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PubMed1995

The impact of family history of colon cancer on survival after diagnosis with colon cancer.

BACKGROUND: The impact of family history of colon cancer on survival after diagnosis with colon cancer is generally unknown. It is possible that family history is indicative of a genetically inherited form of disease which may alter survival. METHODS: The Utah Population Database was used to evaluate survival after diagnosis with colon cancer among 2236 first primary colon cancer cases. This database includes detailed information about family history and is linked to the Utah Cancer Registry to obtain tumour information. RESULTS: Stage at diagnosis was the primary factor associated with death from all causes and from colon cancer. An older age at diagnosis, being female, and having a tumour in the ascending segment of the colon also were associated with poorer survival, although after adjusting for stage at diagnosis these associations disappeared. Having a family history of colon cancer had little impact on survival patterns although there were suggestions that men who were diagnosed at age < or = 55 were more likely to die from all causes as well as colon cancer if they had a sibling with colon cancer (hazard rate ratio [HRR] 2.50, 95% confidence interval [CI]: 1.03-6.10) relative to men > 55 without a sibling with colon cancer. CONCLUSIONS: From these data it appears that the major factor which increases survival is being diagnosed at an early stage of disease. These data also suggest that younger men who have a sibling with colon cancer may have a different form of colon cancer which increases their risk of dying.

Aged↗
PubMed2000

Colon interposition for esophageal replacement: an alternative technique based on the use of the right colon.

OBJECTIVE: To describe the technique and results of an alternative colon interposition procedure in which the ascending and transverse colon is used as graft, but that still relies on the left colonic artery for blood supply. SUMMARY BACKGROUND DATA: The standard procedure to obtain a left colon interposition graft requires ligation of the middle colic artery and mobilization of the left and right flexure. This approach carries a risk because preparation of the left flexure may damage arterial or venous collaterals located at this site that are crucial for graft perfusion. METHODS: The authors modified the standard technique so that mobilization of the left flexure is no longer necessary. To obtain a colon interposition graft that is long enough, the ascending colon was included into the graft by ligating the middle and the right colic artery. The left colic artery remained the blood-supplying vessel. From January 1997 to June 1998, 15 patients underwent modified colon interposition with a cervical anastomosis (12 esophagectomies, 3 esophagogastrectomies). RESULTS: In all cases, intraoperative blood supply from the left colic artery to the proximal ascending colon was sufficient. After surgery, four major complications occurred (27%). Endoscopy demonstrated a vital graft in all patients. In one patient a leakage of the cervical anastomosis was observed. One patient died of herpes pneumonia. Postoperative artificial ventilation was required for an average of 2.8 +/- 4.6 days, the average intensive care unit stay was 6.9+/-4.5 days, and the average total hospital stay was 24.1 +/- 15.1 days. CONCLUSION: An intact left colic artery, including its collaterals at the splenic flexure, supplies sufficient blood to the proximal ascending colon after central ligation of the middle and right colic artery. Even without mobilization of the left flexure, a sufficient graft length can be obtained. Preliminary complication rates with the use of this technique for colon interposition are in the range of those found for the standard colon interposition technique. These modifications may represent an alternative to established procedures for creating a colon interposition graft.

Anastomosis, Surgical↗
PubMed1987

Dose-related inhibition of colon carcinogenesis by dietary piroxicam, a nonsteroidal antiinflammatory drug, during different stages of rat colon tumor development.

The effect of four dose levels of piroxicam administered during different stages of colon tumor development was studied in male F344 rats to obtain a data base on the efficacy of piroxicam as an inhibitor of colon carcinogenesis. Piroxicam was added at levels of 25, 50, 75, and 150 ppm to the NIH-07 open-formula diet and fed to male F344 rats starting 1, 13, and 23 wk after the carcinogen administration. At 7 wk of age, while the animals were consuming the control diet, all animals except the vehicle-treated controls were given s.c. injection of azoxymethane (CAS:25843-45-2; 29.6 mg/kg body weight, once) to induce intestinal tumors. Forty wk after AOM injection, all animals were necropsied, and tumor incidences were compared among the various dietary groups. Colon tumor incidence (percentage of animals with tumors) was inhibited in a dose-dependent manner in rats fed the diets containing 25, 50, 75, and 150 ppm piroxicam starting 1 and 13 wk after carcinogen treatment. The colon tumor incidences in animals fed the diets containing 0, 25, 50, 75, and 150 ppm of piroxicam starting at 1 wk after carcinogen treatment were 89, 61, 58, 50, and 39%, respectively. When the diets containing 0, 25, 50, 75, and 150 ppm were fed 13 wk after carcinogen treatment, the colon tumor incidences were 89, 69, 69, 44, and 33%, respectively. Colon tumor multiplicity (tumors/animal; tumors/tumor-bearing animal) was also significantly inhibited in animals fed the diets containing 25 to 150 ppm piroxicam starting 1 and 13 wk after carcinogen administration. The number of colon tumors/animal was inhibited by about 80 to 84% in animals fed the 150 ppm piroxicam diet. When the diets containing different levels of piroxicam were fed 23 wk after carcinogen treatment, the colon tumor incidence was significantly inhibited in animals fed the 75 and 150 ppm piroxicam diets. The colon tumor incidences in animals fed the diets containing 0, 25, 50, 75, and 150 ppm were 89, 78, 67, 64, and 64%, respectively. The colon tumor multiplicity (colon tumors/animal) was slightly but significantly inhibited in animals fed the diets containing 25 to 150 ppm piroxicam. The results of this study demonstrate that increasing levels of piroxicam in the diet, when fed 1 or 13 wk after carcinogen insult, inhibit colon tumor incidence in a dose-dependent manner.

Animals↗
PubMed1995

DNA aneuploidy in morphologically normal colons from patients with colon cancer.

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)

Adenocarcinoma↗
PubMed2001

Colonic motility in chronic ulcerative proctosigmoiditis and the effects of nicotine on colonic motility in patients and healthy subjects.

BACKGROUND: Nicotine decreases diarrhoea and pain in ulcerative colitis without reducing inflammation. AIMS: (i) To evaluate the effect of ulcerative proctosigmoiditis on motor functions of an uninflamed segment of descending colon; and (ii) to assess nicotine's effects on colonic motor functions in patients and healthy subjects. METHODS: In healthy subjects (n=30) and patients with ulcerative colitis (13; 11 active, two quiescent colitis), we studied the effects of intravenous nicotine on colonic transit of solid residue by scintigraphy (healthy subjects) and on colonic motility in healthy subjects and 11 patients. RESULTS: In ulcerative colitis, fasting colonic motility was increased, whereas motor response to a meal was significantly reduced; compliance was unchanged. In healthy subjects, high-dose nicotine induced transient high amplitude propagated contractions and relaxation of the descending colon followed by decreased phasic contractions. This dose also accelerated colonic transit. Low-dose nicotine (mimicking a transdermal nicotine patch) reduced colonic compliance in healthy subjects, but did not affect motor function in ulcerative colitis. CONCLUSIONS: Ulcerative proctosigmoiditis increases fasting colonic motility and reduces tone response to a meal in the descending colon without affecting colonic compliance, suggesting changes in physiological responses but not intrinsic wall properties. Nicotine has dose-dependent effects on colonic motor activity in healthy subjects.

Adult↗
PubMed1999

Presence of well-differentiated distal, but not poorly differentiated proximal, rat colon carcinomas is correlated with increased cell proliferation in and lengthening of colon crypts.

To determine whether colon crypt proliferative parameters were significantly altered by the stage of colon carcinogenesis or the type or location of colon tumors in rats, male Sprague-Dawley rats received an injection of the carcinogen 1,2-dimethylhydrazine (12 mg DMH base/kg body weight) or DMH vehicle once a week for 8 weeks, then were killed 24 weeks later. Three hours before sacrifice, rats were injected with 1 mg/kg body weight colchicine to arrest mitotic cells at metaphase. Transverse sections of the colon mucosa were taken 6 cm from the anus and at least 3 cm from any tumor, fixed in formalin, then stained with hematoxylin & eosin (H&E) for analyses of proliferative parameters. Only complete, mid-axial crypts were scored for mitotic count (MC), crypt proliferative zone (PZ) height and crypt height (CH). Serial tumor sections were stained with H&E for histological evaluation or used in immunohistochemical detection of transforming growth factor alpha (TGF alpha). DMH treatment significantly increased MC, PZ and CH regardless of tumor status. The PZ and CH of rats with a carcinoma located in the distal colon were significantly increased compared with DMH-treated rats without an adenocarcinoma (AC) or with rats which had a tumor located in the proximal colon. Distal colon ACs were found to be well differentiated and to have greater TGF alpha immunoreactivity than the generally less differentiated proximal colon carcinomas. Distal colon AC production and systemic circulation of a soluble colon crypt stimulating factor such as TGF alpha may explain the significant increase in PZ and CH in histologically normal colonic mucosa located away from the tumor.

1,2-Dimethylhydrazine↗
PubMed1991

Carcinoma of the colon in asbestos-exposed workers: analysis of asbestos content in colon tissue.

Epidemiological studies have indicated an increased incidence of carcinoma of the colon in asbestos workers. The present study evaluated the colon tissue asbestos burden, by light and electron microscopic analytic techniques, in patients with a history of occupational asbestos exposure and colon cancer. Asbestos fibers and/or asbestos bodies were present in colon tissue from 14 of 44 (31.8%) asbestos workers with colon carcinoma (range 142,199 to 15,231, 543 fibers/g/wet weight, mean 2,517,823). Chrysotile was identified in 9 patients and amosite in 3 patients. Both amosite and chrysotile were found in the colonic wall in one individual. Other forms of asbestos (e.g., crocidolite, tremolite, or anthophyllite) were not found. Asbestos fibers and asbestos bodies were not found in colon tissue from 20 control patients (colon carcinoma and no asbestos exposure). Asbestos fibers frequently enter and reside in the wall of the colon and are often intimately associated with tumor tissue at the site of colon carcinoma in workers with asbestos exposure and colon carcinoma.

Asbestos↗
PubMed1988

Myoelectric spiking activity of right colon, left colon, and rectosigmoid of healthy humans.

The tip of an intraluminal probe was positioned in the cecum, and before and after a standard meal (greater than 800 kcal), the rapid myoelectrical activity of the right, the left, and the rectosigmoid colon in six healthy subjects was recorded. In each colonic site, we recorded two different patterns of spike bursts: Short spike bursts and long spike bursts, as previously described. We observed no difference in either the duration or the amplitude of the two kinds of spike bursts among the three different parts of the colon. Before the meal, the number of long spike bursts was lower in the right than in the left colon (P less than 0.01) and than in the rectosigmoid (P less than 0.01). After the meal, a significant activity increase in long spike bursts lasted 20 min in the right colon (P less than 0.001), 100 min in the left colon, and in the rectosigmoid (P less than 0.001-P less than 0.05). This activity was always significantly less intense in the right colon than in the two other sites (P less than 0.001-P less than 0.01) and was less marked in the left colon than in the rectosigmoid (P 0.01-P less than 0.05). The short spike burst activity remained unchanged. These results provide evidence for the heterogeneity of motility in the different parts of the colon, with a relative hypomotility of the right colon compared to the left colon and the rectosigmoid in the healthy human.

Adult↗
PubMed2003

Oestrogen receptor beta (ERbeta) is abundantly expressed in normal colonic mucosa, but declines in colon adenocarcinoma paralleling the tumour's dedifferentiation.

Oestrogen Receptor beta (ERbeta) may protect against prostate and mammary cell proliferation and malignant transformation. Epidemiological studies indicate that oestrogens may reduce colon cancer risk. Since ERalpha is minimally expressed in normal and malignant colon, the aim of this study was to investigate the expression of ERbeta in both normal colonic wall and colon cancer. ERbeta expression was evaluated by immunohistochemistry in 90 cases of colon adenocarcinoma and nearby (>30-cm away) normal colonic wall, using a monoclonal antibody. Moderate or strong nuclear immunostaining was detected in superficial and crypt epithelium, endothelial cells, vascular smooth muscle cells, lymphocytes, enteric neurons and smooth muscular cells of the normal colonic wall. Superficial epithelial cells in normal colon demonstrated a significantly higher ERbeta expression than colon adenocarcinoma cells in both genders. The decline in ERbeta expression paralleled the loss of differentiation of malignant colon cells, regardless of the tumour's localisation. These findings suggest a protective role for ERbeta against colon carcinogenesis.

Adenocarcinoma↗
PubMed2000

Red meat and colon cancer: dietary haem, but not fat, has cytotoxic and hyperproliferative effects on rat colonic epithelium.

High intake of red meat is associated with an increased risk of colon cancer. It has been suggested that fat from red meat is responsible, because high fat intake increases the concentration of cytotoxic lipids in the colon. Experimental studies have not unequivocally supported such a role for fat, however. Recently, we showed that dietary haem, which is abundant in red meat, increased colonic cytotoxicity and epithelial proliferation. In this study, we wanted to clarify whether dietary fat affects colon cancer risk by itself or by modulating the detrimental effects of haem on the colonic epithelium. Rats were fed control or haem-supplemented diets with 10%, 25% or 40% of the energy derived from fat for 14 days. Faeces were collected for biochemical analyses. Colonic cytotoxicity was determined from the degree of lysis of erythrocytes by faecal water. Colonic epithelial proliferation was measured in vivo using [(3)H]thymidine incorporation. Increasing the fat content of the control diets stimulated faecal disposal of both fatty acids and bile acids. It also increased the concentration of fatty acids, but not that of bile acids, in faecal water in control rats. The cytolytic activity of faecal water and colonic epithelial proliferation were unaffected. Dietary haem increased faecal cation content and cytolytic activity of faecal water at all fat levels, suggesting that the colonic mucosa was exposed to high amounts of luminal irritants. This effect was smaller in rats on the low-fat diet. Dietary haem also increased colonic epithelial proliferation at all fat levels. The haem-induced effects were independent of fatty acids or bile acids in the faecal water. In western societies, 30-40% of ingested energy is supplied by dietary fat, so our results suggest that the association between consumption of red meat and risk of colon cancer is mainly due to its haem content, and is largely independent of dietary fat content.

Animals↗
PubMed2005

Alteration of gene expression in macroscopically normal colonic mucosa from individuals with a family history of sporadic colon cancer.

PURPOSE: We have shown that the expression of several genes associated with human colon cancer is altered in the morphologically normal colonic mucosa (MNCM) of APC(min) mice and humans with colon cancers. To determine whether these alterations also occur in the MNCM of individuals who have not developed colon cancer but are at high risk of doing so, we measured gene expression in the MNCM of individuals with a family history of colon cancer. METHODS: Expression of 16 genes in the MNCM of 12 individuals with a first-degree relative with sporadic colon cancer and 16 normal controls were measured by quantitative reverse transcription-PCR. All subjects tested had normal colonoscopic examinations. Biopsy samples of MNCM were obtained from the ascending, transverse, descending, and rectosigmoid regions of the colon (2-8 biopsy samples were obtained from each region). RESULTS: Relative to normal controls, the expression of several genes, including PPAR-gamma, SAA1, and IL-8 were significantly altered in the macroscopically normal rectosigmoid mucosa from individuals with a family history of colon cancer. CONCLUSIONS: Molecular abnormalities that precede the appearance of adenomatous polyp are present in the MNCM of individuals who have a family history of colon cancer. This observation raises the possibility of screening for individuals who are at an increased risk of developing colon cancer by analysis of gene expression in rectosigmoid biopsy samples. To assess this possibility, prospective studies will be needed to determine whether or not altered gene expression is associated with the subsequent development of adenomatous polyps and/ or colonic carcinomas.

Adolescent↗
PubMed2001

Colonic endocrine cells in rats with chemically induced colon carcinoma.

Colonic carcinoma was induced in male Sprague-Dawley rats by injecting them with 1,2-dimethylhydrazine dihydrochloride. Control rats were injected with EDTA solution. Tissue specimens of colon from four groups of animals: (i) rats without tumour, (ii) with dysplasia and lymphoid hyperplasia, (iii) with colonic adenocarcinoma, and (iv) controls, were investigated. The colonic endocrine cells were detected by immunocytochemistry and quantified by computerised image analysis. Peptide YY (PYY)- and serotonin-immunoreactive cells were found in the colon of all the groups investigated. There were few somatostatin- or enteroglucagon-immunoreactive cells and no pancreatic polypeptide (PP)-immunoreactive cells in the colon of any of the groups studied. The density of PYY-immunoreactive cells increased significantly in rats with dysplasia and lymphoid hyperplasia and in rats with colon carcinoma. There was no statistically significant difference as regards cell secretory index (CSI) or nuclear area of PYY-immunoreactive cells in any of treated groups examined. Nor was there any statistically significant difference between all treated animal groups and controls, as regards cell density, CSI, or nuclear area of serotonin-immunoreactive cells. The present observations in an animal model of human colon carcinoma support the assumption that neuroendocrine peptides in the gut are involved in the carcinogenesis of colorectal carcinoma. However, The nature of the changes in the colonic endocrine cells observed here differed from those in patients with colon carcinoma, possibly due to a difference between the response of young rats to an induced colon carcinoma and a spontaneously developed carcinoma in elderly humans, or due to a species difference.

1,2-Dimethylhydrazine↗
PubMed2004

Effects of mu and kappa opioid receptor agonists and antagonists on contraction of isolated colon strips of rats with cathartic colon.

AIM: To study the effects of mu and kappa opioid receptor agonists and antagonists on the isolated colon strips of rats with cathartic colon. METHODS: Cathartic colon model was established by feeding rats with contact laxatives, and effects of mu and kappa opioid receptor agonists and antagonists on electricity-stimulated contraction of isolated colon strips of rats with cathartic colon were observed. RESULTS: Compared with control group, exogenous mu and kappa agonists inhibited significantly electricity-stimulated contraction of strips of cathartic colon (8.50+/-0.89 mm, 6.24+/-0.91 mm, 3.35+/-0.6 mm vs 11.40+/-0.21 mm P<0.01; 8.98+/-0.69 mm, 6.89+/-0.71 mm, 4.43+/-0.99 mm vs 11.40+/-0.21 mm, P<0.01). In contrast, the exogenous mu antagonist significantly enhanced electricity-stimulated contraction of isolated colon strips (13.18+/-0.93 mm, 15.87+/-0.98 mm, 19.46+/-1.79 mm vs 11.40+/-0.21 mm, P<0.01), but kappa antagonist had no effect on the isolated colon strips of rats with cathartic colon. CONCLUSION: Mu and kappa opioid receptors are involved in the regulation of colon motility of rats with cathartic colon.

Analgesics, Opioid↗
PubMed1996

Evaluation in rats of the dose-response relationship among colonic mucosal growth, colonic fermentation, and dietary fiber.

The dose-response relationship among dietary fiber, colonic fermentation, fecal weight, and mucosal growth were evaluated in this study. The morphometric parameter of total mucosal volume was used to assess diet-induced differences in colonic mucosal growth. Dietary fibers with a wide range of fermentability and that have previously been shown to inhibit the development of colonic neoplasia in rats were used. Sprague-Dawley rats were fed Purina Rodent Chow, AIN-76a fiber-free diet, or an AIN-76a diet supplemented with three different dietary fibers, (cellulose, guar gum, or wheat bran) at 2, 5, 10, or 15% of the diet. Diets were fed for 28 days. Total colonic mucosal volume was determined using stereologic principles and computerized image analysis; 48-hr fecal weight was measured; and the concentration of short-chain fatty acids (SCFA) in colonic contents was determined at study termination. Each type of fiber induced a dose-dependent increase in total mucosal volume of the colon and fecal weight. Mucosal volume and fecal weight were closely correlated (R2 > 0.95). Total mucosal volume was not correlated with the concentration of total SCFA or butyrate in the colon. These results indicate that diet-induced change in colonic mucosal growth, as measured by total mucosal volume, is positively correlated with fecal weight and not related to alterations in colonic fermentation. Enhanced colonic mucosal growth occurs in rats fed dietary fibers that have previously been shown to inhibit the development of genotoxin-induced colonic neoplasia in rats.

Animals↗
PubMed2000

Expression of H type 1 antigen of ABO histo-blood group in normal colon and aberrant expressions of H type 2 and H type 3/4 antigens in colon cancer.

We have immunohistochemically examined the distribution of the H antigens of type 1, type 2 and type 3/4 chains of the ABO(H) histo-blood group system in human normal colon and in colon cancer using three monoclonal antibodies specific for each of the H type 1/2, H type 2, and the H type 3/4 chain. We unexpectedly found that mucosa of the normal colon from secretors but not that from nonsecretors expressed only H type 1 and did not express H type 2 or H type 3/4. The H type 1 was expressed in goblet cells. Positive goblet cells expressing H type 1 were decreased in number progressively from the proximal colon to the rectum. In tumors, 4 (57%) of 7 cancer tissues of the proximal colon from secretors expressed no H type 1, whereas all 8 cancer tissues of the distal colon from secretors expressed H type 1. The aberrant expressions of H type 2 and H type 3/4 (47 and 67%, respectively) were found in cancer tissues from both the proximal and the distal colon. Tumors from nonsecretors did not express any H antigens. Our results suggested that the expression of H type 1 in the normal colon and the aberrant expressions of H type 2 and H type 3/4 in colon cancer tissues were regulated by FUT2-encoded Se type alpha(1,2)fucosyltransferase. However, UEA-I-positive substance(s) rather than H type 2 were uniquely expressed throughout the normal colon and in colon cancers from both secretors and nonsecretors.

ABO Blood-Group System↗
PubMed1995

Liver colonization competence governs colon cancer metastasis.

Tumors that metastasize do so to preferred target organs. To explain this apparent specificity, Paget, > 100 years ago, formulated his seed and soil hypothesis; i.e., the cells from a given tumor would "seed'' only favorable "soil'' offered by certain groups. The hypothesis implies that cancer cells must find a suitable "soil'' in a target organ--i.e., one that supports colonization--for metastasis to occur. We demonstrate in this report that ability of human colon cancer cells to colonize liver tissue governs whether a particular colon cancer is metastatic. In the model used in this study, human colon tumors are transplanted into the nude mouse colon as intact tissue blocks by surgical orthotopic implantation. These implanted tumors closely simulate the metastatic behavior of the original human patient tumor and are clearly metastatic or nonmetastatic to the liver. Both classes of tumors were equally invasive locally into tissues and blood vessels. However, the cells from each class of tumor behave very differently when directly injected into nude mouse livers. Only cells from metastasizing tumors are competent to colonize after direct intrahepatic injection. Also, tissue blocks from metastatic tumors af fixed directly to the liver resulted in colonization, whereas no colonization resulted from nonmetastatic tumor tissue blocks even though some growth occurred within the tissue block itself. Thus, local invasion (injection) and even adhesion to the metastatic target organ (blocks) are not sufficient for metastasis. The results suggest that the ability to colonize the liver is the governing step in the metastasis of human colon cancer.

Adenocarcinoma↗
PubMed1998

Alterations in colonic anatomy induced by chronic stimulant laxatives: the cathartic colon revisited.

Cathartic colon is a historic term for the anatomic alteration of the colon secondary to chronic stimulant laxative use. Because some have questioned whether this is a real entity, we investigated changes occurring on barium enema in patients ingesting stimulant laxatives. Our study consisted of two parts. In part 1, a retrospective review of consecutive barium enemas performed on two groups of patients with chronic constipation (group 1, stimulant laxative use [n=29]; group 2, no stimulant laxative use [n=26]) was presented to a radiologist who was blinded to the patient group. A data sheet containing classic descriptions of cathartic colon was completed for each study. Chronic stimulant laxative use was defined as stimulant laxative ingestion more than three times per week for 1 year or longer. To confirm the findings of the retrospective study, 18 consecutive patients who were chronic stimulant laxative users underwent barium enema examination, and data sheets for cathartic colon were completed by another radiologist (part 2). Colonic redundancy (group 1, 34.5%; group 2, 19.2%) and dilatation (group 1, 44.8%; group 2, 23.1%) were frequent radiographic findings in both patient groups and were not significantly different in the two groups. Loss of haustral folds, however, was a common finding in group 1 (27.6%) but was not seen in group 2 (p < 0.005). Loss of haustral markings occurred in 15 (40.5%) of the total stimulant laxative users in the two parts of the study and was seen in the left colon of 6 (40%) patients, in the right colon of 2 (13.3%) patients, in the transverse colon of 5 (33.3%) patients, and in the entire colon of 2 (13.3%) patients. Loss of haustra was seen in patients chronically ingesting bisacodyl, phenolpthalein, senna, and casanthranol. We conclude that long-term stimulant laxative use results in anatomic changes in the colon characterized by loss of haustral folds, a finding that suggests neuronal injury or damage to colonic longitudinal musculature caused by these agents.

Aged↗
PubMed2005

One-stage resection without colonic lavage in emergency surgery of the left colon.

OBJECTIVE: Intra-operative colonic lavage is a widespread procedure introduced to decompress and clean the colon of its faecal load during emergency surgery of the left colon in order to perform a safe anastomosis. This type of lavage is never performed at our institution. The aim of this study was to evaluate the safety and acceptability of emergency left-sided colectomy without colonic lavage in a consecutive series of patients admitted at our department for perforation and obstruction of the left colon. PATIENTS AND METHODS: All 44 patients (29 with obstruction and 15 with perforation) on whom a one-stage left-sided colon resection was performed without colonic lavage between January 1998 and June 2004 were evaluated in a retrospective review. During this period all patients with acute disease of the left colon underwent a one stage resection without colonic lavage. The only exclusion criteria for anastomosis were: haemodynamic instability, ASA > 3, unresectable tumour. Death, anastomotic leakage and wound infection were main outcome measures. RESULT: The leak rate was 4.5% and mortality 2.3% due to one case of postoperative myocardial infarction. A 16% morbidity rate was recorded due to 4 wound infections and 3 minor complications. CONCLUSION: The procedure is safe. The low morbidity and mortality of one stage resection without colonic lavage can justify future prospective studies enrolling a large number of patients to compare its results with those obtained by one stage resection with colonic lavage.

Anastomosis, Surgical↗