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1.
Arq. bras. cardiol ; 117(4): 626-636, Oct. 2021. tab, graf
Article in English, Portuguese | LILACS | ID: biblio-1345231

ABSTRACT

Resumo Fundamento: Estudos epidemiológicos recentes demonstraram que alterações na microbiota e seus metabólitos estão associadas à hipertensão arterial sistêmica. A Helicobacter pylori (H. pylori) é um dos patógenos bacterianos mais comuns, e a possível associação entre a infecção por H. pylori e a hipertensão é controversa. Objetivos: Este estudo teve o objetivo de esclarecer a associação entre eles e proporcionar uma nova base teórica para detectar a patogênese da hipertensão. Métodos: Foram selecionados estudos caso-controle e transversais sobre a associação entre H. pylori e hipertensão, publicados de 1996 a 2019 indexados nos bancos de dados PubMed, Google Scholar, Chinese Wan Fang Data, e Chinese National Knowledge Infrastructure (CNKI). As razões de chance (RC) combinadas e o intervalo de confiança (IC) 95% foram estimados. O I² foi realizado para avaliar a heterogeneidade estatística. O viés de publicação foi avaliado utilizando-se os testes de Beggs e de Egger. Os dados extraídos foram analisados no software Stata 12.0. A significância estatística foi definida com um p-valor < 0,05. Resultados: Foram cadastrados 17 estudos envolvendo 6376 casos de hipertensão e 10850 controles. A taxa de infecção por H. pylori em pacientes hipertensos e em controles foi de 64,9% e 56,3%, respectivamente. Foi demonstrada uma associação significativamente positiva entre a infecção por H. pylori e a hipertensão, com uma RC global de 2,07 (IC 95%: 1,46-2,94; p < 0,05). A análise de subgrupos revelou que a prevalência de infecção por H. pylori foi associada à hipertensão na região da Ásia e no grupo de caso-controle, as RC (IC 95%) foram 2,26 (1,51-3,38) e 2,53 (1,72-3,72), respectivamente. Depois de estratificar por métodos de detecção, ainda existiam diferenças entre os subgrupos (todos p < 0,05). Conclusão: Esta metanálise indicou que a infecção por H. pylori está associada positivamente à hipertensão.


Abstract Background: Recent epidemiological studies have shown that alterations in microbiota and its metabolites are associated with systemic arterial hypertension. Helicobacter pylori (H. pylori) is one of the most common bacterial pathogens, and the potential association between H. pylori infection and hypertension are controversial. Objective: This study aimed to clarify their association and provide a new theoretical basis for uncovering the pathogenesis of hypertension. Methods: Case-control and cross-sectional studies on the association between H. pylori and hypertension published from 1996 to 2019 indexed in PubMed, Google Scholar, Chinese Wan Fang Data, and Chinese National Knowledge Infrastructure (CNKI). The pooled odds ratios (OR) and 95% confidence interval (CI) were estimated. I2 was performed to evaluate the statistical heterogeneity. Publication bias was evaluated using Begg's and Egger's test. The extracted data was analyzed in Stata 12.0. Statistical significance was defined as p-value < 0.05. Results: A total of 17 studies involving 6,376 cases of hypertension and 10,850 controls were enrolled. H. pylori infection rate in hypertension patients and controls were 64.9% and 56.3%, respectively. A significantly positive association was shown between H. pylori infection and hypertension with an overall OR of 2.07 (95% CI: 1.46-2.94; p < 0.05). Subgroup analysis revealed that the prevalence of H. pylori infection was associated with hypertension in the region of Asia and the case-control group, ORs (95% CI) were 2.26 (1.51-3.38) and 2.53 (1.72-3.72), respectively. After stratifying by detection methods, differences still existed in subgroups (all p < 0.05). Conclusion: This meta-analysis indicated that H. pylori infection is positively associated with hypertension.


Subject(s)
Humans , Hypertension/epidemiology , Odds Ratio , Cross-Sectional Studies , Helicobacter pylori , Helicobacter Infections/complications , Helicobacter Infections/epidemiology
2.
Arq. gastroenterol ; 58(1): 114-119, Jan.-Mar. 2021. tab, graf
Article in English | LILACS | ID: biblio-1248992

ABSTRACT

ABSTRACT Helicobacter pylori is the main etiological agent of all malignant tumors caused by an infectious disease. It is a major, at times dominant, factor in the pathogenesis of a large spectrum of diseases such as acute and chronic gastritis, gastric and duodenal ulcers, gastric carcinoma, and lymphoma. Epidemiological and experimental studies suggest that H. pylori chronic infection may be related to different extragastric diseases, including colorectal neoplasms. This concise review aims to explore the association of H. pylori infection with colorectal cancer and adenoma, including the recent epidemiological findings, the diagnostic methods employed to detect H. pylori and virulent factors, and the potentially involved mechanisms. Furthermore, is attempted to establish the current data integration for causal inference using the Bradford-Hill causality criteria. The weak, although global, strength of the epidemiological positive association between H. pylori infection and colonic neoplasms associated to new mechanisms postulated to explain this interaction, including intestinal dysbiosis, should stimulate future studies. Prospective confirmatory studies to establish the role of H. pylori eradication in the process of carcinogenic transformation of the colonic epithelium may define its eventual role in the treatment and prevention of colonic neoplasms.


RESUMO Helicobacter pylori é o principal agente etiológico dos tumores malignos causados por doenças infecciosas. Constitui fator importante, às vezes dominante, na patogênese de um amplo espectro de doenças como gastrite aguda e crônica, úlceras gástricas e duodenais, carcinoma gástrico e linfoma. Estudos epidemiológicos e experimentais sugerem que a infecção crônica por H. pylori pode estar relacionada a diferentes doenças extragástricas, incluindo neoplasias colorretais. Esta concisa revisão tem como objetivo explorar a associação da infecção por H. pylori com câncer colorretal e adenoma, incluindo os recentes achados epidemiológicos, os métodos de diagnóstico empregados para detectar H. pylori e seus fatores de virulência com os mecanismos potencialmente envolvidos nesta relação. Além disso, procura-se estabelecer a integração dos dados atuais na busca de inferência causal com o emprego dos critérios de causalidade de Bradford-Hill. A associação epidemiológica positiva entre infecção por H. pylori e neoplasias do cólon embora classificada como fraca - porém global - do ponto de vista epidemiológico, quando associada a mecanismos recentemente postulados para explicar essa interação, incluindo disbiose intestinal, deverá estimular a realização de investigações futuras. Estudos prospectivos confirmatórios para estabelecer o papel da erradicação do H. pylori no processo de transformação carcinogênica do epitélio do cólon são aguardados para definir seu eventual papel no tratamento e prevenção de neoplasias do cólon.


Subject(s)
Humans , Stomach Neoplasms/etiology , Stomach Neoplasms/epidemiology , Colorectal Neoplasms/etiology , Colorectal Neoplasms/epidemiology , Helicobacter pylori , Helicobacter Infections/complications , Helicobacter Infections/epidemiology , Gastritis , Prospective Studies
3.
Ciencia Tecnología y Salud ; 8(2): 166-183, 2021. il 27 c
Article in Spanish | LILACS-Express | LILACS, LIGCSA, DIGIUSAC | ID: biblio-1353093

ABSTRACT

El cáncer gástrico (CG) es la neoplasia del tubo digestivo más prevalente en el mundo, asociada a factores genéticos del hospedero y externos, como infección por Helicobacter pylori. La patogénesis incluye inflamación crónica mediada por citocinas del microambiente tumoral, detectables sistémicamente. Estudios previos reportan niveles séricos de citocinas y su contribución al diagnóstico de CG. El presente estudio analiza el perfil de citocinas del tipo de Th1(IFNγ), Th2(IL-4 e IL-10), Th17(Th-17A) y otras pro inflamatorias: IL-1ß, IL-6 y TNF-α, en plasma de 70 casos de pacientes con CG comparándolos con 132 sujetos sanos equiparables en edad y sexo. Los casos provinieron del Hospital Roosevelt e Instituto Nacional de Cancerología de Guatemala (Incan) y formaron parte de un estudio previo. Se analizó la base de datos clínicos, patológicos y epidemiológicos. Se midieron los niveles de citocinas utilizando el sistema "MSD MULTI-SPOT Assay System". La edad promedio de los casos fue 59.5 años, (DE 13.0), 51%, eran positivos para IgG anti H. pylori. Un 71% presentó adenocarcinoma grado III (Borrman), según clasificación de Lauren 55% tenían tipo intestinal. Las siete citocinas cuantificadas se encontraron significativamente elevadas (p < .05) en el plasma de los casos respecto a sus controles. Los casos de CG tipo difuso presentaron niveles de IFNγ significativa-mente elevados. Por regresión logística, las citocinas IL-6 e IL-10, están asociadas significativamente a CG (p < .05) independientemente del estatus de infección por H. pylori. Se destacan la IL-6 e IL-10 como las principales citocinas asociadas a la presencia de CG.


Gastric cancer (GC) is the most prevalent gastrointestinal neoplasm in the world, associated with host and external genetic factors, such as Helicobacter pylori infection. The pathogenesis includes chronic inflammation mediated by cytokines of the tumor microenvironment, systemically detectable. Previous studies report serum levels of cyto-kines and their contribution to the diagnosis of GC. The present study analyzes the profile of cytokines of the type Th1 (IFNγ), Th2 (IL-4 and IL-10), Th17 (Th-17A) and other pro-inflammatory: IL-1ß, IL-6 and TNF-α, in plasma of 70 cases of patients with GC compared with 132 healthy subjects comparable in age and sex. The cases came from the Roosevelt Hospital and the National Cancer Institute of Guatemala -Incan- and were part of a previous study. The clinical, pathological and epidemiological databases were analyzed. Cytokine levels were measured using the "MSD MULTI-SPOT Assay System". The average age of the cases was 59.5 years, (SD 13.0), 51% were positive for IgG anti H. pylori, 71% had grade III adenocarcinoma (Borrman), according to Laurenís classification, 55% had intestinal type. The seven cytokines quantified were found to be significantly elevated (p < .05) in the plasma of the cases compared to their controls. The diffuse GC cases presented significantly elevated IFNγ levels. By logistic regression, the cytokines IL-6 and IL-10 are significantly associated with GC (p < .05) regardless of the H. pylori infection status. IL-6 and IL-10 stand out as the main cytokines associated with the presence of GC.


Subject(s)
Humans , Male , Female , Adolescent , Adult , Middle Aged , Plasma/chemistry , Stomach Neoplasms/complications , Cytokines/analysis , Interleukin-6/analysis , Interleukin-1/analysis , Interleukin-10/analysis , Th2 Cells , Th17 Cells , Immunoglobulin G/analysis , Adenocarcinoma/complications , Biomarkers, Tumor/analysis , Helicobacter Infections/complications , Th1 Cells , Gastrointestinal Tract/pathology , Tumor Microenvironment , Neoplasms/complications
4.
Rev. cuba. med. mil ; 49(4): e616, tab
Article in Spanish | LILACS, CUMED | ID: biblio-1156518

ABSTRACT

Introducción: El Helicobacter pylori se ha relacionado con el desarrollo de gastritis crónica atrófica, metaplasia intestinal y displasia, lesiones que pueden evolucionar a carcinoma gástrico. Existen investigaciones que demuestran que la erradicación de esta bacteria disminuye el riesgo de progresión histopatológica de las lesiones preneoplásicas, excepto la metaplasia intestinal y la displasia. Se realizó una revisión de los artículos publicados en las bases de datos Pubmed, Scielo, Medline y Cochrane, relacionados con el tema. Objetivo: Profundizar en los conocimientos relacionados con la infección por Helicobacter pylori y cáncer gástrico. Desarrollo: El adenocarcinoma es el tumor gástrico más frecuente y el Helicobacter pylori es el agente etiológico principal. En poblaciones de riesgo elevado, el adenocarcinoma gástrico de tipo intestinal, se precede de lesiones preneoplásicas (atrofia, metaplasia intestinal y displasia) que evoluciona al cáncer invasor. Conclusiones: Helicobacter pylori favorece la carcinogénesis gástrica, aunque existen otros factores de riesgo para el surgimiento del cáncer gástrico como son: la historia familiar, la pobre ingestión de frutas y vegetales y el bajo nivel socioeconómico(AU)


Introduction: Helicobacter pylori has been linked to the development of chronic atrophic gastritis, intestinal metaplasia, and dysplasia, lesions that can progress to gastric carcinoma. There is research showing that the eradication of this bacterium reduces the risk of histopathological progression of preneoplastic lesions, except for intestinal metaplasia and dysplasia. A bibliographic review was made of the articles published in the Pubmed, Scielo, Medline and Cochrane data bases, related to the topic, belonging to authors dedicated to the study of this problem. Objective: To go deepen in the knowledge related to Helicobacter pylori infection and gastric cancer. Development: Adenocarcinoma is the most frequent gastric tumor and Helicobacter pylori is the main etiologic agent. In high-risk populations, gastric adenocarcinoma of the intestinal type, is preceded by preneoplasic lesions (atrophy, intestinal metaplasia, and dysplasia), that progresses to invasive cancer. Conclusions: Helicobacter pylori favors gastric carcinogenesis, although there are other risk factors for the development of gastric cancer such as: family history, poor intake of fruits and vegetables, and low socioeconomic leve(AU)


Subject(s)
Animals , Stomach Neoplasms/epidemiology , Helicobacter Infections/complications , Helicobacter Infections/drug therapy
5.
Prensa méd. argent ; 106(7): 439-443, 20200000.
Article in English | LILACS, BINACIS | ID: biblio-1366962

ABSTRACT

Background: There are many studies highlight the association between Helicobacter pylori seropositivity with typhoid fever in human populations and there is no study in Iraq. Aim: Our study designed to estimate the correlation between seroprevelace of H. pylori and Typhoid fever in clinically examined patients as dyspeptic and typhoid fever infected. Methods: From May (2016) to February (2018), a total of 213 patients (134 females and 79 male) attending an enterology outpatient clinic in AL-Najaf province, Iraq. The patients with age range from 10 to 90 years and with symptoms of dyspepsia and typhoid fever (as fever, diarrhea, headache), were referred to serologic diagnosis of antibodies against H. pylori (IgG) and Typhoid (IgG and/or IgM), using the Rapid Tests Cassette. Results: Of a total of 213 clinically examined as dyspeptic and typhoid fever infected patients,134 (63.0%) were females and 79 (37.0%) were males.In this study, 82 (38.5 %) of 213 patients were seropositive for typhoid fever and 131 patients were seronegative. Moreover, 128 (60.1 %) of 213 patients were seropositive for H.pylori IgG (51 case,39.8%, typhoid seropositive, and 77 case,60.2%, typhoid seronegative) and 82 were seronegative. The serologic co-infection diagnosed in 51 (24.0%) patients. The seropositivity of typhoid fever was higher in H. pylori seropositive patients, co-infections (62.2 %), than H. pylori seronegative patients (37.8%). The co-infection was more in female (64.7%) than male (35.3%). In respect of age H. pylori seropositivity was more prevelance (25.8%) in 30s age group where as co-infection was more prevalence in 40s age group (29.4%). But the statistical analysis showed insignificant association of H. pylori with typhoid fever (P value = 0.6203), gender (P value = 0.4770) and age groups (P value = 0.0745). Conclusion: Our study indicates that H. pylori seropositive dyspepsia more susceptiple to typhoid fever particularly in female and 40s ages and suggest there was insignificant relationship amongst seropositivity of H. pylori and typhoid fever within dyspepsia patient


Subject(s)
Humans , Adolescent , Adult , Middle Aged , Aged , Typhoid Fever/diagnosis , Helicobacter Infections/complications , Dyspepsia/complications
7.
Rev. méd. Chile ; 147(11): 1382-1389, nov. 2019. tab, graf
Article in Spanish | LILACS | ID: biblio-1094167

ABSTRACT

Background Chile has one of the highest mortality rates by gastric cancer (GC) worldwide. Primary prevention of GC and detection of pre-neoplastic and early neoplastic lesions should be a national priority. Aim To assess the impact of the protocolization of endoscopy referral and the use of H. pylori stool antigen test (HPSA) in the management of dyspepsia to decrease the waiting list for endoscopy and increase the detection of gastric pre-neoplastic and early neoplastic lesions. Material and Methods We included all patients referred to the Endoscopy Unit of a regional hospital, from January 2015 to December 2017. We also included patients with known pre-neoplastic lesions and all those with first degree relatives with GC. We implemented protocols for referral of patients with dyspepsia considering the use of HPSA test, prioritizing to endoscopy those with a higher risk of GC. Results A total of 4,641 endoscopies and 2,631 HPSA tests were carried out. After the adoption of these protocols, we observed a 52% decrease in the waiting time for endoscopy. The GC detection rate in this period was 1.8 to 3.1 cases per 100 endoscopies. After the adoption of the protocols, we observed a significant increase in early GC detection rate (from none in 2015 to 13% in 2017, p = 0.03). Conclusions The protocolization of the referral for endoscopy associated with widespread use of HPSA test in the management of patients with dyspepsia, are successful strategies to decrease waiting lists for endoscopy and optimize the detection rate of pre-neoplastic lesions and early GC.


Subject(s)
Humans , Precancerous Conditions/diagnosis , Waiting Lists , Helicobacter pylori/isolation & purification , Helicobacter Infections/diagnosis , Dyspepsia/diagnosis , Feces/microbiology , Antigens, Bacterial/analysis , Precancerous Conditions/microbiology , Primary Health Care , Referral and Consultation , Helicobacter Infections/complications , Helicobacter Infections/microbiology , Sensitivity and Specificity , Early Diagnosis , Dyspepsia/microbiology , Endoscopy/statistics & numerical data
8.
Int. j. morphol ; 37(3): 917-927, Sept. 2019. graf
Article in Spanish | LILACS | ID: biblio-1012376

ABSTRACT

El carcinoma gástrico (CG) de tipo intestinal se origina en un epitelio displásico, que a su vez se desarrolla en medio de una atrofia gástrica (AG) y metaplasia intestinal (MI). La infección por Helicobacter pylori (HP) es la causa más frecuente de AG, causando una pangastritis atrófica multifocal. Entre otras condiciones que producen inflamación crónica de la mucosa gástrica se encuentran también la gastritis autoinmune y la anemia perniciosa. El marco conceptual sobre el cual descansa gran parte de la investigación actual y nuestra comprensión de los cambios que ocurren en la mucosa gástrica se debe a la denominada "cascada de Correa"; quien planteó que la mucosa gástrica crónicamente inflamada, da paso a la AG, que va adquiriendo focos de MI y en dicho epitelio se desarrollará finalmente una displasia (DIS). Se ha acuñado el término lesiones preneoplásicas gástricas (LPG), para referirse a: AG, MI y DIS.Después de la erradicación de HP, se ha demostrado una reducción general de la incidencia de CG; efecto que no es tan claro, cuando la pangastritis por HP ha evolucionado a AG extensa. De tal modo que el efecto de la erradicación de HP medido a través de EC, ha sido poco consistente. La AG grave diagnosticada por histología representa la condición de mayor riesgo. Por otra parte, la MI puede ser de tipo intestinal (delgado-entérica ó incompleta) y la colónica (colónica ó completa) considerándose a esta última, como la variedad de peor pronóstico. El diagnóstico histológico de este tipo de lesiones determina que quien las padece, debe someterse a vigilancia endoscópica. El objetivo de este manuscrito fue resumir la evidencia existente respecto de las LPG, en términos de su caracterización morfológica y sus repercusiones diagnóstico-terapéuticas (significado patológico, graduación del riesgo, vigilancia recomendada; y factores de riesgo).


Gastric carcinoma (GC) of intestinal type, originates from a dysplastic epithelium, which in turn develops in the midst of gastric atrophy (GA) and intestinal metaplasia (IM). Helicobacter pylori (HP) infection is the most frequent cause of GA, causing a multifocal atrophic pangastritis. Among other conditions that produce chronic inflammation of gastric mucosa are also autoimmune gastritis and pernicious anemia. The conceptual framework on which much of current research rests and our understanding of the changes that occur in the gastric mucosa is due to the so-called "Correa waterfall"; who stated that gastric mucosa chronically inflamed, gives way to the GA, which is acquiring foci of IM and in said epithelium a dysplasia (DIS) will eventually develop. The term precancerous conditions (PCC) of the gastric mucosa have been coined to refer to: GA, IM and DIS. After HP eradication, a general reduction in the incidence of GC has been demonstrated; effect that is not so clear, when pangastritis by HP has evolved to extensive GA. Thus, the effect of HP eradication measured through clinical trials has been inconsistent. Severe GA diagnosed represents the highest risk condition. On the other hand, IM can be enteric (grade I), enterocolic (grade II) or colonic (grade III); considering IM III as the variety with the worst prognosis. Histological diagnosis of gastric PCC, determines that the one who suffers them, must undergo endoscopic surveillance. The aim of this manuscript was to update morphological aspects and diagnostic-therapeutic scope of gastric PCC.


Subject(s)
Humans , Precancerous Conditions/pathology , Stomach Neoplasms/pathology , Precancerous Conditions/microbiology , Stomach Neoplasms/microbiology , Risk Factors , Helicobacter pylori , Helicobacter Infections/complications , Helicobacter Infections/pathology , Risk Assessment , Gastritis, Atrophic/microbiology , Gastritis, Atrophic/pathology , Intestines/microbiology , Intestines/pathology , Metaplasia/microbiology , Metaplasia/pathology
9.
Arq. gastroenterol ; 56(3): 264-269, July-Sept. 2019. tab, graf
Article in English | LILACS | ID: biblio-1038716

ABSTRACT

ABSTRACT BACKGROUND: It is widely assumed that gender, age, gastritis and Helicobacter pylori , all have some degree of correlation and, therefore, can synergistically lead to the development of gastric cancer. OBJECTIVE: In this cross-sectional study, we expected to observe the above mentioned correlation in the analysis of medical records of 67 patients of both sexes (female, n=44), mean age ± standard deviation: 41±12 years old, all from Belém (capital of Pará State, Brazilian Amazon), a city historically known as one with the highest gastric cancer prevalence in this country. METHODS: All patients were submitted to upper gastrointestinal endoscopy for gastric biopsy histopathological analysis and rapid urease test. All diagnoses of gastritis were recorded considering its topography, category and the degree of inflammatory activity, being associated or not associated with H. pylori infection. RESULTS: The results show that no statistically relevant associations were found among the prevalences of the observed variables. CONCLUSION: The authors hypothesize that observed risk factors associated to gastric cancer might be lesser synergistic than is usually expected.


RESUMO CONTEXTO: É amplamente assumido que gênero, idade, gastrite e Helicobacter pylori , todos têm algum grau de correlação e, portanto, podem sinergicamente levar ao desenvolvimento de câncer gástrico. OBJETIVO: Neste estudo transversal, esperamos observar a correlação acima mencionada na análise de prontuários de 67 pacientes de ambos os sexos (sexo feminino, n=44), média de idade ± desvio padrão: 41±12 anos, todos de Belém (capital do Estado do Pará, Amazônia Brasileira), uma cidade historicamente conhecida como sendo uma das que apresenta maior prevalência de câncer gástrico no país. MÉTODOS: Todos os pacientes foram submetidos à endoscopia digestiva alta para análise histopatológica da biópsia gástrica e teste rápido da urease. Todos os diagnósticos de gastrite foram registrados considerando sua topografia, categoria e grau de atividade inflamatória, sendo associada ou não associada à infecção por H. pylori . RESULTADOS: Os resultados mostram que não foram encontradas associações estatisticamente relevantes entre as prevalências das variáveis observadas. CONCLUSÃO: Os autores levantam a hipótese de que os fatores de risco associados ao câncer gástrico podem ser menos sinérgicos do que o esperado.


Subject(s)
Humans , Male , Female , Adult , Stomach Neoplasms/microbiology , Urease/analysis , Helicobacter Infections/complications , Gastric Mucosa/microbiology , Gastric Mucosa/pathology , Stomach Neoplasms/pathology , Stomach Neoplasms/epidemiology , Biopsy , Brazil/epidemiology , Sex Factors , Prevalence , Cross-Sectional Studies , Endoscopy, Digestive System , Helicobacter pylori , Helicobacter Infections/enzymology , Helicobacter Infections/epidemiology , Age Factors , Sex Distribution , Gastritis/microbiology , Gastritis/pathology , Intestinal Mucosa/enzymology , Middle Aged
11.
Rev. medica electron ; 40(2): 433-444, mar.-abr. 2018. ilus
Article in Spanish | LILACS, CUMED | ID: biblio-902310

ABSTRACT

RESUMEN La Organización Mundial de la Salud señala que el cáncer gástrico es una neoplasia frecuente en el mundo contemporáneo. Constituye la segunda causa de muerte en el hombre y la tercera en las mujeres. Numerosos son los factores de riesgo que se asocian con la aparición del cáncer gástrico, en determinadas regiones del mundo. El descubrimiento del Helicobacter pylori y la asociación con las enfermedades gastroduodenales ha revolucionado los aspectos fisiopatológicos y terapéuticos hasta el punto de considerar la bacteria como agente precursor del cáncer gástrico. Por tal motivo se realizó una revisión de los factores de riesgo y el papel del Helicobacter pylori en la formación de la neoplasia gástrica, con el objetivo de aportar conocimientos relacionados con el cáncer gástrico y su prevención (AU).


ABSTRACT The World Health Organization points out that gastric cancer is a frequent neoplasia in the contemporary world. It is the second cause of death in men and the third one in women. There are several risk factors associated to the development of gastric cancer in specific regions of the world. The discovery of Helicobacter pylori and its association to gastro duodenal diseases has renewed the physiopathological and therapeutic aspects up to the point of considering the bacteria as precursor agent of gastric cancer. For that cause, it was carried out a review of the risk factors and the role of Helicobacter pylori in the formation of gastric neoplasia, with the objective of giving out knowledge related to gastric cancer and its prevention (AU).


Subject(s)
Humans , Stomach Neoplasms/diagnosis , Stomach Neoplasms/mortality , Stomach Neoplasms/prevention & control , Stomach Neoplasms/epidemiology , Risk Factors , Helicobacter Infections/complications , Helicobacter Infections/etiology , Helicobacter Infections/epidemiology , Preventive Health Services , Bibliography of Medicine , Developed Countries , Indicators of Morbidity and Mortality , Epidemiologic Methods , Helicobacter pylori , Developing Countries , Health Promotion
12.
Rev. medica electron ; 40(1): 159-171, ene.-feb. 2018. ilus
Article in Spanish | LILACS, CUMED | ID: biblio-902277

ABSTRACT

RESUMEN La infección por la bacteria Helicobacter pylori ocurre a nivel mundial, aunque es más frecuente en países en vías de desarrollo y en comunidades en condiciones socioeconómicas pobres, donde existe hacinamiento o migración de regiones de prevalencia alta. La infección ocurre principalmente durante la infancia y se incrementa con la edad. Se realizó una revisión exhaustiva donde se explican de manera explícita los mecanismos que desencadenan la respuesta inflamatoria una vez que la bacteria coloniza el estómago, que incluye dos etapas: la primera caracterizada por la llegada y penetración del microorganismo al moco gástrico, donde se asienta y se multiplica y la segunda etapa caracterizada por una amplificación de esta respuesta inflamatoria. El conocimiento de estos mecanismos etiopatogénicos no sólo ayuda a la erradicación de la bacteria, sino que contribuye a la regulación del sistema neuroinmune antes, durante y después del daño tisular, para lograr una regeneración tisular adecuada, mejorar la capacidad funcional del órgano sangrante e impedir la evolución tórpida de la enfermedad (AU).


ABSTRACT The infection by Helicobacter pylori occurs worldwide, although it is more frequent in developing countries and in communities with poor socioeconomic conditions, where there is overcrowding or migration from regions of high prevalence. The infection occurs mainly during the childhood and increases with age. An exhaustive review was carried out where the mechanisms unchaining the inflammatory answer after the bacteria colonizes the stomach are explained in an explicit way. It has two stages: the first one is characterized by the microorganism arrival and penetration to the gastric mucus, where it settles and multiplies, and the second stage characterized by an amplification of the inflammatory answer. The knowledge of these etiopathogenic mechanisms does not only help the eradication of the bacteria but also contributes to the regulation of the neuroimmune system before, during and after tissue damage, for reaching an adequate tissue regeneration, improving the functional capacity of the bleeding organ, and preventing the disease torpid evolution (AU).


Subject(s)
Humans , Helicobacter pylori , Helicobacter Infections/complications , Helicobacter Infections/etiology , Systemic Inflammatory Response Syndrome , Virulence Factors , Gastrointestinal Hemorrhage/etiology , Neuroimmunomodulation , Epidemiologic Factors , Inflammation Mediators , Immunity, Mucosal , Neurogenic Inflammation
14.
Arq. gastroenterol ; 54(4): 297-299, Oct.-Dec. 2017. tab
Article in English | LILACS | ID: biblio-888214

ABSTRACT

ABSTRACT BACKGROUND: As being the first bacteria determined to be carcinogenic, Helicobacter pylori (H. pylori) is a pathogen localized in the stomach in more than half of the world population. Some earlier studies have found a relation between tissue histocompatibility antigens and gastric cancers depending on the regions. OBJECTIVE: The present study aimed to determine the distribution of human leukocyte antigen (HLA) class I and class II antigens in H. pylori-positive pediatric patients with active gastritis and duodenal ulcer, excluding cancer cases, in our center. METHODS: The study included 40 patients diagnosed with H. pylori-positive active gastritis and duodenal ulcer and 100 controls consisting of healthy donor candidates. The HLA class I and class II antigens were studied in the isolated DNA samples using the polymerase chain reaction sequence-specific oligonucleotide probes. RESULTS: The frequency of HLA-B*51 antigen was significantly higher in the patient group than in the control group (40% vs 17%; P=0.003). There was no difference between the two groups in terms of the frequencies of HLA-A, HLA-C, HLA-DR, and HLA-DQ antigens. CONCLUSION: It was determined that HLA-B*51 plays a critical role in H. pylori infection.


RESUMO CONTEXTO: Determinada como sendo a primeira bactéria cancerígena, o Helicobacter pylori (H. pylori) é um patógeno localizado no estômago em mais da metade da população mundial. Alguns estudos anteriores têm encontrado uma relação entre câncer gástrico e antígenos de histocompatibilidade de tecido dependendo das regiões. OBJETIVO: O presente estudo teve como objetivo determinar a distribuição em nosso centro do antígeno leucocitário humano (HLA) de classe I e antígenos classe II em pacientes pediátricos H. pylori-positivos com gastrite e úlcera duodenal ativas, excluindo casos de câncer. MÉTODOS: O estudo incluiu 40 pacientes H. pylori-positivos diagnosticados com gastrite e úlcera duodenal ativas e 100 controles consistindo de candidatos doadores saudáveis. Foram estudadas nas amostras de DNA isoladas o antígeno leucocitário humano classe I e antígenos classe II, utilizando-se as cadeias de sequência específica de polimerase do oligonucleotideo. RESULTADOS: A frequência do antígeno HLA - B * 51 foi significativamente maior no grupo de pacientes do que no grupo controle (40% vs 17%; P=0,003). Não houve diferença entre os dois grupos em termos das frequências dos antígenos HLA-A, HLA-DR, HLA-DQ e HLA-C. CONCLUSÃO: Determinou-se que o HLA - B * 51 desempenha um papel crítico na infecção pelo H. pylori.


Subject(s)
Humans , Male , Female , Child , Histocompatibility Antigens Class I/immunology , Histocompatibility Antigens Class II/immunology , Helicobacter pylori , Helicobacter Infections/immunology , Duodenal Ulcer/immunology , Gastritis/immunology , Case-Control Studies , Helicobacter Infections/complications , Gastritis/microbiology
15.
Clinics ; 72(3): 150-153, Mar. 2017. tab, graf
Article in English | LILACS | ID: biblio-840051

ABSTRACT

OBJECTIVE: Esophageal squamous cell carcinoma is one of the most common esophageal diseases in the developing world, but the relationship between esophageal squamous cell carcinoma and Helicobacter pylori infection remains a neglected topic. The primary objective of this study was to determine the association between Helicobacter pylori infection and esophageal squamous cell carcinoma. A second purpose was to determine the incidence and factors associated with Helicobacter pylori infection following esophagectomy. METHOD: The microorganism was identified by testing the gastric biopsy materials from 95 esophageal squamous cell carcinoma patients (66 females; 39 were esophagectomized) for urease activity in a medium containing urea and a power of hydrogen detection reagent and comparing the results with those from a healthy population. Differences in patient characteristics were assessed with chi-square tests and t-tests for categorical and continuous factors, respectively. RESULTS: The patients with esophageal squamous cell carcinoma had a significantly lower prevalence of Helicobacter pylori compared with the healthy population (p<0.001). The naive and esophagectomized patients, in contrast, showed no significant differences in Helicobacter pylori infection (p>0.005). Patients with esophageal squamous cell carcinoma showed a significant association between leukocytosis and hypoglobulinemia and the presence of Helicobacter pylori infection (p=0.023 and p=0.045, respectively). CONCLUSION: These results suggest that Helicobacter pylori is not an etiological factor in patients with esophageal squamous cell carcinoma. We found a statistically significant negative correlation between esophageal squamous cell cancer and Helicobacter pylori infection. These findings may guide new strategies for esophageal squamous cell carcinoma therapy.


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Aged, 80 and over , Carcinoma, Squamous Cell/microbiology , Esophageal Neoplasms/microbiology , Helicobacter Infections/complications , Helicobacter pylori/isolation & purification , Biopsy , Carcinoma, Squamous Cell/pathology , Case-Control Studies , Esophageal Neoplasms/pathology , Helicobacter Infections/pathology , Helicobacter pylori/pathogenicity , Retrospective Studies , Risk Factors , Sex Factors , Statistics, Nonparametric
16.
An. bras. dermatol ; 92(1): 52-57, Jan.-Feb. 2017. tab, graf
Article in English | LILACS | ID: biblio-838027

ABSTRACT

Abstract: BACKGROUND: Psoriasis is a chronic inflammatory disease that affects the skin and joints and has a multifactorial etiology. Recently, it has been suggested that Helicobacter pylori infection may contribute as a trigger for the development of the disease. OBJECTIVES: To determine the prevalence of H. pylori seropositivity in patients with psoriasis and to evaluate the relation between disease severity and H. pylori infection. METHODS: H. pylori infection was assessed in psoriatic patients and controls by using H. pylori IgG quantitative enzyme immunoassay (ELISA test). The patients were classified according to the severity of the disease (PASI score). RESULTS: One hundred and twenty six patients with psoriasis (73 females and 53 males); mean age 50.48 years; 65 patients (51.59%) had severe psoriasis, 40 (31.75%) moderate psoriasis and 21 (16.67%) mild psoriasis. Twenty one healthy volunteers included as a control group, mean age of 41.05 years, 13 females and 8 males. One hundred and eleven patients with psoriasis tested serologically, 80 (72.07%) were seropositive compared with 7 positive volunteers (33.33%; P=0.002). Forty-nine (75.38%) patients with severe psoriasis were positive, 25 (62.50%) with moderate psoriasis were positive and 6 (28.57%) with mild psoriasis were positive (P=0.045). Study limitations: none. CONCLUSIONS: H. pylori infection influences the development of psoriasis and severity of the disease.


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Psoriasis/microbiology , Helicobacter pylori , Helicobacter Infections/complications , Severity of Illness Index , Enzyme-Linked Immunosorbent Assay , Case-Control Studies , Seroepidemiologic Studies , Helicobacter Infections/diagnosis , Helicobacter Infections/immunology
17.
Säo Paulo med. j ; 135(1): 29-33, Jan.-Feb. 2017. tab
Article in English | LILACS | ID: biblio-846275

ABSTRACT

ABSTRACT CONTEXT AND OBJECTIVE: Helicobacter pylori (H. pylori) is a chronic infectious pathogen with high prevalence. This study investigated the interaction between environmental tobacco exposure and H. pylori infection on the incidence of chronic tonsillitis in Chinese children. DESIGN AND SETTING: Cross-sectional study performed in an outpatient clinic in China. METHODS: Pediatric patients with chronic tonsillitis were enrolled. H. pylori infection was determined according to the presence of H. pylori CagA IgG antibodies. Serum cotinine levels and environmental tobacco smoke (ETS) exposure were determined for all participants. RESULTS: There was no significant difference in H. pylori infection between the children with chronic tonsillitis and children free of disease, but there was a significant difference in ETS between the two groups (P = 0.011). We next studied the association between ETS and chronic tonsillitis based on H. pylori infection status. In the patients with H. pylori infection, there was a significant difference in ETS distribution between the chronic tonsillitis and control groups (P = 0.022). Taking the participants without ETS as the reference, multivariate logistic regression analysis showed that those with high ETS had higher susceptibility to chronic tonsillitis (adjusted OR = 2.33; 95% CI: 1.67-3.25; adjusted P < 0.001). However, among those without H. pylori infection, ETS did not predispose towards chronic tonsillitis. CONCLUSION: Our findings suggest that tobacco exposure should be a putative mediator risk factor to chronic tonsillitis among children with H. pylori infection.


RESUMO CONTEXTO E OBJETIVO: Helicobacter pylori (H. pylori) é um patógeno infeccioso crônico com alta prevalência. Este estudo investigou a interação entre exposição à fumaça ambiental do tabaco (FAT) e infecção pelo H. pylori sobre a incidência de amigdalite crônica em crianças chinesas. TIPO DE ESTUDO E LOCAL: Estudo transversal desenvolvido num ambulatório na China. MÉTODOS: Pacientes pediátricos com amigdalite crônica foram recrutados. A infecção por H. pylori foi determinada segundo a presença de anticorpos H. pylori CagA IgG. Foi determinado o nível de cotinina sérica e exposição à FAT de todos os participantes. RESULTADOS: Não houve diferença significativa entre crianças com amigdalite crônica na infecção por H. pylori e sem amidalite, mas existia diferença significativa na FAT entre os dois grupos (P = 0,011). Em seguida, estudamos a associação entre FAT e amigdalite crônica com base no status de infecção por H. pylori. Nos pacientes com infecção por H. pylori, houve diferença significativa na distribuição de FAT entre os grupos de amigdalite crônica e controle (P = 0,022). Tomando os participantes sem FAT como referência, a análise de regressão logística multivariada mostrou que aqueles com alta FAT tinha maior susceptibilidade à amigdalite crônica (OR ajustado IC = 2,33, 95%: 1,67-3,25, ajustado P < 0,001). No entanto, naqueles sem infecção por H. pylori, a FAT não predispôs a amigdalite crônica. CONCLUSÃO: Nossos achados sugerem que a exposição ao tabaco é um fator de risco para amigdalite crônica em crianças com infecção por H. pylori.


Subject(s)
Humans , Male , Female , Child , Tobacco Smoke Pollution/adverse effects , Tonsillitis/etiology , Helicobacter Infections/complications , Bacterial Proteins/blood , Chronic Disease , Cross-Sectional Studies , Risk Factors , Helicobacter pylori/immunology , Helicobacter Infections/diagnosis , Antibodies, Bacterial/blood , Antigens, Bacterial/blood
18.
Rev. chil. pediatr ; 87(4): 245-249, ago. 2016. ilus, graf
Article in Spanish | LILACS | ID: lil-796809

ABSTRACT

La participación de mecanismos epigenéticos, junto con infecciones en etapas tempranas de la vida, moldean lesiones premalignas del cáncer, en particular el cáncer gástrico, uno de los tumores más frecuentes en Chile, Latinoamérica y el mundo. El principal objetivo de este artículo, como parte de la serie de revisiones en torno a mecanismos epigenéticos en el desarrollo de enfermedades crónicas, es actualizar el rol de alteraciones epigenéticas (i.e. metilación del ADN) en el contexto de la infección crónica por H. pylori en las etapas precursoras del cáncer gástrico. Las investigaciones desarrolladas en esta área permiten delinear desafíos e interrogantes, en los cuales la pediatría tiene un papel preponderante en el desarrollo de estrategias de prevención y detección temprana de esta enfermedad.


The role of epigenetics and infectious diseases at early stages of life influence pre-malignant lesions of cancer, in particular, gastric cancer, one of the most frequent tumours in Chile, Latin America, and worldwide. This article examines the role of H.pylori and epigenetic alterations (i.e. DNA methylation) at early stages of gastric cancer and proposes, from the paediatric point of view, strategies for prevention and early detection.


Subject(s)
Humans , Child , Stomach Neoplasms/prevention & control , Helicobacter Infections/complications , Epigenesis, Genetic , Stomach Neoplasms/genetics , Stomach Neoplasms/microbiology , Chile , Helicobacter pylori/isolation & purification , Helicobacter Infections/microbiology , Helicobacter Infections/epidemiology , DNA Methylation , Early Detection of Cancer/methods
19.
Rev. Col. Bras. Cir ; 43(4): 235-242, July-Aug. 2016. tab, graf
Article in English | LILACS | ID: lil-794943

ABSTRACT

ABSTRACT Objective: to evaluate the influence of Duodenal reflux in histological changes of the gastric mucosa of rats infected with Helicobacter pylori submitted to pyloroplasty. Methods: after two weeks of acclimation, we infected 30 male Wistar rats with Helicobacter pylori. We randomly divided them into three groups: one submitted to pyloroplasty, another to partial gastrectomy and the third, only infected, was not operated. After six months of surgery, euthanasia was carried out. Gastric fragments were studied by light microscopy to count the number of H. pylori, and to observe the histological changes (gastritis, metaplasia, dysplasia and neoplasia). We confirmed these changes by immunohistochemistry using the molecular markers PCNA and TGF-beta. Results: the animals submitted to pyloroplasty had higher percentage of colonization by H. pylori (median=58.5; gastrectomy=16.5; control=14.5). There was a positive correlation between the amount of H. pylori and the occurrence of chronic gastritis present in the antral fragments. Neoplasia occurred in 40% of rats from the group submitted to pyloroplasty. The staining with PCNA and TGF-ß confirmed the histopathological changes visualized by optical microscopy. Conclusions: the antral region was the one with the highest concentration of H. pylori, regardless of the group. There was a positive correlation between the appearance of benign disorders (chronic gastritis, metaplasia, dysplasia) and cancer in mice infected with H. pylori submitted to pyloroplasty.


RESUMO Objetivo: avaliar a influência do refluxo duodenogástrico nas alterações histológicas da mucosa gástrica de ratos, infectados por Helicobacter pylori, submetidos à piloroplastia. Método: após duas semanas de aclimatação, 30 ratos machos da raça Wistar, foram infectados com o microorganismo patogênico H. pylori. De forma aleatória, foram divididos em três grupos: um submetido à piloroplastia, outro à gastrectomia parcial e o terceiro, apenas infectados, não foi operado. Após seis meses de operados, procedeu-se a eutanásia. Os fragmentos gástricos foram estudados por microscopia óptica, para a contagem da quantidade de H. pylori, e para a observação das alterações histológicas (gastrite, metaplasia, displasia e neoplasia). A confirmação dessas alterações foi feita por imuno-histoquímica, utilizando os marcadores moleculares PCNA e TGFbeta. Resultados: os animais submetidos à piloroplastia tiveram maior percentual de colonização por H. pylori (mediana=58,5; gastrectomia=16,5; controle=14,5). Houve correlação positiva entre quantidade de H. pylori e ocorrência de gastrite crônica presente nos fragmentos do antro. Ocorreu 40% de neoplasia no grupo submetido à piloroplastia. A marcação de PCNA e TGF-beta confirmou as alterações histopatológicas visibilizadas à microscopia óptica. Conclusões: a região do antro foi a que apresentou a maior concentração de H. pylori, independente do grupo. Houve correlação positiva entre e o aparecimento de alterações benignas (gastrite crônica, metaplasia, displasia), e de neoplasia nos ratos infectados com H. pylori submetidos à piloroplastia.


Subject(s)
Animals , Male , Rats , Helicobacter pylori , Helicobacter Infections/complications , Duodenogastric Reflux/complications , Gastric Mucosa/pathology , Pylorus/surgery , Random Allocation , Helicobacter Infections/surgery , Rats, Wistar , Duodenogastric Reflux/surgery , Gastrectomy
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