RESUMO
Gastric biopsies of the non neoplastic area of 46 patients with gastric cancer and 59 gastric biopsies of dyspeptic patients without gastric cancer were reviewed by one pathologist, without knowing from which group they were coming, to determine the histopathologic findings. The results of both groups were compared. Intestinal metaplasia was found to be significantly higher in gastric cancer patients than in patients without neoplasia (54,3 and 25,4% respectively) (p=0,001). Also in patients with cancer and intestinal metaplasia, this was of the complete type in about 80% of the cases. A number of items were assessed using logistic regression, we found that the presence of complete metaplasia, gastric atrophy and hypertrophy of the mucinogenous vacuole correlates with the presence of gastric cancer (p=0,0159 0,0080 y 0,0280 respectively). H.pylori presence was similar in both groups. The study was done between November 1997 and November 1998 at the Cayetano Heredia National Hospital and the National Institute of Neoplastic Diseases.
Assuntos
Mucosa Gástrica/patologia , Gastrite/patologia , Neoplasias Gástricas/patologia , Idoso , Biópsia , Doença Crônica , Dispepsia/patologia , Feminino , Gastrite Atrófica/patologia , Helicobacter pylori/isolamento & purificação , Humanos , Hipertrofia , Masculino , Metaplasia , Pessoa de Meia-IdadeRESUMO
INTRODUCTION: Nodular gastritis is a frequent endoscopic finding at our hospital, of 3600 upper endoscopies done from 1994 to 1997, 261 presented with this endoscopic characteristic. The aim of this study is to find whether there is any particular histopathological pattern in nodular gastritis. MATERIAL AND METHODS: 112 gastric biopsies of patients with an endoscopic diagnosis of nodular gastritis were compared to a control group of 111 gastric biopsies of patients with the same age and sex but without this endoscopic finding of nodular gastritis. Patients with peptic ulcer, duodenitis and neoplasia were excluded. Biopsies were blindly reviewed by one experienced pathologist. The following parameters were considered: presence and type of gastritis, grade of mucosal inflammation, presence and percentage of complete or incomplete metaplasia, presence and grade of inflammatory activity, presence and number of lymphoid follicles (primary and secondary), presence and number of eosinophils in the mucosa, presence of H. pylori and presence of epithelial edema. RESULTS: Patients with nodular gastritis were constituted by 62 women and 50 men, the control group by 62 women and 49 men. The average age for the nodular gastritis group was 37 + 17 years (16-82 years) and the control group 38+17 years ( 16-82 years). Both groups had the same number of lymphoid follicles (primary and secondary). Statistical differences were found in relation to : grade of mucosal inflammation (p: 0.042), presence of superficial eosinophils on the surface (p: 0.019) and presence of Helicobacter pylori (p: 0.024). CONCLUSIONS: Nodular gastritis is a chronic gastritis with superficial eosinophilic infiltration, moderate inflammation and an important inflammatory activity associated with the presence of H. pylori. There is no relation with the presence and number of lymphoid follicles. The nodular pattern seen on endoscopy could be related to inflammation mediated by the eosinophil and probably induced by H.pylori or other factors as infectious agents, environment, nutritional, or other individual factors not considered in this study.
Assuntos
Gastrite/patologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Estudos de Casos e Controles , Método Duplo-Cego , Feminino , Hospitais , Humanos , Masculino , Pessoa de Meia-IdadeAssuntos
Gastrite/microbiologia , Infecções por Helicobacter/epidemiologia , Helicobacter pylori , Adolescente , Adulto , Fatores Etários , Biópsia , Doença Crônica , Feminino , Gastrite/epidemiologia , Gastrite/patologia , Gastrite/fisiopatologia , Infecções por Helicobacter/patologia , Infecções por Helicobacter/fisiopatologia , Humanos , Masculino , Peru/epidemiologia , Prevalência , Índice de Gravidade de DoençaRESUMO
We compared the prevalence of gastric metaplasia of the duodenal mucosa (GM) and its characteristics in 204 Peruvian patients from a low socioeconomic level with the corresponding prevalence reported in dyspeptic patients from a developed country, the United Kingdom. Gastric metaplasia was significantly less prevalent in the Peruvian than in the United Kingdom series. However, when present, GM was not significantly different in extent or frequency of colonization by Helicobacter pylori or association with active duodenitis, despite a higher prevalence of H. pylori-associated gastritis. Hypochlorhydria was markedly more frequent in the Peruvian than in the United Kingdom series. The finding of a low prevalence of H. pylori-colonized GM in patients with previously reported low prevalence of duodenal ulcer gives further support to a pathogenic link between both conditions.
Assuntos
Dispepsia/epidemiologia , Dispepsia/patologia , Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/patologia , Helicobacter pylori/isolamento & purificação , Mucosa Intestinal/patologia , Estômago/patologia , Adolescente , Adulto , Idoso , Duodeno , Dispepsia/microbiologia , Feminino , Infecções por Helicobacter/microbiologia , Humanos , Mucosa Intestinal/microbiologia , Masculino , Metaplasia/epidemiologia , Metaplasia/microbiologia , Metaplasia/patologia , Pessoa de Meia-Idade , Peru/epidemiologia , Prevalência , Fatores Socioeconômicos , Estômago/microbiologia , Reino Unido/epidemiologiaRESUMO
Evidence is presented suggesting that infection by Helicobacter pylori triggers and continuously contributes to the pathophysiology of progressive gastric changes that can ultimately lead to gastric cancer. In Peru, especially in population groups of low socioeconomic status, infection by H. pylori begins earlier in life and is more prevalent and persistent than in developed countries. The infection produces a destructive lesion of the mucinous surface epithelium which probably enables other aggressive luminal factors to cause further mucosal damage. As a consequence, active chronic gastritis appears. The gastritis is of the superficial type at the beginning but may progressively change to atrophic. Chronic atrophic gastritis is found more frequently and at a younger age in dyspeptic patients with low socioeconomic status--that is, in patients having higher prevalence of persistent infection by H. pylori since earlier in life. When chronic atrophic gastritis becomes severe and extensive, hypochlorhydria ensues. Hypochlorhydria favors the appearance of bacterial overgrowth, nitrites, and N-nitroso compounds in the gastric lumen. N-nitroso compounds, because of their mutagenic-carcinogenic properties, probably induce gastric premalignant lesions like intestinal metaplasia and dysplasia of the gastric mucosa. Oral bismuth therapy apparently reverses H. pylori-associated gastric dysplasia. It is proposed that future programs designed for the control of gastric cancer would be incomplete if they do not include further evaluation of the many effects of infection by H. pylori on the gastric mucosa and of cost-effective methods to eradicate the infection.
Assuntos
Gastrite Atrófica/patologia , Infecções por Helicobacter/patologia , Helicobacter pylori , Lesões Pré-Cancerosas/patologia , Neoplasias Gástricas/etiologia , Fatores Etários , Gastrite Atrófica/complicações , Gastrite Atrófica/epidemiologia , Infecções por Helicobacter/complicações , Humanos , Peru/epidemiologia , Pobreza , PrevalênciaRESUMO
We report a study of 127 patients examined with esophago-gastroduodenoscopy and with a diagnosis of chronic gastritis (by biopsy), and gastric peptic ulcer and duodenal peptic ulcer (endoscopically). Brushing samples and biopsies were taken from the esophagus, stomach, and duodenum. Gram stains of brush-collected samples, culture of brush samples and biopsies were performed in order to detect the presence of PC. In cases of chronic active gastritis, PC was found in 91% of patients. It was found in 73% and 84%, respectively, of cases of gastric and duodenal ulcer. PC was found with equal frequency in the cardia and body as in the antrum of infected individuals, but no confirmed cases of colonization of the esophagus or duodenum were found. The most efficient methods for identifying PC colonization were (in descending order of efficiency), silver stain of biopsies, Gram stain of brushings, hematoxylin-eosin stain of biopsies, culture of biopsies, and culture of brushings. In some cases, we have identified PC in the esophagus and duodenum by gram stain and culture, but no not by silver stain or H&E stain of biopsies, suggesting that contamination from other areas of the stomach may be an occasional problem in sampling these areas for PC.
Assuntos
Infecções por Campylobacter/complicações , Campylobacter/isolamento & purificação , Gastrite/etiologia , Úlcera Péptica/etiologia , Piloro/microbiologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Infecções por Campylobacter/diagnóstico , Criança , Pré-Escolar , Feminino , Gastrectomia , Gastrite/patologia , Técnicas Histológicas , Humanos , Masculino , Pessoa de Meia-Idade , Úlcera Péptica/diagnósticoRESUMO
We report a study of 127 patients examined with esophago-gastroduodenoscopy and with a diagnosis of chronic gastritis (by biopsy), and gastric peptic ulcer and duodenal peptic ulcer (endoscopically). Brushing samples and biopsies were taken from the esophagus, stomach, and duodenum. Gram stains of brush-collected samples, culture of brush samples and biopsies were performed in order to detect the presence of PC. In cases of chronic active gastritis, PC was found in 91
of patients. It was found in 73
and 84
, respectively, of cases of gastric and duodenal ulcer. PC was found with equal frequency in the cardia and body as in the antrum of infected individuals, but no confirmed cases of colonization of the esophagus or duodenum were found. The most efficient methods for identifying PC colonization were (in descending order of efficiency), silver stain of biopsies, Gram stain of brushings, hematoxylin-eosin stain of biopsies, culture of biopsies, and culture of brushings. In some cases, we have identified PC in the esophagus and duodenum by gram stain and culture, but no not by silver stain or H&E stain of biopsies, suggesting that contamination from other areas of the stomach may be an occasional problem in sampling these areas for PC.