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PubMed1992

The role of pathology in pelvic ileal reservoir surgery.

The increasing use and success of pelvic ileal reservoir surgery places an ever more demanding role onto the surgical pathologist. Close surgical and pathological cooperation is critical for preoperative patient selection, for intraoperative diagnostic confirmation and for postoperative follow up. The long term consequences of pouch construction are, as yet, unknown, but there is much evidence to substantiate the need for life-long surveillance by clinical, endoscopic and pathological means to maximise the benefits of the pelvic ileal reservoir to the patient. This paper reviews the pathological input into these aspects of pelvic ileal reservoir surgery together with a critical appraisal of the likely long term consequences of pelvic ileal reservoir construction.

Adenomatous Polyposis Coli↗
PubMed1986

An assessment of inflammation in the reservoir after restorative proctocolectomy with ileoanal ileal reservoir.

The significance of inflammation of the mucosa of the ileal reservoir after restorative proctocolectomy is not known although in some cases it appears to be associated with symptoms when the condition has been referred to as pouchitis. This investigation has aimed to determined the prevalence of inflammation, to define pouchitis and to examine some factors which might be related to inflammation. Mucosal biopsies from the ileal reservoir were studied in 90 patients at up to 62 months after closure of the ileostomy. A histological grading system (0-6) was used to assess the severity of inflammation. Some degree of chronic and acute inflammation was found in 87% and 30% of cases respectively. The prevalence of a grade of 4 or more was 23% and 3.5%. There was a correlation between severity of chronic and acute inflammation. Severe histological acute inflammation (grade 4-6) was associated with sigmoidoscopic features of inflammation and with increased frequency of defaecation. Of 55 patients sigmoidoscoped by one clinician, 6 (11%) had pouchitis which was characterised by macroscopic inflammation of the reservoir, diarrhoea and a histological grade of 4 or more. The severity of chronic inflammation was not related to frequency of defaecation. Histological inflammation could not be correlated with the type of reservoir, residual volume after evacuation of a known volume of stool substitute introduced per anum into the reservoir or compliance of the reservoir. Acute inflammation was significantly more severe in patients with ulcerative colitis than in those with familial adenomatous polyposis.

Adenomatous Polyposis Coli↗
PubMed1991

Lectin staining of neoplastic and normal background colorectal mucosa in nonpolyposis and polyposis patients.

A lectin histochemistry approach was adopted for comparative assessment of a colon cancer risk. Binding of Ulex europaeus agglutinin-I (UEA-I), peanut agglutinin (PNA), Griffonia simplicifolia agglutinin-II (GSA-II), and Dolichos biflorus agglutinin (DBA) was investigated in tumor and background tissue from a total of 34 adenoma and 44 cancer patients and compared with reaction patterns in control and familial adenomatous polyposis (FAP) patients. Adenoma patients with UEA-I positive rectal mucosa were found to have a 33.3 percent familial history of large bowel cancer, which was significantly higher (P less than 0.05) than the respective 4.0 percent figure for patients with negative rectal mucosa. In the cancer patients, an even stronger correlation was noted, with a 63.2 percent UEA-I positive family history association being recorded, as opposed to 4.0 percent in the negative rectal mucosa patients (P less than 0.01). Thus, the results suggest that, apparently, normal rectal background mucosa of individuals genetically at high risk for colon and rectal cancer demonstrates a specific lectin binding ability similar to that of FAP patients and that the simple method using UEA-I staining of rectal biopsy specimens can be of practical use in identification of high-risk colorectal cancer.

Adenoma↗
PubMed1995

Risk of residual rectal mucosa after proctocolectomy and ileal pouch-anal reconstruction with the double-stapling technique. Postoperative endoscopic follow-up study.

PURPOSE: This study was designed to assess the risk of retained rectal mucosa after proctocolectomy and ileal pouch-anal anastomosis with the double-stapling technique. METHODS: A total of 113 patients underwent proctocolectomy with an ileal pouch-anal reconstruction. In 57 patients the anastomosis between pouch and proximal anal canal was performed using the double-stapling technique. In 26 patients the procedure was carried out without a protecting ileostomy. Of the remaining 31 patients with a proximal ileostomy, 15 underwent endoscopy six weeks postoperatively. Circular biopsies were taken just distal from the pouch-anal anastomosis. RESULTS: Histologic examination revealed rectal mucosa in at least one biopsy in 7 of 15 patients. At follow-up (mean 18 months) no (distal) pouchitis was clinically noticed. In one patient with familial polyposis, a few polyps, distal of the anastomosis, had to be endoscopically removed. CONCLUSIONS: Double-stapled ileal pouch-anal anastomosis has a considerable risk of residual rectal mucosa, because of combined linear transection and circular stapling with bilateral dog-ear formation of rectal mucosa. Residual rectal mucosa did not seem to influence clinical results at follow-up.

Adenomatous Polyposis Coli↗
PubMed1989

Tissue-specific expression of c-Ha-ras in premalignant gastrointestinal mucosae.

The molecular mechanisms underlying premalignant gastrointestinal diseases, such as ulcerative colitis and Barrett's esophagus, remain unknown. For this reason, the expression of the protooncogene c-Ha-ras was studied in ulcerative colitis and Barrett's esophagus. Total cellular RNA was extracted from different regions of the gastrointestinal tract in these two diseases. Expression of c-Ha-ras was greater in proximal than in distal colon and undetectable in Barrett's esophagus. These regional differences in expression were not seen with the control gene beta-actin or with the protooncogenes c-myc and p53. In order to evaluate structural factors contributing to expression, amplification and methylation of c-Ha-ras DNA were studied in these tissues by Southern and slot blotting. No amplification of c-Ha-ras or six other protooncogenes was detected. These data suggest tissue-specific regulation of c-Ha-ras expression in the gastrointestinal tract in certain premalignant disease states.

Adenomatous Polyposis Coli↗
PubMed1995

Intraoperative small bowel enteroscopy in familial adenomatous and familial juvenile polyposis.

BACKGROUND: In familial adenomatous polyposis and juvenile polyposis, polyps can occur throughout the gastrointestinal tract. METHODS: We report seven patients with familial adenomatous polyposis and two patients with juvenile polyposis who underwent small bowel enteroscopy at the time of exploratory celiotomy either for colectomy or other pathology. RESULTS: Polyps in the jejunum and/or ileum were noted in five of nine (56%) patients at enteroscopy. In three of nine (33%) patients these polys were adenomatous. Two of these patients had polyps in the jejunum and in the ileum, whereas one patient had jejunal adenomas alone. These polyps were from 3 mm to 30 mm in size. The remaining two patients with polyps had lymphoid hyperplasia in the ileum. All three patients who had adenomas at intraoperative small bowel enteroscopy had duodenal adenomas at esophagogastroduodenoscopy. At the age of 14 years, one patient had an intramucosal carcinoma in a small bowel juvenile polyp. CONCLUSION: Baseline small bowel enteroscopy should be considered at the time of surgical exploration in patients with asymptomatic familial adenomatous polyposis and juvenile polyposis. In patients with duodenal polyps, enteroscopy should be performed at the time of surgery. Biopsy and/or excision of larger polyps should be performed because these polyps may harbor a carcinoma.

Adenomatous Polyposis Coli↗
PubMed2001

Disease model: familial adenomatous polyposis.

Mutations in the APC gene are responsible for familial adenomatous polyposis (FAP) and for the majority of sporadic colorectal cancers. The establishment of genotype-phenotype correlations in FAP is often complicated by the great clinical variability observed among carriers of the same APC mutation even within the same kindred. This variability is likely to arise from the interaction of genetic and environmental modifying factors, the dissection of which ideally requires the employment of mouse models where the effects of specific Apc mutations are analyzed in an inbred, homogeneous genetic background and a controlled environment. The availability of different Apc mouse models allows not only the establishment of more precise genotype-phenotype correlations but has also provided very important clues for the understanding of the function of APC in homeostasis and tumorigenesis. Also, the close phenotypic resemblance to the human disease makes these mice unique preclinical models to test chemopreventive and therapeutic interventions.

Adenomatous Polyposis Coli↗
PubMed2002

When is molecular genetic testing for colorectal cancer indicated?

The genetic mutations causing many of the syndromes which confer a high inherited risk of colorectal cancer have now been identified. These include familial adenomatous polyposis, hereditary non-polyposis colorectal cancer, Peutz-Jeghers syndrome, Cowden's syndrome and juvenile polyposis. In all these diseases, the precise mutation is nearly always unique to a particular family; there are few mutation hot spots. This means that mutation detection is technically demanding. Nonetheless, genetic testing can now be used clinically to confirm the diagnosis in affected individuals, and to predict whether an "at risk" family member has inherited the disease and should therefore have endoscopic screening. Because current technology does not detect all mutations, a negative result in a definitely affected individual is diagnostically unhelpful and does not allow predictive testing of other family members. When a mutation can be detected, it is diagnostically very useful, and allows better management of all family members.

Adenomatous Polyposis Coli↗
PubMed2000

Genotype and phenotype factors as determinants for rectal stump cancer in patients with familial adenomatous polyposis. Hereditary Colorectal Tumors Registry.

OBJECTIVE: To identify factors influencing the occurrence of cancer in the rectal remnant in patients with familial adenomatous polyposis (FAP) after colectomy and ileorectal anastomosis (IRA). SUMMARY BACKGROUND DATA: The risk for rectal cancer in patients with FAP after colectomy and IRA remains a major concern. METHODS: Between 1955 and 1997, 371 patients (206 men, 165 women) from the Registry of Hereditary Colorectal Tumors underwent colectomy and IRA as a primary surgical procedure. Survival was estimated using the Kaplan-Meier method. Cox proportional hazard models were fitted to assess the relative excess risk of rectal cancer and to control for confounding factors. A multivariate analysis was performed to assess the relation between cancer risk in the rectum and sex, age, number of rectal polyps, colon cancer, and APC germline mutation. RESULTS: Median follow-up was 81 months. Eighty-nine patients (24%) had colon cancer at the time of surgery. The APC mutation was found in 200 patients. In 27 patients, cancer developed in the retained rectum 1 to 26 years after surgery. The incidence of rectal carcinoma appears to increase with time: at 10, 15, and 20 years after surgery, the cumulative risk was 7.7%, 13.1%, and 23.0%, respectively. Multivariate analysis identified as independent predictors the presence of colon cancer at IRA and a mutation occurring between codons 1250 and 1464; both factors increased the risk nine times. CONCLUSIONS: The presence of cancer at IRA and APC mutation type are the most important risk factors for the future development of cancer in the rectal remnant in patients with FAP.

Adenomatous Polyposis Coli↗
PubMed2004

Adenomatous colonic polyps are rare in ulcerative colitis.

BACKGROUND: Uncertainty exists as to whether dysplastic polyps in ulcerative colitis should always be managed as dysplasia-associated lesions/masses requiring colectomy, or whether some can be managed by polypectomy. The prevalence of non-inflammatory polyps in ulcerative colitis is unknown. AIM: To compare dysplastic polyp occurrence in patients with ulcerative colitis and in patients without inflammatory bowel disease. METHODS: The clinical, endoscopic and histological records of 150 ulcerative colitis patients (median disease duration, 10 years; 57% with pancolitis) undergoing colonoscopy were scrutinized for any polyp history. Two hundred and five patients undergoing colonoscopy for altered bowel habit, but without features suggestive of polyp presence, were used as a control group. Immunohistochemical staining of flat and polypoid mucosa for p16, beta-catenin, p53 and cyclo-oxygenase-2 was compared in the two groups. RESULTS: Only six (4%) ulcerative colitis patients had ever had dysplastic polyps. Two had single adenomatous polyps proximal to the colitis segment. Of the four patients with dysplastic polyps within colitic mucosa, two were treated endoscopically, but in two the lesions were considered to be dysplasia-associated lesions/masses and colectomy was advised. In contrast, 24 controls had at least one adenomatous polyp (chi(2) = 6.7, P < 0.01). Ten (6.7%) ulcerative colitis patients and 24 (12%) control patients had metaplastic polyps (N.S.). Immunohistochemical staining was not discriminatory. CONCLUSION: Despite the increased cancer risk in long-standing ulcerative colitis, adenomatous polyps arise less frequently in ulcerative colitis patients than in patients without ulcerative colitis.

Adenomatous Polyposis Coli↗
PubMed2005

A characterization of anaerobic colonization and associated mucosal adaptations in the undiseased ileal pouch.

INTRODUCTION: The resolution of pouchitis with metronidazole points to an anaerobic aetiology. Pouchitis is mainly seen in patients with ulcerative colitis pouches (UCP). We have recently found that sulphate reducing bacteria (SRB), a species of strict anaerobe, colonize UCP exclusively. Herein, we aimed to correlate levels of different bacterial species (including SRB) with mucosal inflammation and morphology. METHODS: Following ethical approval, fresh faecal samples and mucosal biopsies were taken from 9 patients with UCP and 5 patients with familial adenomatous polyposis pouches (FAPP). For the purposes of comparison, faecal samples and mucosal biopsies were also taken from the stomas of 7 of the 9 patients with UC (UCS). Colonization by four types of strict anaerobes (SRB, Clostridium perfringens, Bifidobacteria and Bacteroides) as well as by three types of facultative anaerobes (Enterococci, Coliforms and Lactobacilli) was evaluated. Inflammatory scores and mucosal morphology were assessed histologically in a blinded fashion by a pathologist. RESULTS: In general, strict anaerobes predominated over facultative in the UCP (P = 0.041). SRB were present in UCP exclusively. Even after exclusion of SRB from total bacterial counts, strict anaerobes still predominated. In the UCS, facultative anaerobes predominated. Strict and facultative anaerobes were present at similar levels in the FAPP. Enterococci were present at significantly reduced levels in the UCP when compared with the UCS (P = 0.031). When levels of SRB and other anaerobic species were individually correlated with mucosal inflammation and morphology, no trends were observed. CONCLUSION: We have previously identified that SRB exclusively colonize UCP. In addition we have now identified a novel increase in the strict/facultative anaerobic ratio within the UCP compared to UCS. These stark differences in bacterial colonization, however, appear to have limited impact on mucosal inflammation or morphology.

Adenomatous Polyposis Coli↗
PubMed2004

Genetic polymorphisms of human flavin monooxygenase 3 in sulindac-mediated primary chemoprevention of familial adenomatous polyposis.

PURPOSE: Sulindac is a nonsteroidal anti-inflammatory drug (NSAID) effective in regressing adenomas in patients with familial adenomatous polyposis (FAP). However, a recent randomized trial showed that sulindac, when compared with placebo, failed to prevent the development of adenomatous polyps in genotypically positive but phenotypically negative FAP patients. The present study determined whether polymorphisms in the gene encoding flavin monooxygenase 3 (FMO3), a hepatic microsomal enzyme that inactivates sulindac, played a role in determining the efficacy of sulindac in preventing polyposis in this cohort of FAP patients. EXPERIMENTAL DESIGN: Genotyping was performed on seven established FMO3 polymorphisms previously shown to have functional relevance-M66I, P153L, E158K, V257M, E305X, E308G, and R492W-in 21 and 20 FAP patients, who received sulindac and placebo, respectively. RESULTS: None of the 41 patients exhibited heterozygous or homozygous M66I and R492W variant alleles, or homozygous P153L, V257M, and E305X variant alleles. Among sulindac-treated patients who did not develop adenomas ("responders"), 4 (33%) were homozygous for E158K and 2 (17%) were homozygous for E308G variant alleles. In contrast, none of the patients on sulindac who developed adenomas ("nonresponders") exhibited homozygosity for either of the two variant alleles. In addition, polymorphisms in the E158K or E308G allele were associated with a significant reduction in mucosal prostanoid levels in patients treated with sulindac. CONCLUSIONS: Polymorphisms in FMO3, particularly at the E158K and E308G loci, may reduce activity in catabolizing sulindac and result in an increased efficacy to prevent polyposis in FAP.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

[Magnifying colonoscopy in the diagnosis of colorectal carcinoma invading the submucosa in familial adenomatous polyposis].

The development of colonoscopy with image magnification has enable to study the colonic mucosa in detail and to do differential diagnosis between neoplastic and non-neoplastic lesions from the observation of pit patterns. The results are comparable to stereomicroscopy being possible to predict the histologic diagnosis. In a patient with familial adenomatous polyposis magnifying colonoscopy was performed and this method demonstrated a wide variation of benign polypoid lesions and the morphological features of early colorectal cancer. In this patient, the evaluation by image magnification, together with indigo carmin 0.4% chromoscopy, showed a wide variety of lesions in the colon and rectum: laterally spreading tumor in the cecum, with IIIL + IV pits, subpediculate polyp in the transverse colon with approximately 2.0 cm diameter and IV + V pits, flat elevated lesions IIIL type, and in the sigmoid colon IIa + IIc lesion with V type of Kudo's classification were observed. The evaluation of pit patterns of the lesions in the transverse and sigmoid colon has enable to do the endoscopic diagnosis of the lesion with submucosal invasion.

Adenocarcinoma↗
PubMed2005

Determination of optical properties of normal and adenomatous human colon tissues in vitro using integrating sphere techniques.

AIM: The purpose of the present study is to compare the optical properties of normal human colon mucosa/submucosa and muscle layer/chorion, and adenomatous human colon mucosa/submucosa and muscle layer/chorion in vitro at 476.5, 488, 496.5, 514.5 and 532 nm. We believe these differences in optical properties should help differential diagnosis of human colon tissues by using optical methods. METHODS: In vitro optical properties were investigated for four kinds of tissues: normal human colon mucosa/submucosa and muscle layer/chorion, and adenomatous human colon mucosa/submucosa and muscle layer/chorion. Tissue samples were taken from 13 human colons (13 adenomatous, 13 normal). From the normal human colons a total of 26 tissue samples, with a mean thickness of 0.40 mm, were used (13 from mucosa/submucosa and 13 from muscle layer/chorion), and from the adenomatous human bladders a total of 26 tissue samples, with a mean thickness of 0.40 mm, were used (13 from mucosa/submucosa and 13 from muscle layer/chorion). The measurements were performed using a double-integrating-sphere setup and the optical properties were assessed from these measurements using the adding-doubling method that was considered reliable. RESULTS: The results of measurement showed that there were significant differences in the absorption coefficients and scattering coefficients between normal and adenomatous human colon mucosa/submucosa at the same wavelength, and there were also significant differences in the two optical parameters between both colon muscle layer/chorion at the same wavelength. And there were large differences in the anisotropy factors between both colon mucosa/submucosa at the same wavelength, there were also large differences in the anisotropy factors between both colon muscle layer/chorion at the same wavelength. There were large differences in the value ranges of the absorption coefficients, scattering coefficients and anisotropy factors between both colon mucosa/submucosa, and there were also large differences in these value ranges between both colon muscle layer/chorion. There are the same orders of magnitude in the absorption coefficients for four kinds of colon tissues. The scattering coefficients of these tissues exceed the absorption coefficients by at least two orders of magnitude. CONCLUSION: There were large differences in the three optical parameters between normal and adenomatous human colon mucosa/submucosa at the same laser wavelength, and there were also large differences in these parameters between both colon muscle layer/chorion at the same laser wavelength. Large differences in optical parameters indicate that there were large differences in compositions and structures between both colon mucosa/submucosa, and between both colon muscle layer/chorion. Optical parameters for four kinds of colon tissues are wavelength dependent, and these differences would be useful and helpful in clinical applications of laser and tumors photodynamic therapy (PDT).

Adenomatous Polyposis Coli↗