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PubMed2002

Culture-independent microbial community analysis reveals that inulin in the diet primarily affects previously unknown bacteria in the mouse cecum.

Inulin is a well-known fructose-based prebiotic which has been shown to stimulate the growth of bifidobacteria, a bacterial group generally considered beneficial for intestinal health. In the present study, we analyzed inulin-associated shifts in the total bacterial community of wild-type mice and mice carrying a genetically inactivated adenomatous polyposis coli tumor suppressor gene by using DNA-based approaches independent of bacterial culturability. Mice were fed a high-fat, nonfiber diet with or without inulin inclusion at a 10% (wt/wt) concentration. Cecal contents were analyzed after 0, 3, and 9 weeks on the experimental diets. Inulin inclusion significantly affected the total bacterial community structure of the cecum as determined by both a nonselective percent-guanine-plus-cytosine-based profiling analysis and a more specific 16S ribosomal DNA sequence analysis. The shifts included stimulation of bifidobacteria and suppression of clostridia, but sequence comparison revealed that the major shifts were within previously unknown bacterial taxa. Concomitantly, significantly higher bacterial densities, determined by flow cytometry, were observed with the inulin-amended diet, and the metabolism of the cecal bacterial community was altered, as indicated by higher levels of residual short-chain fatty acids, particularly lactic acid. With regard to all of the microbiological parameters measured, the wild-type mice and mice carrying a genetically inactivated adenomatous polyposis coli tumor suppressor gene were essentially identical. Studies of the implications of pre- and probiotics may need to be expanded to include careful analysis of their effects on the entire microbial community, rather than just a few well-known species. Further studies are needed to increase our understanding of the possible roles of currently unknown gastrointestinal bacteria in health and disease.

Animal Feed↗
PubMed2000

[Turcot syndrome].

Turcot syndrome is the association of colorectal polyposis with primary neuroepithelial tumors of the central nervous system such as glioblastoma and medulloblastoma. Including putative patients, more than 150 familial or sporadic cases of the syndrome have been reported in literature. Since early reports, there is considerable controversy regarding the modality of genetic transmission and the distinction from other syndromes like familial adenomatous polyposis(FAP). Recent molecular evidence suggests that Turcot syndrome could be divided into the following two entities based on the distinct genetic backgrounds. (1) True Turcot syndrome(autosomal recessive): Intestinal polyps are less in number(< 100), large in size and apt to transform to the malignant tumor. Brain tumor is mainly diagnosed as glioblastoma or astrocytoma and mismatch repair genes might be involved. (2) FAP-associated type(autosomal dominant): Predisposing to medulloblastoma.

Base Pair Mismatch↗
PubMed2003

Oral melanosis: a case report of Peutz-Jegher's Syndrome in Suva, Fiji.

This paper reports on a case of oral melanosis resultng from Peutz-Jeghers Syndrome, a hereditary disease characterized by harmatomatous polyposis and by mucocutaneous melanic pigmentation, in a 14-year-old Fijian girl with a family history of the disease. The patient underwent surgery for treatment of an intestinal obstruction due to a small intestine intussusception. Recognition of the characteristic pigmentation by dentists may lead to early diagnosis of associated harmatomatous polyps or neoplastic disease that may be life threatening.

Adolescent↗
PubMed2006

Novel and recurrent germline alterations in the MLH1 and MSH2 genes identified in hereditary nonpolyposis colorectal cancer patients in Slovakia.

Hereditary non-polyposis colorectal cancer (HNPCC) is associated with germline mutations in DNA mismatch repair genes, predominantly MSH2 and MLH1. Mutation carriers develop cancers in the colorectum, endometrium, ovary, stomach, small intestine and the upper urinary tract. We describe here the results of a mutational analysis of 11 unrelated HNPCC patients by direct genomic sequencing of MLH1 and MSH2. The alterations found include 7 novel changes and 4 different pathogenic mutations described previously in Poland, Moldavia, Finland, Germany, France and USA. Four novel pathogenic mutations in the MLH1 gene include two frameshift mutations (c.1150delG and c.1210_1211delCT), one missense mutation (c.793C>A) and one intron-exon border mutation (c.546- 2A>C). The last change resulted in the skipping of exon 7, as shown by sequencing of RT-PCR products. The only novel MSH2 pathogenic change was a nonsense mutation c.1129C>T. The novel intronic change c.381-41A>G in MLH1 was found in a patient carrying a previously-described mutation in the MSH2 gene. Interestingly, two unrelated patients carried also a novel change in the promoter region of MLH1 in one of the CpG islands (c.-269C>G). However, this alteration does not abrogate transcription, as shown by RT-PCR analysis. In summary, most (approximately 80%) pathogenic germline mutations detected in the studied group of patients by direct genomic sequencing of MLH1 and MSH2 were located in the MLH1 gene. These and previous data indicate that the majority of germline point mutations and small deletions/insertions in HNPCC families in Slovakia affect the MLH1 locus.

Adaptor Proteins, Signal Transducing↗
PubMed1996

Loss of heterozygosity of multiple tumor suppressor genes in human gastric cancers by polymerase chain reaction.

Loss of heterozygosity (LOH) occurring on various chromosomes has been described in the majority of human tumors and its targets are believed to be tumor suppressor genes. Although allelic deletion of the p53 gene (over 60%) has been frequently observed in gastric cancer, as well as in other human malignancies, LOH of other tumor suppressor genes is still discrepant in gastric cancer. To our knowledge, simultaneous analysis of LOH using PCR in adenomatous polyposis coli (APC), deleted in colon cancer (DCC), and retinoblastoma susceptibility (Rb) genes has not yet been reported in sporadic gastric cancer. We examined 21 advanced gastric cancers (12 intestinal type and 9 diffuse type) for LOH at the APC, DCC, and Rb loci using PCR. Inclusion of these tumor suppressor genes in the allelic deletions was directly ascertained by performing PCR at polymorphic sites within the genes. LOH occurred in 30% of informative cases at APC, in 27% of informative cases at DCC, and in 30% of informative cases at Rb. Thirty-three percent of tumors informative at all loci (fully informative) lost heterozygosity at all three loci. There were no significant differences among histologic types in the prevalence of LOH at any locus and no correlations between losses involving APC, DCC, and Rb genes. These data suggest that inactivation of APC, DCC, and Rb is involved in the development and progression of some human gastric cancers regardless of histologic type.

Base Sequence↗
PubMed2000

ACP Best practice no 159. Examination of large intestine resection specimens.

Macroscopic examination of large intestinal resection specimens by the surgical pathologist provides important diagnostic and prognostic information. This review summarises current recommended protocols and evidence based guidelines for gross description, dissection, and histological block selection in both neoplastic and non-neoplastic colorectal disease. Specific lesions discussed include colorectal cancer, polypectomies and polyposis syndromes, and inflammatory bowel disease. Microscopic examination is briefly described, with emphasis on certain pitfalls that might be encountered in routine practice. A section covering special techniques for the investigation of occult bleeding is included.

Clinical Protocols↗
PubMed1988

[Diffuse pseudopolyposis of the colon: developmental form or cicatricial of hemorrhagic rectocolitis?].

The authors report the case of a patient with generalized polyposis associated with ulcerative colitis. The diagnosis of polyposis was made 20 years after the onset of colitis. The patient presented with the unusual clinical manifestations, ie poor general condition and severe denutrition, following a severe relapse of colitis. The mucosal surface of the entire colon, except the rectum, was covered by innumerable polyps, without any macroscopic or microscopic evidence of ulceration. Intestinal protein loss, as assessed by alpha-1-antitrypsin clearance, was very high (470 ml/d). Acute mucosal inflammation, as assessed by histologic study and by 111-Indium-labelled-leukocyte scintigraphy, was also present. The patient responded dramatically to total colectomy with ileorectal anastomosis. Histologically, the polyps were filiform, with a central core, containing vessels and smooth muscle fibers. This observation demonstrates that generalized polyposis, generally considered to be an asymptomatic sequela of ulcerative colitis, can also be associated with severe attacks of colitis.

Adult↗
PubMed1987

The familial polyposis coli register.

Familial polyposis coli is an inherited condition in which many hundreds of adenomatous polyps develop in the colorectum usually during the second decade of life. There is a high incidence of associated carcinoma, a risk which approximates to 100% in untreated patients. Adenomas and carcinomas also occur in the upper gastro-intestinal tract though to a lesser extent. A policy of cancer prevention based on the genetic origin and natural course of the disease requires the identification of family members at risk in order that detection and surgical removal of the polyps can be effected before any malignant change has occurred. The identification of persons at risk requires knowledge of affected families. The establishment and maintenance of regional registers of polyposis coli families is advocated.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

Peroral sustained-release indomethacin treatment for rectal adenomas in familial adenomatous polyposis: a pilot study.

BACKGROUND/AIMS: The efficacy of peroral sustained-release indomethacin on rectal adenomas in colectomized patients with familial adenomatous polyposis and its toxicity were evaluated preliminarily. METHODOLOGY: A total of seven colectomized patients with familial adenomatous polyposis were treated with peroral sustained-release indomethacin at the usual clinical doses. The numbers of rectal polyps before and after treatment and approximately one year after cessation of treatment were counted using a flexible colonoscope and compared. RESULTS: After treatment, reductions of rectal polyp size were observed in all patients. Numbers of the rectal polyps also decreased significantly after treatment (median, 1; range, 0 to 30) compared with those before treatment (median, 19; range, 4 to 78) (P = 0.023). However, Grade 4 anemia due to lower intestinal ulcers occurred in two patients. Moreover, one year after termination of the treatment, increase in the size and number of rectal polyps was observed in six patients. CONCLUSIONS: Because of incomplete efficacy and severe toxicity, general use of this treatment for familial adenomatous polyposis patients must be deemed inappropriate.

Adenoma↗
PubMed1993

Operation and abdominal desmoid tumors in familial adenomatous polyposis.

Abdominal desmoid tumors (ADT) have become an important problem because of the increased survival of patients with familial adenomatous polyposis (FAP). Of 240 patients operated upon for FAP between 1978 and 1991, 29 (16 men and 13 women) had ADT. Diagnosis was made at laparotomy in 19 patients, while an abdominal mass or intestinal obstruction was the principal cause of discovery in the ten remaining patients. Twenty ADT were discovered after a previous laparotomy performed an average of three years earlier. Nine ADT occurred in 146 patients who had previously undergone a coloproctectomy and ileal pouch-anal anastomosis and eight occurred in 74 patients who had abdominal colectomy and ileorectal anastomosis. Desmoid tumors were responsible for eight instances of intestinal obstruction and one instance of small intestinal perforation. One death was directly related to ADT. In four of nine patients, ADT was responsible for a deterioration of the functional results of ileoanal anastomosis, but pouch removal was not necessary. Conversion of ileorectal anastomosis to ileoanal anastomosis and excision of carcinomas that occur in the residual rectum after ileorectal anastomosis were impossible because of ADT in three and two patients, respectively. Complete surgical removal of the tumor was possible in seven patients only and four patients had a recurrence. None of the medical therapies used (sulindac, tamoxifen and chemotherapy) were effective. The results of this study confirm the high incidence, severity and absence of effective treatment of ADT in FAP. Desmoid tumors occurring after ileorectal anastomosis seem to be more severe than after ileoanal anastomosis because, in the former instance, they may interfere with the further management of the rectal stump.

Abdominal Muscles↗
PubMed1999

Combined restorative proctocolectomy and pancreaticoduodenectomy for familial adenomatous polyposis.

This is a case report on FAP in a 41-year-old woman in which preoperative examination showed a giant tubulovillous adenoma of the descending duodenum surrounding the papilla of Vater, in addition to pancolon adenomatous polyposis, and isolated adenomas in the gastric antrum and corpus. As it was impossible to remove the giant villous adenoma in the duodenum endoscopically, prophylactic surgical treatment was chosen consisting of restorative proctocolectomy and additional pancreaticoduodenectomy. Flat tubulovillous adenomas in the gastric corpus were successfully removed by total snare biopsies before operation. FAP coli patients treated by prophylactic surgery are now known to be at risk of developing adenomas anywhere in the intestine and many affected patients later die from upper gastrointestinal tumors. In this single case report, the simultaneous occurrence of FAP coli and giant villous adenoma of the duodenum indicates the frequent outcome of this genetic alteration requiring lifelong surveillance. This rare case report includes a short survey of the relevant literature.

Adenomatous Polyposis Coli↗
PubMed1993

Randomized controlled trial of the effect of sulindac on duodenal and rectal polyposis and cell proliferation in patients with familial adenomatous polyposis.

Twenty-four patients with familial adenomatous polyposis who had previously undergone prophylactic colectomy and had advanced duodenal polyposis were entered into a randomized trial to assess the effect of the non-steroidal anti-inflammatory drug sulindac on duodenal and rectal polyps. Polyp size and number were assessed by videotaped duodenoscopy (and rectoscopy in 14 patients) at entry and after 6 months of treatment; the tapes were compared by two assessors who were unaware of the randomization and the shuffled chronological order of the recordings. Mucosal cell proliferation was measured by in vitro incorporation of 5-bromo-2'-deoxyuridine. Sulindac therapy was associated with a reduction in epithelial cell proliferation in the duodenum (median labelling index (LI) 15.8 versus 14.4 per cent, P = 0.003) and a trend towards duodenal polyp regression (P = 0.12). In the rectum, cell proliferation showed a marked reduction (median LI 8.5 versus 7.4 per cent, P = 0.018), and significant (P = 0.01) polyp regression was seen. Rectal polyposis was less severe than that in the duodenum and responded more dramatically. Sulindac is a possible treatment for patients in whom rectal polyps have failed to show significant regression after ileorectal anastomosis and who are unsuitable for pouch surgery; it may be useful in early duodenal polyposis or as an adjunct after duodenal clearance.

Adenomatous Polyposis Coli↗
PubMed1996

The tumor suppressor protein APC colocalizes with beta-catenin in the colon epithelial cells.

The APC gene is mutated in familial adenomatous polyposis and sporadic colorectal tumors. The product of this gene is a 300 kDa cytoplasmic protein associated with catenin. In the present study, we examined the subcellular localization of the APC protein and beta-catenin in the mouse colon by double-labeling immunocytochemistry. While the APC protein was localized in the lateral and apical cytoplasm and in microvilli of the epithelial cells, beta-catenin was present exclusively in the lateral cytoplasm. Double-labeling-immunoelectron microscopy demonstrated precise colocalization of the APC protein and beta-catenin along the lateral plasma membrane. These results suggest that the APC protein functions in cooperation with beta-catenin in the lateral cytoplasm but has other functions independent of beta-catenin in the apical cytoplasm and in microvilli.

Adenomatous Polyposis Coli Protein↗
PubMed1990

Pouchitis and gastric hyposecretion: cause or effect?

Pouchitis is a well recognized entity but its aetiology is still controversial. The aim of this study is to determine if gastric acidity has a role in the physiopathology of this problem. In a series of 70 consecutive patients with pelvic reservoir (65 mucosal ulcerative colitis (UC), 5 familial adenomatous polyposis (FAP], 15 patients developed pouchitis. Ten patients responded favourably to metronidazole. Five patients had several episodes of resistant pouchitis. Two of these (with FAP) developed recurrent bouts of pouchitis while on cimetidine therapy for severe peptic disease. Both patients were improved on sucralfate and symptoms did not recur after highly selective vagotomy. The other three patients began to complain of pouchitis one to six years after the fabrication of the reservoir. Gastric studies were undertaken to determine the fasting gastric pH. The values were high in all three cases despite normal stimulation tests and normal gastric biopsy. After pouch removal for toxic dilatation (without obstruction) in one of these patients, the gastric pH returned to normal. From these preliminary results, it seems that pouchitis might be associated with hypochlorhydria. It might also be possible that certain physiologic properties of the reservoir reduce gastric acidity and so create recurrent bouts of pouchitis. Further studies are needed to evaluate the physiologic consequences of the pelvic ileal reservoir on gastric physiology.

Adenomatous Polyposis Coli↗
PubMed1987

Upper gastrointestinal neoplasia in familial polyposis.

Upper gastrointestinal (UGI) endoscopy was performed in 41 asymptomatic American patients with familial polyposis to assess the prevalence of gastric and duodenal polyps and to characterize their pathological features. Eighteen patients (44%) had UGI endoscopic abnormalities. Six patients had both gastric and duodenal lesions. Eight patients had only gastric polyps, and four had duodenal polyps only. The presence of other extracolonic expressions of polyposis had a suggestive but statistically insignificant correlation with UGI polyps. Patients with familial polyposis and duodenal adenomatous polyps are at high risk for the development of periampullary cancer; screening and identification of these individuals is recommended.

Adenomatous Polyposis Coli↗
PubMed1995

Randomized trial to determine the optimum level of pouch-anal anastomosis in stapled restorative proctocolectomy.

PURPOSE: This study was undertaken to identify the optimum level of stapled ileal pouch-anal anastomosis. METHOD: A prospective, randomized trial was completed to compare double-stapled ileoanal anastomosis placed at the top of anal columns (high, n = 26) with anastomosis at the dentate line (low, n = 21). RESULTS: There was no significant difference in the overall complication rate between operations (high, n = 7, vs. low, n = 8; P < 0.21). Pouch-anal functional score (scale 0-12; 0 = excellent, 12 = poor) was significantly better in the high anastomosis group (median (range): 2 (1-9) vs. 5.5 (1-12); P < 0.05). Incontinence occurred in only two patients randomized to high anastomosis compared with six in the low anastomosis group. Nocturnal soiling was reported in three patients after high anastomosis and in six patients after dentate line anastomosis. Both operations caused a significant but comparable reduction of maximum and resting pressure (31 percent after high anastomosis (P < 0.05); 23 percent after low anastomosis (P < 0.05)). However, a significant fall in functional length of the anal canal was only seen after a low pouch-anal anastomosis (P < 0.05). CONCLUSION: Stapled pouch-anal anastomosis at the top of anal columns gives better functional results compared with a stapled anastomosis at the dentate line.

Adenomatous Polyposis Coli↗