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A patient, who proved to have a chylous cyst of the colon, presented with bright red rectal bleeding and an abnormality on barium enema suggesting a colonic polyp. We review such an unusual presentation and other reported cases.
For transitional cell carcinoma of the urinary bladder, an eighty-two-year-old man underwent cystoprostatectomy. His urine was diverted to a defunctionalized right colonic segment used to replace his bladder. Four months after the surgery, gross hematuria appeared; endoscopy disclosed an adenomatous polyp in the substitute bladder. We review the incidence and origin of neoplasia in colonic segments used for urinary diversion.
PURPOSE: The authors evaluated computed tomographic (CT) virtual colography for the detection of simulated polyps under ideal conditions, as well as the effects on lesion conspicuity of (a) collimation, (b) table pitch, and (c) orientation of the colon lumen with respect to the gantry. MATERIALS AND METHODS: Pig colon was resected and cleansed, and polyps with diameters of 3, 7, and 10 mm were created. Each specimen was scanned with collimation of 5 and 7 mm and table pitch of 1.0, 1.6, and 2.0 at angles of 0 degrees, 45 degrees, and 90 degrees to the gantry. The initial two-dimensional (2D) images were reconstructed at 1-mm intervals (2D reconstructions), from which three-dimensional (3D) virtual colography images were generated. Polyp conspicuity on the initial and reconstructed 2D images and the 3D reconstructions was evaluated on a three-point scale: 0 = polyp not depicted, 1 = polyp faintly depicted, and 2 = polyp clearly depicted. RESULTS: The 10-mm-diameter polyp was clearly depicted (grade 2 conspicuity) on every initial and reconstructed 2D image and 3D reconstruction without regard to collimation, table pitch, or angle to the gantry. The 7-mm-diameter polyp was clearly depicted (grade 2 conspicuity) on every initial and reconstructed 2D image, but conspicuity on 3D reconstructions varied as the imaging parameters varied. The 3-mm-diameter polyp was faintly depicted (grade 1 conspicuity) on the initial and reconstructed 2D images and 3D reconstructions, but conspicuity varied on the 3D reconstructions as the imaging parameters varied. CONCLUSION: CT virtual colography helped detection of small mucosal polyps regardless of the angle of the colon lumen to the gantry at which they were obtained.
4000 male probands aged 45 to 69 were investigated in a field trial according to random distribution for undetected intestinal bleeding with the Haemoccult - method. With a participation of 28% only 39 out of a total of 65 positive cases could be evaluated. Four cases of colon or rectal carcinoma and four cases of colonic polyps were ascertained. In view of complete lack of experience with false negative test results the Haemoccult test is at present a useful addition to the diagnostic possibilities. However, in suspected cases even a repeatedly negative test cannot replace complete colo-rectal investigation.
Currently, selenium (in the form of high selenium containing yeast or selenomethionine) is being evaluated for anticancer effects against both human colon polyp recurrence and human prostate cancer, respectively. Chemical speciation analysis of the high selenium containing yeast indicates that selenomethionine (SeMet) is a major constituent of selenized yeast. We tested the hypothesis that SeMet might affect colon cancer cell growth by mechanisms involving cyclooxygenases (COX). The growth of all four-colon cancer cell lines tested was inhibited by selenomethionine. Furthermore, selenomethionine decreased COX-2 protein and PGE2 levels in HCA-7 cells. Selenomethionine suppressed COX-2 RNA levels in HCA-7 cells which could account for decreased COX-2 protein levels. Finally, the addition of PGE2 protected cells from the antiproliferative effects of selenomethionine in a concentration dependent manner. Selenomethionine might regulate COX-2 at the transcriptional level. These data suggests that Se-Met-induced cell growth inhibition may be, in part, mediated by COX-2 dependent mechanisms. The results of this study support the use of selenium agents in colon cancer chemoprevention trials.
Heavy drinking is associated with many gastrointestinal symptoms and diseases, such as rapid intestinal transit time, diarrhea, colon polyps, and colorectal cancer. Acetaldehyde produced from ethanol by intestinal microbes has recently been suggested to be one of the pathogenetic factors related to alcohol-associated gastrointestinal morbidity. Furthermore, acetaldehyde is absorbed from the colon into portal blood and may thus contribute to the development of alcoholic liver injury. The present study was aimed to investigate the significance of gut aerobic flora in intracolonic acetaldehyde formation. For this study, 58 male Wistar rats (aged 9 to 11 weeks) were used. Half of the rats received ciprofloxacin for four consecutive days. Control rats (n = 29) received standard chow. On the fifth day of treatment, 1.5 g/kg body weight of ethanol was administered intraperitoneally to 19 rats receiving ciprofloxacin and 19 control rats. Ten ciprofloxacin-treated and 10 control rats received equal volumes of physiological saline intraperitoneally. Two hours after the injection of ethanol or saline, the samples of colonic contents and blood were obtained. Acetaldehyde and ethanol levels of the samples were determined by headspace gas chromatography. The intracolonic acetaldehyde level 2 hr after ethanol administration was 483+/-169 microM (maximum: 2.7 mM). High intracolonic acetaldehyde after ethanol injection was significantly reduced by ciprofloxacin treatment. After ciprofloxacin, intracolonic acetaldehyde levels before and after the injection of ethanol were 25+/-4.8 and 23+/-15 microM, respectively. Ciprofloxacin treatment resulted also in significantly higher blood (p < 0.005) and intracolonic (p < 0.0001) ethanol levels than in the control animals. Furthermore, ciprofloxacin treatment totally abolished the formation of endogenous ethanol in the large intestine. This study demonstrates that alcoholic fermentation and intracoIonic acetaldehyde production can be blocked by diminishing the amount of intracolonic aerobic bacteria with ciprofloxacin. Our findings indicate that the bacteriocolonic pathway for ethanol oxidation is mediated almost exclusively by gut aerobic microbes, and this knowledge may provide new insights into the studies on the pathogenesis of alcohol-related gastrointestinal symptoms and diseases.
The use of a 4- x 4-inch gauze pad at the suction port during snare colonoscopic polypectomy facilitates the retrieval of polyps. This technique is a simple, rapid, and cost-effective method of retrieving small polyps for pathologic evaluation.
Turcot's syndrome, the association of brain tumor (usually glioblastoma, medullo-blastoma, or astrocytoma) and colonic polyps, is a very rare condition of which about 20 cases have been reported. It has been described only once previously with cancer in a third organ system. In this paper, we report a child affected with colonic polyposis and astrocytoma (i.e., Turcot's syndrome) associated with intestinal non-Hodgkin's lymphoma.
Continued monitoring of a family for new malignant tumors has revealed diverse immunological and neoplastic disorders during a 15-year period. In 1966, the proband developed lymphoma. In 1975, his antibody titers to Epstein-Barr virus (EBV) became elevated, and again, he developed a malignant lymphoma. He also had borderline hypo-immunoglobulin A, died of glioblastoma multiforme in 1977, and at autopsy, had adenomatous colonic polyps. His eldest brother has normal immunoglobulin levels, but developed immune thrombocytopenia in 1973 and had elevated EBV antibody titers in 1980. Another brother had hypo-immunoglobulin A, thymoma in 1965, and adenomas and adenocarcinoma of the colon. Two other brothers succumbed to glioblastoma in 1968 and 1969. The father of the proband had bronchiectasis in 1952, hypo-immunoglobulin M documented in 1972, and elevated EBV antibody titers 5 years preceding development of a malignant lymphoma. The latter contained 10 EBV genome equivalents/cell by EBV viral DNA/DNA reassociation kinetics analysis. The proband's grandmother had died of an immunoglobulin G-secreting myeloma in 1977, and his grandfather had borderline low immunoglobulin M, elevated EBV antibody titers, and hypopharyngeal carcinoma in 1980. Predisposition to oncogenesis in this family was probably inherited.
Computer-aided diagnosis for computed tomographic colonography is in its infancy but has the potential to improve sensitivity and decrease costs for colonic polyp detection. This article reviews the current state of research in this nascent field and explores major challenges and avenues for future work.
The authors present the case of a 39-year-old woman with Gardner syndrome who died from marked hyponatremia and hypokalemia. Gardner syndrome is a rare variant of the familial adenomatous polyposis syndrome in which the affected individual develops thousands of polyps within the gastrointestinal tract, with a 100% risk of eventual malignant change. Individuals with Gardner syndrome also develop a variety of extra gastrointestinal abnormalities. In the case presented, a woman with a clinical history of Gardner syndrome who had previously undergone a total colectomy with ileorectal anastomosis presented to the hospital with a recent history of sore throat, fever, diarrhea, and abdominal pain. The symptoms were considered clinically to be due to a viral gastroenteritis. She was admitted to the hospital, where she had episodes of collapse believed to be vasovagal in origin. She suffered a cardiorespiratory arrest and died 24 hours after admission. After her death, electrolyte estimation performed on blood taken shortly before death revealed severe hyponatremia and hypokalemia. Postmortem examination showed the gastric mucosa to be virtually covered by innumerable adenomatous and hyperplastic polyps. Fewer polyps were seen within the small bowel. There was no evidence of malignancy. The features were consistent with Gardner syndrome. Hyponatremia and hypokalemia have been described in patients with villous adenomas and in familial adenomatous polyposis syndromes associated with numerous colonic polyps. The cause of death in this case was considered to be hyponatremia and hypokalemia associated with florid gastric polyps in a woman with Gardner syndrome. Viral gastroenteritis contributed to the death by causing further electrolyte depletion. To the best of the authors' knowledge, death in Gardner syndrome has not been described as attributable to such metabolic disturbance, in particular in those who have only gastric, small bowel, and rectal polyps remaining after total colectomy.
Genetic factors can dramatically influence the risk of colorectal cancer, and the molecular bases of many hereditary colorectal cancer syndromes, including familial adenomatous polyposis (FAP), attenuated FAP (AFAP), and hereditary nonpolyposis colorectal cancer (HNPCC) have been elucidated. Additional syndromes continue to be defined as new genes, including MYH , are linked to the development of colonic polyps and cancer. The risks of colorectal cancer are variable and depend on the specific germline alterations. Some mutations are associated with a 100% lifetime risk of developing cancer, while others are associated with only a mild increase in risk. Although there are overlapping clinical features in many of these syndromes, they can be distinguished by the age at cancer diagnosis, inheritance pattern, number and distribution of polyps, specific histologic features of the cancers, and the presence of distinctive extracolonic features. The introduction and refinement of genetic testing has provided a new and invaluable tool for the diagnosis and assessment of cancer risk for suspected cases of hereditary colon cancer.
Cronkhite-Canada syndrome is generally accepted as being a benign disorder. We herein present a 66-year-old-male patient with Cronkhite-Canada syndrome who had a carcinoma of the sigmoid colon along with multiple colonic polyps, which included juvenile-type polyps, adenomas, and hyperplastic polyps. In the world literature, there have been 34 cases of Cronkhite-Canada syndrome associated with colorectal carcinoma among the 280 reported cases of this syndrome. This report thus adds to the growing evidence that Cronkhite-Canada syndrome may be a premalignant condition for colorectal carcinoma. A periodic examination of the colon is therefore advised in order to detect any development of colorectal carcinoma at an early stage.
The juvenile form is the usual type of colonic polyp seen during childhood. However, mixed forms associating juvenile and adenomatous polyps have been reported. A syndrome including the association of generalized juvenile polyposis, pulmonary arteriovenous malformation, and hypertrophic osteoarthropathy has been described in three cases; however, this is the first report of the association of mixed juvenile and adenomatous polyposis, pulmonary arteriovenous malformation, and hypertrophic osteoarthropathy.
A rabbit antiserum prepared to 2nd-trimester fetal organ extracts and absorbed with adult tissue (anti-STFa) was used to detect antigens common to 2nd-trimester fetal large bowel, normal adult stomach, several colon carcinoma cells (in primary and established cultures) and epithelial cells cultured from benign colonic polyps. The frequency of anti-STFa-positive cells was highest in cultures derived from benign tumors known to be associated with a greater degree of premalignancy. Thus, the percentage of antigen-positive cells increased from 18 and 43% to 70% of cultures from tubular, villotubular and villous adenomas, respectively. Considerable heterogeneity in the distribution of antigen-containing cells was evident within any given area of a positive culture. Absorption experiments, using a spectrum of fetal and normal adult tissue extracts, indicated that the adenoma-carcinoma specificity resides in fetal, but not adult, large bowel and normal adult stomach.
AIM: To determine the real association between serum lipid levels and colonic polyp formation. METHODS: We performed a large scale retrospective study to analyze the correlation between the incidence of colorectal adenoma or carcinoma and the fasting serum levels of total cholesterol (TC) and triglycerides (TG) in patients who underwent total colonoscopy for screening for colon cancer. RESULTS: Both levels were significantly elevated in patients with adenomas as compared with patients without any neoplastic lesion (TC 207.6+/-29.5 vs 199.5+/-34.3, n=4883, P<0.001; TG 135.0+/-82.2 vs 108.7+/-71.5, n=4874, P<0.001). The difference was significant in patients with tubular adenoma but not in those with villous or serrated adenoma. Multiple logistic regression analysis including age and sex revealed that TG was an independent correlation factor in male (P<0.01), but not in female patients. The level of TG in patients with invasive carcinoma did not show a significant elevation from that in patients with adenoma. These findings suggest that hypertriglyceridemia is an independent risk factor for colonic adenoma in men. CONCLUSION: Although a high level of serum triglyceride does not appear to be mechanically involved in the development of carcinoma, reduction of serum TG and intensive surveillance with total colonoscopy may have benefit in men with hypertriglyceridemia.
In an effort to generate a good mouse model for human colorectal cancer, we generated mice which carry a mutation in the adenomatous polyposis coli (Apc) gene. Mice which are heterozygous for the mutation, designated Apc1638, develop colonic polyps and tumors of the small intestine. Neoplasms were found in 96% of animals studied, and they included adenomas, adenocarcinomas, and polypoid hyperplasias. The mice developed an average of 3.3 tumors, with the highest number in duodenum, followed by jejunum, stomach, ileum, and colon. Focal areas of dysplasias were observed in the colonic mucosa in 50% of mice which were 10 months old or older. These results suggest that mice carrying the Apc1638 mutation can serve as a good model to study the initiation, progression, and inhibition of gastrointestinal tumors.
We have recently proposed the existence of a bacteriocolonic pathway for ethanol oxidation [i.e., ethanol is oxidized by alcohol dehydrogenases (ADHs) of intestinal bacteria resulting in high intracolonic levels of reactive and toxic acetaldehyde]. The aim of this in vitro study was to characterize further ADH activity of some aerobic bacteria, representing the normal human colonic flora. These bacteria were earlier shown to possess high cytosolic ADH activities (Escherichia coli IH 133369, Klebsiella pneumoniae IH 35385, Klebsiella oxytoca IH 35339, Pseudomonas aeruginosa IH 35342, and Hafnia alvei IH 53227). ADHs of the tested bacteria strongly preferred NAD as a cofactor. Marked ADH activities were found in all bacteria, even at low ethanol concentrations (1.5 mM) that may occur in the colon due to bacterial fermentation. The Km for ethanol varied from 29.9 mM for K. pneumoniae to 0.06 mM for Hafnia alvei. The inhibition of ADH by 4-methylpyrazole was found to be of the competitive type in 4 of 5 bacteria, and Ki varied from 18.26 +/- 3.3 mM for Escherichia coli to 0.47 +/- 0.13 mM for K. pneumoniae. At pH 7.4, ADH activity was significantly lower than at pH 9.6 in four bacterial strains. ADH of K. oxytoca, however, showed almost equal activities at neutral pH and at 9.6. In conclusion, NAD-linked alcohol dehydrogenases of aerobic colonic bacteria possess low apparent Km's for ethanol. Accordingly, they may oxidize moderate amounts of ethanol ingested during social drinking with nearly maximal velocity. This may result in the marked production of intracolonic acetaldehyde. Kinetic characteristics of the bacterial enzymes may enable some of them to produce acetaldehyde even from endogenous ethanol formed by other bacteria via alcoholic fermentation. The microbial ADHs were inhibited by 4-methylpyrazole by the same competitive inhibition as hepatic ADH, however, with nearly 1000 times lower susceptibility. Individual variations in human colonic flora may thus contribute to the risk of alcohol-related gastrointestinal morbidity, such as diarrhea, colon polyps and cancer, and liver injury.