AIM： To determine the association of Helicobacter pylori （H pylorl） CagA^＋ infection and pro-inflammatory polymorphisms of the genes interleukin （IL）-IRN and IL-1B with the risk of gastric atrophy and peptic ulc...AIM： To determine the association of Helicobacter pylori （H pylorl） CagA^＋ infection and pro-inflammatory polymorphisms of the genes interleukin （IL）-IRN and IL-1B with the risk of gastric atrophy and peptic ulcers in a dyspeptic population in Costa Rica, a country with high incidence and mortality of gastric cancer. METHODS： Seven biopsy specimens, a fasting blood sample and a questionnaire concerning nutritional and sociodemographic factors were obtained from 501 consecutive patients who had undergone endoscopy for dyspeptic symptoms. A histopathological diagnosis was made. Pepsinogen concentrations were analyzed by enzyme linked immunosorbent assay （ELISA）. Infection with H pylori CagA^＋ was determined by serology and polymerase chain reaction （PCR）. IL-1B and IL-1RN polymorphisms genotyping was performed by PCRrestriction fragment length polymorphism （PCR-RFIP）and PCR respectively. RESULTS： In this dyspeptic population, 86% were Hpylori positive and of these, 67.8% were positive for CagA. Atrophic antral gastritis （AAG） was associated with CagA^＋ status [odd ratio （OR） = 4.1; P 〈 0.000] and fruit consumption （OR = 0.3; P 〈 0.00）. Atrophic body gastritis （ABG） was associated with pepsinogen PGI/PGII 〈 3.4 （OR = 4.9; P 〈 0.04） and alcohol consumption （OR = 7.3; P 〈 0.02）. Duodenal ulcer was associated with CagA^＋ （OR = 2.9; P 〈 0.04） and smoking （OR = 2.4; P 〈 0.04）. PGI 〈 60 μg/L as well as PGI/PGII 〈 3.4 were associated with CagA^＋. CONCLUSION： In a dyspeptic population in Costa Rica, H pylori CagA^＋ is not associated with ABG, but it is a risk factor for AAG. The pro-inflammatory cytokine poly- morphisms IL-1B ＋ 3945 and IL-1RN are not associated with the atrophic lesions of this dyspeptic population.展开更多
Helicobacter pylori(H. pylori) infection is a wellestablished risk factor for the development of gastric cancer(GC), one of the most common and deadliest neoplasms worldwide. H. pylori infection induces chronic inflam...Helicobacter pylori(H. pylori) infection is a wellestablished risk factor for the development of gastric cancer(GC), one of the most common and deadliest neoplasms worldwide. H. pylori infection induces chronic inflammation in the gastric mucosa that, in the absence of treatment, may progress through a series of steps to GC. GC is only one of several clinical outcomes associated with this bacterial infection, which may be at least partially attributed to the high genetic variability of H. pylori. The biological mechanisms underlying how and under what circumstances H. pylori alters normal physiological processes remain enigmatic. A key aspect of carcinogenesis is the acquisition of traits that equip preneoplastic cells with the ability to invade. Accumulating evidence implicates H. pylori in the manipulation of cellular and molecular programs that are crucial for conferring cells with invasive capabilities. We present here an overview of the main findings about the involvement of H. pylori in the acquisition of cell invasive behavior, specifically focusing on the epithelial-to-mesenchymal transition, changes in cell polarity, and deregulation of molecules that control extracellular matrix remodeling.展开更多
基金Supported by The Centre Culturel et de Cooperation Scientifique de l'Ambassade de France au Costa Rica and the University of Costa Rica, No. 742-99-340
文摘AIM： To determine the association of Helicobacter pylori （H pylorl） CagA^＋ infection and pro-inflammatory polymorphisms of the genes interleukin （IL）-IRN and IL-1B with the risk of gastric atrophy and peptic ulcers in a dyspeptic population in Costa Rica, a country with high incidence and mortality of gastric cancer. METHODS： Seven biopsy specimens, a fasting blood sample and a questionnaire concerning nutritional and sociodemographic factors were obtained from 501 consecutive patients who had undergone endoscopy for dyspeptic symptoms. A histopathological diagnosis was made. Pepsinogen concentrations were analyzed by enzyme linked immunosorbent assay （ELISA）. Infection with H pylori CagA^＋ was determined by serology and polymerase chain reaction （PCR）. IL-1B and IL-1RN polymorphisms genotyping was performed by PCRrestriction fragment length polymorphism （PCR-RFIP）and PCR respectively. RESULTS： In this dyspeptic population, 86% were Hpylori positive and of these, 67.8% were positive for CagA. Atrophic antral gastritis （AAG） was associated with CagA^＋ status [odd ratio （OR） = 4.1; P 〈 0.000] and fruit consumption （OR = 0.3; P 〈 0.00）. Atrophic body gastritis （ABG） was associated with pepsinogen PGI/PGII 〈 3.4 （OR = 4.9; P 〈 0.04） and alcohol consumption （OR = 7.3; P 〈 0.02）. Duodenal ulcer was associated with CagA^＋ （OR = 2.9; P 〈 0.04） and smoking （OR = 2.4; P 〈 0.04）. PGI 〈 60 μg/L as well as PGI/PGII 〈 3.4 were associated with CagA^＋. CONCLUSION： In a dyspeptic population in Costa Rica, H pylori CagA^＋ is not associated with ABG, but it is a risk factor for AAG. The pro-inflammatory cytokine poly- morphisms IL-1B ＋ 3945 and IL-1RN are not associated with the atrophic lesions of this dyspeptic population.
基金Supported by Vicerrectoría de Investigación of the University of Costa Rica,No.B6A11,No.B7281 and No.90912
文摘Helicobacter pylori(H. pylori) infection is a wellestablished risk factor for the development of gastric cancer(GC), one of the most common and deadliest neoplasms worldwide. H. pylori infection induces chronic inflammation in the gastric mucosa that, in the absence of treatment, may progress through a series of steps to GC. GC is only one of several clinical outcomes associated with this bacterial infection, which may be at least partially attributed to the high genetic variability of H. pylori. The biological mechanisms underlying how and under what circumstances H. pylori alters normal physiological processes remain enigmatic. A key aspect of carcinogenesis is the acquisition of traits that equip preneoplastic cells with the ability to invade. Accumulating evidence implicates H. pylori in the manipulation of cellular and molecular programs that are crucial for conferring cells with invasive capabilities. We present here an overview of the main findings about the involvement of H. pylori in the acquisition of cell invasive behavior, specifically focusing on the epithelial-to-mesenchymal transition, changes in cell polarity, and deregulation of molecules that control extracellular matrix remodeling.
