BACKGROUND AND AIMS: Previous reports have suggested a possible association between hyperplastic polyposis and colorectal neoplasms. Increased gastrin may be the link between these two conditions insofar as gastrin has been reported to be a growth-promoting tumoural agent. This report describes gastric polyposis, hypergastrinaemia and colorectal neoplasms in four elderly patients. METHODS: Four male patients with no family history of cancer, who were found to have multiple gastric hyperplastic polyps, hypergastrinaemia and colorectal cancers or an adenomatous polyp, were evaluated. Assessment included clinical evaluation, biochemical and haematological profiles, fasting gastrin levels, Helicobacter pylori serology, cobalamin, parietal cell antibodies, gastroscopy with biopsies of polyps and gastric mucosa, urease tests, and colonoscopy with biopsies of colorectal neoplasms. Immunohistochemistry of specimens from gastric polyps and colonic carcinomas was performed for chromogranin A, synaptophysin, Leu 7, neuron-specific enolase and gastrin. RESULTS: The mean age at diagnosis of gastric polyps was 71.2 years and at removal of colorectal neoplasm was 70.0 years. In two patients, the gastric lesion was diagnosed before the colonic lesion and conversely in the two remaining patients. Gastrin was very high (1604 pg/ml; normal level, < 115 pg/ml) in one patient with pernicious anaemia, and the mean level for the other three was 324 pg/ml. H. pylori were found in two patients. Immunohistochemistry failed to identify neuroendocrine cells in the hyperplastic gastric polyps and three of the colonic carcinomas. CONCLUSIONS: Occurrence of sporadic colorectal neoplastic lesion in patients with diffuse hyperplastic gastric polyposis and hypergastrinaemia may represent a new syndrome. Gastrin is not secreted by the gastric polyps or colonic carcinomas and may be related to gastric mucosal changes and H. pylori colonization. In patients with hyperplastic gastric polyposis and hypergastrinaemia, colorectal neoplasms should be ruled out.
BACKGROUND AND AIMS: Previous reports have suggested a possible association between hyperplastic polyposis and colorectal neoplasms. Increased gastrin may be the link between these two conditions insofar as gastrin has been reported to be a growth-promoting tumoural agent. This report describes gastric polyposis, hypergastrinaemia and colorectal neoplasms in four elderly patients. METHODS: Four male patients with no family history of cancer, who were found to have multiple gastric hyperplastic polyps, hypergastrinaemia and colorectal cancers or an adenomatous polyp, were evaluated. Assessment included clinical evaluation, biochemical and haematological profiles, fasting gastrin levels, Helicobacter pylori serology, cobalamin, parietal cell antibodies, gastroscopy with biopsies of polyps and gastric mucosa, urease tests, and colonoscopy with biopsies of colorectal neoplasms. Immunohistochemistry of specimens from gastric polyps and colonic carcinomas was performed for chromogranin A, synaptophysin, Leu 7, neuron-specific enolase and gastrin. RESULTS: The mean age at diagnosis of gastric polyps was 71.2 years and at removal of colorectal neoplasm was 70.0 years. In two patients, the gastric lesion was diagnosed before the colonic lesion and conversely in the two remaining patients. Gastrin was very high (1604 pg/ml; normal level, < 115 pg/ml) in one patient with pernicious anaemia, and the mean level for the other three was 324 pg/ml. H. pylori were found in two patients. Immunohistochemistry failed to identify neuroendocrine cells in the hyperplastic gastric polyps and three of the colonic carcinomas. CONCLUSIONS: Occurrence of sporadic colorectal neoplastic lesion in patients with diffuse hyperplastic gastric polyposis and hypergastrinaemia may represent a new syndrome. Gastrin is not secreted by the gastric polyps or colonic carcinomas and may be related to gastric mucosal changes and H. pylori colonization. In patients with hyperplastic gastric polyposis and hypergastrinaemia, colorectal neoplasms should be ruled out.
Authors: Karen D Papay; Vincent G Falck; Steen S Poulsen; Remo Panaccione; Jens F Rehfeld; Martin A Storr Journal: Nat Rev Gastroenterol Hepatol Date: 2010-08-31 Impact factor: 46.802