiliary diseases. Nevertheless, no explanation that justifies the presence of the bacterium in the human liver has been proposed. We evaluated the presence of Helicobacterin the liver of patients with hepatic diseases of different aetiologies. We prospectively evaluated 147 patients (106 with primary hepatic diseases and 41 with hepatic metastatic tumours) and 20 liver donors as controls. Helicobacter species were investigated in the liver by culture and specific 16S rDNA nested-polymerase chain reaction followed by sequencing. Serum and hepatic levels of representative cytokines of T regulatory cell, T helper (Th)1 and Th17 cell lineages were determined using enzyme linked immunosorbent assay. The data were evaluated using logistic models. Detection of Helicobacter pylori DNA in the liver was independently associated with hepatitis B virus/hepatitis C virus, pancreatic carcinoma and a cytokine pattern characterised by high interleukin (IL)-10, low/absent interferon-γ and decreased IL-17A concentrations (p < 10-3). The bacterial DNA was never detected in the liver of patients with alcoholic cirrhosis and autoimmune hepatitis that are associated with Th1/Th17 polarisation. H. pylori may be observed in the liver of patients with certain hepatic and pancreatic diseases, but this might depend on the patient cytokine profile.

Helicobacter pylori infection is associated with peptic ulcer and gastric carcinoma. The oral cavity may be a reservoir for H. pylori; however, the results of studies on this subject are controversial. We employed single-step and nested polymerase chain reactions (PCR) to detect the presence of the vacA, ureA and 16S rDNA genes of H. pylori in the stomach, saliva and dental plaque of 30 subjects. The results were confirmed by sequencing. Nested 16S rDNA and ureA amplification was achieved in 80% of gastric, 30% of saliva and 20% of dental plaque specimens. Sequencing of 10, seven and four 16S rDNA products from stomach, saliva and dental plaque, respectively, showed > 99% identity with H. pylori. Sequencing of the other four oral cavity PCR products showed similarity with Campylobacter and Wolinella species. Additionally, the vacA genotype identified in the samples of different sites was the same within a given subject.H. pylori may be found in the oral cavity of patients with gastric infection, thus it could be a source of transmission. However, results obtained with detection methods based only on PCR should be interpreted with caution because other microorganisms that are phylogenetically very close to H. pylori are also present in the mouth.

As alterações qualitativas e quantitativas da flora ileal na obstrução biliar e o papel dos sais biliares foram avaliados em ratos. Em animais com obstrução biliar houve aumento da população ileal. Esse efeito é provavelmente causado pela ausência de sais biliares no lúmen ileal, uma vez que em animais cuja dieta foi suplementada com sais biliares houve redução da flora ileal.

Qualitative and quantitative alterations in ileal flora during obstructive jaundice and the role of bile salts were evaluated in rats. Obstructive jaundice was associated with bacterial overgrowth in the ileum. This effect may be due to the reduced concentration of bile salts, since dietary supplementation reduced the small bowel aerobic bacterial flora.

OBJETIVO: Apresentar aspectos relevantes relativos à úlcera péptica gastroduodenal e à infecção pelo Helicobacter pylori na criança e adolescente. FONTES DOS DADOS : Livros técnicos e bases de dados MEDLINE e LILACS de 1966 a 2006. SÍNTESE DOS DADOS : A úlcera péptica na criança e adolescente pode ser primária, associada à infecção pelo H. pylori, ou secundária, na qual os mecanismos etiopatogênicos dependem da doença de base. A infecção é adquirida predominantemente na infância, com taxas de prevalência que variam de 56,8 a 83,1% nas crianças que vivem nas regiões mais pobres do Brasil e de aproximadamente 10% nas crianças abaixo de 10 anos de idade nos países desenvolvidos. A infecção pode ser diagnosticada por métodos invasivos, que investigam a presença da bactéria, ou de DNA, RNA ou produtos bacterianos em fragmentos de biópsia da mucosa gástrica obtida à endoscopia; também pode ser diagnosticada através de métodos não-invasivos, que compreendem a pesquisa de anticorpos anti-H. pylori em amostras de soro, urina ou saliva, a pesquisa de antígenos da bactéria nas fezes e o teste respiratório com uréia marcada com carbono-13. O método de escolha para o diagnóstico da úlcera péptica é a endoscopia digestiva alta, com a vantagem adicional de, durante o procedimento, permitir a obtenção de fragmentos de mucosa gástrica para o diagnóstico da infecção e estudo histopatológico. CONCLUSÕES: A infecção por H. pylori é a principal causa de úlcera péptica na infância. A erradicação da bactéria com antimicrobiano é acompanhada de cura da doença, sendo, portanto, indicada em todas as crianças H. pylori-positivas com úlcera péptica em atividade, recorrente, cicatrizada ou complicada.

OBJECTIVE: To show important aspects of gastroduodenal peptic ulcer and of Helicobacter pylori infection in children and adolescents. SOURCES: Technical textbooks and MEDLINE and LILACS databases including publications between 1966 and 2006. SUMMARY OF THE FINDINGS : The etiology of peptic ulcer in children and adolescents may be primary, associated with H. pylori infection, or secondary, in which etiopathogenic mechanisms rely upon the underlying disease. The infection is acquired predominantly in childhood, with prevalence rates between 56.8 and 83.1% in children who live in the poorest Brazilian regions, amounting to nearly 10% in children aged less than 10 years in industrialized countries. The infection can be diagnosed by invasive methods, which investigate the presence of the bacterium, or of DNA, RNA or bacterial products in biopsy fragments of the gastric mucosa obtained at endoscopic examination; it can also be diagnosed through noninvasive methods, which include the detection of anti-H. pylori antibodies in serum, urine or saliva samples, detection of bacterial antigens in stool samples, and the carbon 13-labeled urea breath test. However, upper gastrointestinal endoscopy is the method of choice for the diagnosis of peptic ulcer, as it allows collecting fragments from the gastric mucosa during the procedure for the diagnosis of infection and for histopathological analysis. CONCLUSIONS: H. pylori infection is the major cause of peptic ulcer among children. Eradication of the bacterium with antimicrobial therapy results in the cure of the disease, and is therefore indicated for all children with H. pylori infection with an active, recurrent, healed, or complicated peptic ulcer.

OBJETIVOS: Analisar o padrão topográfico da gastrite por H. pylori em relação ao status cagA e associação com úlcera duodenal (UD) e carcinoma gástrico precoce (CaGp). MATERIAL E MÉTODO: Estudamos prospectivamente 160 biopsias endoscópicas e 40 peças de gastrectomia por CaGp. Amostras do antro e do corpo na pequena e grande curvaturas, da incisura e do tumor, foram processadas rotineiramente para histologia com histoquímica para caracterização da metaplasia intestinal (MI). O Helicobacter pylori foi avaliado por histologia, imuno-histoquímica, cultura e reação em cadeia de polimerase (PCR) e o status cagA por PCR. A gastrite crônica (GC) foi classificada segundo o sistema Sydney. Realizou-se estudo topográfico em 130 pacientes, analisando os parâmetros de gastrite comparativamente entre as áreas e em relação ao status cagA. RESULTADOS: Cento e vinte e um pacientes apresentaram GC, 24 UD e 14 eram normais. Detectaram-se amostras cagA-positivas em 59 pacientes com GC, 17 com UD e 24 com CaGp. Todos os parâmetros de GC foram significativamente mais intensos nos pacientes infectados por amostras cagA-positivas, que se associavam ainda à presença de atrofia e MI. A MI foi significativamente mais intensa na porção média da pequena curvatura antral do que nas demais regiões. Nos pacientes com GC e CaGp, infectados por amostras cagA-positivas, inflamação e atividade acometiam igualmente o antro e corpo distal, enquanto a atrofia e a MI predominavam no antro, particularmente na pequena curvatura do antro médio. Nos pacientes cagA-negativos a GC era predominantemente antral, e na UD a GC apresentava predominância antral, independentemente do status cagA. CONCLUSÕES: Nossos dados sugerem que o padrão de gastrite por H. pylori se relaciona com fatores de virulência da bactéria. As lesões pré-neoplásicas são significativamente mais intensas na pequena curvatura do antro médio, onde surge a maioria dos carcinomas gástricos (CaG).

AIMS: We aimed to investigate the topographical pattern of H. pylori gastritis in relation to cagA status and association with duodenal ulcer (DU) and early gastric carcinoma (EGCa). MATERIALS AND METHOD: We studied chronic gastritis (CG) in 160 patients submitted to upper endoscopy and in 40 patients with EGCa submitted to gastrectomy. Samples were taken from the antrum and corpus in the lesser and greater curvatures, incisura and from the tumour and were processed routinely for histology and histochemistry for intestinal metaplasia (IM) characterisation. H. pylori was evaluated by histology, immunohistochemistry, culture, and PCR; cagA status was evaluated by polymerase chain reaction (PCR). CG was analyzed according to the updated Sydney System. In 130 patients a topographic study was conducted by the comparative analysis of the gastritis parameters among the areas and according to cagA status. RESULTS: CG was observed in 121 patients, 24 had UD and 14 were normal. cagA-positive strains were detected in 59 patients with GC, 17 DU and 24 EGCa. All gastritis parameters were significantly more intense in the cagA-positive group than in cagA-negative one. Infection by cagA-positive strains was associated with atrophy and IM. IM was significantly more intense in the middle portion of the lesser curvature in the antral mucosa. In CG or EGCa patients infected with cagA-positive strains, inflammation and activity compromised equally the antrum and distal corpus, whereas atrophy and IM were more frequently found in the antral mucosa. In DU, CG was antral-predominant irrespectively of cagA status. CONCLUSIONS: According to our data the topographical pattern of H. pylori-associated gastritis seems to be associated with cagA status. Precancerous lesions were significantly more intense in the antral lesser curvature, where most gastric carcinomas arise.

A prevalência da infecção pelo Helicobacter pylori foi avaliada em amostra randomizada de indivíduos de uma comunidade urbana de baixa renda em Fortaleza, Estado do Ceará. O H. pylori foi detectado em 384 (62.9%) dos 610 participantes. A taxa de infecção foi de 47.5% em indivíduos com seis meses a 10 anos de idade, aumentou para 73.3% entre indivíduos com 11 a 20 anos, e continuou a aumentar com a idade, atingindo 87% naqueles com aproximadamente 60 anos. Após essa idade, a prevalência diminuiu discretamente. A prevalência da infecção aumentou significantemente com a idade (p<0.0001).

The prevalence of Helicobacter pylori infection was assessed in a randomly selected sample of individuals from low-income community in Fortaleza, Northeastern Brazil. Overall, 384 out of 610 participants (62.9%) were H. pylori positive. A 47.5% infection rate was found in subjects aged six months to 10 years old, increased to 73.3% in subjects aged 11-20 years and then continued to increase with age reaching up to 87% in those over 60 years old. After this age group, the prevalence decreased slightly. The prevalence of infection increased significantly with age (p<0.0001).

A prevalência da infecção pelo Helicobacter pylori foi avaliada em amostra randomizada de indivíduos de uma comunidade urbana de baixa renda em Fortaleza, Estado do Ceará. O H. pylori foi detectado em 384 (62.9%) dos 610 participantes. A taxa de infecção foi de 47.5% em indivíduos com seis meses a 10 anos de idade, aumentou para 73.3% entre indivíduos com 11 a 20 anos, e continuou a aumentar com a idade, atingindo 87% naqueles com aproximadamente 60 anos. Após essa idade, a prevalência diminuiu discretamente. A prevalência da infecção aumentou significantemente com a idade (p<0.0001).

The prevalence of Helicobacter pylori infection was assessed in a randomly selected sample of individuals from low-income community in Fortaleza, Northeastern Brazil. Overall, 384 out of 610 participants (62.9%) were H. pylori positive. A 47.5% infection rate was found in subjects aged six months to 10 years old, increased to 73.3% in subjects aged 11-20 years and then continued to increase with age reaching up to 87% in those over 60 years old. After this age group, the prevalence decreased slightly. The prevalence of infection increased significantly with age (p<0.0001).

We investigated the prevalence and the risk factors for infection with Helicobacter pylori in a randomly-selected population of adults from a low-income community in Northeastern Brazil. Helicobacter pylori infection was determined by ELISA. Risk factors were assessed using a structured interview. Two hundred and four individuals were included in the study, including 49 males and 155 females, ranging from 18 to 80 years old. Overall, 165 of 204 participants (80%) were H. pylori positive, without significant gender differences (p= 0.49). The infection rate was of 84.7% in subjects 18 to 30 years of age, increasing to 92% in subjects 46-60 years old. Above 60 years old, the prevalence decreased slightly. As a whole, the prevalence of infection did not increase significantly (p=0.147) with age. There were no significant differences in the prevalence of H. pylori infection, when patients were classified by age, smoking habit, educational level, alcohol consumption, the number of persons per room, the number of children per household, the number of adults per household, cup-sharing, household pets, toilet location, number of persons per bed and medical history of antibiotic and raw vegetable ingestion. In conclusion, no risk factors associated with infection was found in these adults, suggesting that the infection, even in a poor population, may be acquired predominantly during childhood; the relatively high prevalence that we observed may be more due to a cohort effect than to acquisition of infection during adulthood.