Polyps of the colon and rectum.
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DNA aneuploidy is common in colon carcinoma, colonic polyps, and ulcerative colitis. We found an interesting subset of patients with colon cancer. These individuals (14 of 230 cases, 6%) had hypodiploid aneuploidy in their morphologically normal-appearing colonic tissue. The aneuploid fractions were small, making up between 10 to 15% of the total events, and the ploidy pattern was not related to the ploidy pattern of the tumor. The clinical findings of the 14 patients were compared with those of patients who had diploid normal colons by age, location of the tumor, Dukes stage, and percent aneuploidy in the main tumor; the two groups were comparable. Both the normal colon and carcinomas of the 14 cases were studied by a newly developed "enriched" polymerase chain reaction for K-ras mutations. No K-ras mutations were found in the normal tissues, but mutations were found in the tumors of four cases. Cells from some colon cancers have a high degree of genetic instability, as shown by numerous mutations throughout the genome. Analysis of eight matched colon cancers and aneuploid, morphologically normal-appearing colons for genetic alterations, as measured by shifts in the electrophoretic mobility of microsatellite repeat fragments, showed that only one of eight colon cancer samples had microsatellite instability, which is the expected frequency. Taken together, the data suggest that individuals with colon cancer may have morphologically normal colonic tissue, which is genetically abnormal, and this abnormality may precede the development of mutations in K-ras.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to compare double-contrast barium examination (DCBE) and endoscopy in detection of small colonic polyps. In 57 patients DCBE revealed 106 polyps in the large intestine. On total colonoscopy, 62 polyps could be verified. The size of the polyps excised ranged from 2 to 15 mm. Compared with DCBE, colonoscopy verified 48 true positive, 44 false positive and 14 false negative polyps. In revealing a polyp less than 5 mm, DCBE had a sensitivity of 72%, whereas in detection of larger polyps the sensitivity was 81%. Histological verification was available in 52 of the 62 removed polyps. A tubular adenoma was found in 12 of the 29 diminutive polyps verified with histology. DCBE and colonoscopy could not differentiate between adenomas and hyperplastic polyps. Since a polyp less than 5 mm may represent an adenoma, a precancerous lesion, its removal is indicated during colonoscopy after DCBE has detected it.
This study is based on a prospective survey of 212 autopsies that was conducted to determine the prevalence of colon adenomas in Barcelona, Spain. Adenomatous polyps were found in 21.7% of the patients (29.3% of the men and 12.5% of the women); multiple adenomas were found in 40% of the patients. Almost all adenomas were less than 5 mm in diameter, although 6.7% of the ones seen predominantly in the rectosigmoid colon were larger than 1 cm. The prevalence and number of adenomas increases with age. The prevalence of hyperplastic polyps was very low (1.6%). The data shows a relationship between the prevalence of colon adenomas in Spain and the incidence of colon cancer. The prevalence of colon adenomas in Spain is one of the lowest compared with that in other European countries and North America.
BACKGROUND: The effect of sulindac, a nonsteroid antiinflammatory drug, has been reported to cause both regression and suppression of colon polyps in patients with familial adenomatous polyposis and Gardner's syndrome. We report our experience with seven patients with diffuse colonic polyposis treated with sulindac. PATIENTS AND METHODS: Seven patients with familiar adenomatous polyposis, four men and three women (mean age, 30 years; range 16 to 41 years) were included in this study. Two patients that underwent prior colectoctomy with ileorectal anastomosis and had polyps in the rectum were also included. The polyps ranged in size from 0.2 to 2.5 cm; most of them were less than 1 cm. Sulindac was given 150 mg. twice a day. Further colonoscopic examination was done at 6-month intervals during follow-up in all patients. RESULTS: A disappearance or a marked reduction in the number and size of polyps was observed in all patients after 24 months of treatment with sulindac. The drug was well tolerated and no side effects were observed during treatment. CONCLUSION: The authors conclude that sulindac is effective in inducing the regression of rectal polyps in familial, adenomatous polyposis.
BACKGROUND: Body iron stores and dietary iron intake have both been shown to be positively associated with subsequent risk of colon cancer. This finding comes from a cohort study involving 14,000 men, but the positive association occurred in only 12 cases. PURPOSE: We performed a case-control study of 264 men and 98 women to test for an association between serum ferritin levels and the presence of adenoma of the colon that would be independent of other known risk factors. METHODS: Serum ferritin levels were determined in this study from sera, frozen at -80 degrees C for 5-8 years, that had been originally obtained between 1984-1987 at the Walter Reed Army Medical Center from adult male and postmenopausal female patients undergoing routine colonoscopic examination and previously enrolled in a case-control study that assessed the potential dietary and environmental risk factors for colonic neoplasia. The presence of fecal occult blood in the stool or the suggestion of colonic polyps seen on barium enema defined eligibility for the study. Patients with known preexisting colonic disease were excluded. Eligible patients had their blood drawn and serum prepared. Following colonoscopy and histologic review, the patients were classified into three groups: normal (without neoplastic disease), 159 subjects; adenoma, 145 subjects; and colon cancer, 29 subjects. Body iron stores were determined by measuring serum ferritin levels by a competitive-binding radiometric immunoassay. Ferritin levels categorized into quintiles for adenoma were defined. Crude and adjusted odds ratios (ORadj) with 95% confidence intervals (CIs) for cancer and adenoma related to ferritin were calculated, controlling for known or suspected risk factors including sex, age, race, body mass index, family history, tobacco use, and alcohol consumption. RESULTS: Statistically significant associations of adenoma risk were seen in the third ([ORadj] = 3.8; 95% CI = 1.5-9.5) and fourth (ORadj = 5.1; 95% CI = 2.0-12.7) quintiles of ferritin relative to the first quintile, for smoking history (ORadj = 2.4; 95% CI = 1.3-4.3), for male sex (ORadj = 1.9; 95% CI = 1.0-3.7), and for family history of polyps or cancer (ORadj = 1.8; 95% CI = 1.0-3.4). From a second set of analyses that excluded 36 patients with serum ferritin of greater than or equal to 399 ng/mL, the greatest effect of ferritin on adenoma risk by anatomic subsite was seen in the right colon. CONCLUSION: The apparent dose-response for serum ferritin level and adenoma risk suggest that exposure to iron may be related to adenoma formation.
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One hundred seventy-three hyperplastic polyps removed from the colon of 146 patients were carefully examined by light microscopy in order to evaluate the histologic variants. Seventy polyps were also studied histochemically in order to assess the mucin distribution. Seven polyps measured greater than 1 cm. The frequency of hyperplastic foci has been assessed in a review of 1000 colonic adenomas, 50 juvenile, 30 inflammatory, and six Peutz-Jeghers polyps. The vast majority of the hyperplastic polyps showed features similar to those of inflammatory and ischemic bowel mucosa, leading to the suggestion of an inflammatory-ischemic origin of the polyps. The frequent finding of dysplastic features within hyperplastic polyps greater than 1 cm suggests that at least the large polyps are dysplasia-prone.
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The medical records of 214 consecutive inpatients who had a barium enema examination were reviewed, and the clinical indications, efficacy of the barium enema, and patient outcome were correlated to determine the impact of the barium enema on patient management. The most frequent indications were rectal bleeding (33%), abdominal pain (31%), anemia (17%), weight loss (12%), and previous lesions needing reevaluation (12%). Diverticular disease (30%), colonic polyps (10%), and primary or secondary malignancies (12%) were the most common abnormalities detected radiographically. The sensitivity of the barium enema for colonic neoplasms was 89%, with only 1 small cecal polyp being undetected. The effects of barium enema on patient management were serious pathology excluded (64%), diagnosis made that changed therapy (24%), existing therapy continued (10%), and a further study ordered (2%). No serious or life-threatening lesion was missed by barium enema.
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The juvenile polyps are usually benign but there is the possibility of adenomatous degeneration. The authors recall their experience about colon endoscopy. Rectal bleeding was the first symptom that request endoscopy. 23 children were investigated. 10 of them presented with one or more polyps in their colon. All were juvenile polyps. In this article is suggested a diagnostic approach and a follow-up.
A case of Peutz-Jeghers syndrome in which one colonic polyp showed many foci of glandular dysplasia is reported. Peutz-Jeghers polyps are considered to be hamartomatous, and their malignant potential has been considered doubtful. This case is valuable because foci of glandular dysplasia existed within hyperplastic glands. Glands of Peutz-Jeghers polyps are proliferative in nature, and therefore it is not surprising that there are areas of glandular dysplasia and of cancerous change.
In vivo expression of human hereditary tumors are known to be tissue specific; in familial polyposis coli the genotype is expressed solely as colonic polyps that become malignant and in the Gardner syndrome as extracolonic connective tissue tumors and related neoplasms in addition to such colonic lesions. In vitro such tissue specificity was also seen in these 2 syndromes. Increased tetraploidy has been observed only in those cultures derived from tissues, which although appearing normal in the patient, were known to undergo malignant transformation in vivo based on clinical phenotypes and family histories: colonic mucosa in familial polyposis coli, skin and colonic mucosa in the Gardner syndrome. Cultures established from tissues known not to show neoplastic growth or from benign tumors (fibromas, sebaceous cysts and lipomas) did not show increased tetraploidy. Increased tetraploidy in cultures established from these 2 syndromes did not identify all cultured cells with either mutant genotype or those cells showing abnormal benign growths in vivo but rather only in those that are known to undergo malignant transformation in vivo in both syndromes. Such observations suggested that in these 2 syndromes there was a population of tetraploid cells, at least in culture, constantly present which may be relevant to the multi-step process of carcinogenesis.
Four cases of giant inflammatory polyps were found in a series of 86 consecutive colectomies for inflammatory bowel disease. Two presented a distinctive clinical syndrome of abdominal pain and chronic iron-deficiency anemia due to blood loss. Secondary ulceration of the heads of the polyps accounted for the bleeding and anemia, and the size of the polyps accounted for the abdominal pain. In both cases unusually long portions of colon were involved by the giant polyps. The third and fourth cases had rare complications--reactivation of an enterocutaneous fistula and perforation of an acquired diverticulum. These cases demonstrate that giant inflammatory polyps may produce symptoms independently of the underlying inflammatory bowel disease. In reported cases of giant inflammatory polyps, approximately two-thirds had Crohn's disease and one-third had ulcerative colitis. The transverse colon was the commonest location, pain was the commonest symptom, and the polyps were localized to a short segment of colon in the majority of cases. More than 50% of cases mimicked neoplasm on barium enema. Giant inflammatory polyps may produce a variety of distinctive signs and symptoms and deserve independent recognition.
Recent identification of genetic alterations in colon polyps and tumors has allowed construction of a hypothesis for the molecular basis of colon carcinogenesis. The consistency of observed genetic changes has inspired enthusiastic anticipation of new diagnostic tools and interventions for colon cancer. Appropriate animal models are crucial to the testing of molecular postulates as well as the development of markers and therapies for colon carcinogenesis. We discuss herein the various animal models that are currently used for the study of colon cancer as well as those that hold promise for the future. The contributions, drawbacks, and potential uses for the chemical carcinogen model, the multiple intestinal neoplasia model, transgenic animals, and the reconstruction model in the study of colon carcinoma are presented.
To clarify the relationship between tobacco use and risk of colorectal cancer, we evaluated a cohort of 248,046 American veterans followed prospectively for 26 years. In comparison with veterans who had never used tobacco, the risk of death was significantly increased for colon cancer and rectal cancer among current and former cigarette smokers and among pipe or cigar smokers, controlling for social class and occupational physical activity. Rectal-cancer risk was also significantly elevated among users of chewing tobacco or snuff. For both sites, risk increased significantly with pack-years, earlier age at first use, and number of cigarettes. These results reinforce 2 recent reports of the association of cigarette smoking and colorectal cancer in men and women. Inconsistencies in the findings of earlier epidemiologic studies appear to be due in large part to differences in length of follow-up or in choice of controls. Studies with at least 20 years of follow-up or population-based controls have tended to find elevated risk with tobacco smoking, while those with shorter follow-up or hospital controls have not. This, plus the strength and consistency of the association of smoking and colon polyps, suggest that smoking may primarily affect an early stage in the development of colon cancer. If this association is causal, tobacco use may be responsible for 16% of colon-cancer and 22% of rectal-cancer deaths among these veterans.
Dietary fiber consists of the structural and storage polysaccharides and lignin in plants that are not digested in the human stomach and small intestine. A wealth of information supports the American Dietetic Association position that the public should consume adequate amounts of dietary fiber from a variety of plant foods. Recommended intakes, 20-35 g/day for healthy adults and age plus 5 g/day for children, are not being met, because intakes of good sources of dietary fiber, fruits, vegetables, whole and high-fiber grain products, and legumes are low. Consumption of dietary fibers that are viscous lowers blood cholesterol levels and helps to normalize blood glucose and insulin levels, making these kinds of fibers part of the dietary plans to treat cardiovascular disease and type 2 diabetes. Fibers that are incompletely or slowly fermented by microflora in the large intestine promote normal laxation and are integral components of diet plans to treat constipation and prevent the development of diverticulosis and diverticulitis. A diet adequate in fiber-containing foods is also usually rich in micronutrients and nonnutritive ingredients that have additional health benefits. It is unclear why several recently published clinical trials with dietary fiber intervention failed to show a reduction in colon polyps. Nonetheless, a fiber-rich diet is associated with a lower risk of colon cancer. A fiber-rich meal is processed more slowly, which promotes earlier satiety, and is frequently less calorically dense and lower in fat and added sugars. All of these characteristics are features of a dietary pattern to treat and prevent obesity. Appropriate kinds and amounts of dietary fiber for the critically ill and the very old have not been clearly delineated; both may need nonfood sources of fiber. Many factors confound observations of gastrointestinal function in the critically ill, and the kinds of fiber that would promote normal small and large intestinal function are usually not in a form suitable for the critically ill. Maintenance of body weight in the inactive older adult is accomplished in part by decreasing food intake. Even with a fiber-rich diet, a supplement may be needed to bring fiber intakes into a range adequate to prevent constipation. By increasing variety in the daily food pattern, the dietetics professional can help most healthy children and adults achieve adequate dietary fiber intakes.