Characteristics of the gastric mucosa of direct relatives of patients with sporadic gastric carcinoma
Fátima Carneiro, António Taveira‐Gomes, A Cabral-Correia, A Vasconcelos-Teixeira, R Barreira, Manuel Cardoso-Oliveira, M Sobrinho-Simes
Abstract
Fátima Carneiro, António Taveira‐Gomes, A Cabral-Correia, A Vasconcelos-Teixeira, R Barreira, Manuel Cardoso-Oliveira, M Sobrinho-Simes
Abstract
We compared the gastric mucosa lesions of 63 direct relatives of 24 patients with gastric carcinoma with those observed in 151 dyspeptic patients and in seven members of a family with familial gastric carcinoma of diffuse type. We found a higher prevalence of Helicobacter pylori infection (96.8%) and gastritis (98.4%) in the relatives of patients with sporadic carcinoma than in the dyspeptic patients. One-third of the individuals of the former group displayed chronic atrophic gastritis and intestinal metaplasia. Dysplasia was only observed in the group of cancer patient relatives. The relatives of patients with intestinal carcinoma showed a higher prevalence of chronic atrophic gastritis (40.0%), incomplete intestinal metaplasia (22.9%) and dysplasia (5.7%) than the relatives of patients with diffuse carcinoma (10.0%, 0.0% and 0.0%, respectively). The only striking feature that emerged from the comparison of relatives of patients with sporadic gastric carcinoma with the members of the family with familial gastric carcinoma was the significantly higher prevalence of hyperplastic lesions (100%) in the latter group. These results reinforce the existence of two main pathways of carcinogenesis of gastric mucosa, one leading to intestinal carcinoma via chronic atrophic gastritis and intestinal metaplasia and the other leading to diffuse carcinoma via hyperplastic changes.
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We compared the gastric mucosa lesions of 63 direct relatives of 24 patients with gastric carcinoma with those observed in 151 dyspeptic patients and in seven members of a family with familial gastric carcinoma of diffuse type. We found a higher prevalence of Helicobacter pylori infection (96.8%) and gastritis (98.4%) in the relatives of patients with sporadic carcinoma than in the dyspeptic patients. One-third of the individuals of the former group displayed chronic atrophic gastritis and intestinal metaplasia. Dysplasia was only observed in the group of cancer patient relatives. The relatives of patients with intestinal carcinoma showed a higher prevalence of chronic atrophic gastritis (40.0%), incomplete intestinal metaplasia (22.9%) and dysplasia (5.7%) than the relatives of patients with diffuse carcinoma (10.0%, 0.0% and 0.0%, respectively). The only striking feature that emerged from the comparison of relatives of patients with sporadic gastric carcinoma with the members of the family with familial gastric carcinoma was the significantly higher prevalence of hyperplastic lesions (100%) in the latter group. These results reinforce the existence of two main pathways of carcinogenesis of gastric mucosa, one leading to intestinal carcinoma via chronic atrophic gastritis and intestinal metaplasia and the other leading to diffuse carcinoma via hyperplastic changes.
Key concepts: Intestinal metaplasia, Atrophic gastritis, Gastroenterology, Medicine, Dysplasia, Internal medicine, Carcinoma, Cancer