Polyp Dysplasia

An uncontrolled retrospective study of patients who had taken proton pump inhibitors for an average of 33 months found gastric polyps in 17 of 231 patients who underwent two or more endoscopies for complicated gastro-esophageal reflux disease (33). The polyps were generally small (under 1 cm), sessile, and multiple, and were present in the proximal or mid gastric body. Of the 15 polyps removed endoscopically, nine were fundic gland type, four were hyperplastic, and two were inflammatory. None had any dysplasia or carcinoma. 

H. Messmann, R. Knuchel, W. Baumler, A. Holstege, J. Scholmerich (1999). Endoscopic fluorescence detection of dysplasia in patients with Barrett s esophagus, ulcerative colitis, or adenomatous polyps after 5-aminolevulinic acid-induced protoporphyrin IX sensitization. Gastrointest. Endosc., 49, 97-101. 

Polyps between 6 and 9 mm are defined as intermediate lesions. Most of them are eventually found to be low-grade dysplasia adenomas, less than 1% are found to be harbour invasive carcinomas and 30% are found to be hyperplastic lesions. Thus, surveillance either with conventional or virtual colonoscopy may be a reasonable option in these cases... 

Neoplastic lesions, including hyperplasias, dysplasia, adenomatous polyps, and carcinomas are present in rodents and humans. 

Mpofu C, Watson A, Rhodes J (2004) Strategies for detecting colon cancer and/or dysplasia in patients with inflammatory bowel disease. Cochrane Database Syst Rev 2 CD000279 O Brien M, Winawer S, Zauber A et d. (1990) The national polyp study, patient and polyp characteristics associated with high grade dysplasia in colorectal adenomas. Gastroenterology 88 371-379... 

Colorectal cancer is associated with the presence and growth of adenomatous polyps in the bowel, the greatest malignant potential being associated with the larger adenomas. The adenomacarcinoma (or dysplasia-carcinoma) sequence[56] stages the development of colon... 

A large number of clinical intervention studies have examined the effect of supplemental p-carotene on intermediate cancer endpoints, as shown in Table 1. The results of these trials indicate that supplemental p-carotene consistently results in regression of oral precancerous lesions (oral leukoplakia, oral dysplasia), and a decreased frequency of micronucleated buccal mucosal cells. While many of the trials of oral precancerous endpoints were not placebo-controlled, and thus somewhat difficult to interpret because spontaneous regression can occur, those that were placebo-controlled nonetheless demonstrated significant benefit to p-carotene relative to placebo. From Table 1 it appears that the chemopreventive efficacy of p-carotene varies by site, with evidence for efficacy in the oral cavity and possibly esophagus, mixed evidence in cervix and lung, and convincing evidence of a lack of efficacy in the prevention of recurrent colorectal polyps. 

In view of the above discussion, it can be appreciated that the suppression of aberrant proliferation, in our model caused by enhanced GJC between these minimally mutated cells and surrounding normal cells, could effectively inhibit the development of cells bearing multiple mutations required for full carcinogenic potential. In a clinical context, populations of cells which have not yet acquired the full neoplastic potential can be recognized in the colon as polyps, and in many epithelia as dysplasias. 

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