Evaluation of the oncogenic risk of diffuse gastric polyposis. A case report

OBJECTIVES: Benign polyps of the stomach undergo malignant transformation at a rate correlating to the histological type and size of the proliferative lesion. It has been shown that gastric carcinogenesis is a multi-step process, supported by multiple genetic and molecular alterations, and mutations at both the c-Ki-Ras gene and the HER2 gene are involved. Among the various pathogenetic hypotheses explaining the histomorphologic progression of gastric lesions, the one proposed by Correa (with the sequence: gastritis-intestinal metaplasia-dysplasia-gastric carcinoma) is greatly favored, whereas the direct sequence from adenoma to carcinoma, though generally accepted for colon cancer, is questioned. MATERIALS AD METODS: We report a case of a 50-year-old woman who was taking warfarin and was affected by severe sideropenic anemia (Hb 4.1 g/dl). The gastrin levels were within normal ranges. Esophagogastroduodenoscopy showed diffuse gastric polyposis marked out by more than 1.000 polyps scattered over the entire gastric cavity with signs of diffuse oozing. Colonoscopy showed the presence of a 3-cm wide pedunculated polyp of the ascending colon, which was removed by diathermy and resulted a tubulo-villous adenomatous polyp at histological examination. The patient was treated by total gastrectomy with Roux-Y esophagojejunostomy. Histological examination showed the presence of diffuse gastric polyposis with the contemporary occurrence of hyperplastic polyps and mixed hyperplastic and adenomatous polyps, with a tubular pattern and the focal aspect of serrate adenoma. The perilesional gastric mucosa was characterized by the presence of either atrophic or metaplastic areas and by a mild dysplasia. Immunohistochemistry showed that both beta-catenin and E-cadherin were expressed as a membrane diffuse positivity in the glandular epithelium of the polyps and the low grade dysplastic components. P53 protein expression was detected only in the hyperplastic areas with low grade dysplasia, the same areas where Ki-67 antigen positive cells were more frequently found. EGF receptor overexpression was detected at the level of the resting cells of the deep portion of foveola. The proliferative index ki-67 was highest among the dysplastic foci. Molecular assays failed to show the presence of c-Ki-Ras gene mutations, similarly HER2 amplification was not detected. CONCLUSIONS: This is the first case report of sporadic diffuse hyperplastic and adenomatous polyposis of the stomach. We speculate that the evolutive potential of precancerous gastric lesions into frank neoplasia may be assumed by immunohistochemistry and molecular assay. The absence of both high-grade dysplastic lesions and outbreaks of neoplastic transformation well correlated with the histochemical and molecular features, confirming the highly proliferative pattern of the polyps in the lack of signs of malignant progression.