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PubMed1992

Gastroduodenal polyps in patients with familial adenomatous polyposis.

A review of the endoscopy reports and pathology results from esophagogastroduodenoscopy (EGD) of all patients with familial adenomatous polyposis (FAP) undergoing such an examination was performed. Two hundred forty-seven patients were identified, with an overall prevalence of duodenal adenomas of 66 percent and of fundic gland polyps of 61 percent. Analysis of our more recent experience (1986 to 1990) shows the prevalence to be 88 percent and 84 percent, respectively. A normal-appearing papilla was adenomatous in 50 percent of cases. No case of periampullary carcinoma developed in patients under surveillance. Routine EGD is indicated for patients with FAP. Duodenal adenomas and fundic gland polyps will occur in the majority of patients.

Adenomatous Polyposis Coli↗
PubMed1997

[Cronkhite-Canada syndrome. Epidemiology, symptoms, morphology and therapy based on a case report and literature review].

Juvenile polyposis was first described by Cronkhite and Canada in 1955. This disease is characterized by juvenile intestinal polyps and ectodermal abnormalities. The etiology of Cronkhite-Canada syndrome (CCS), however, is still not well understood. Interestingly among patients with CCS a significant correlation (16.5%) with intestinal carcinomas has been observed. Thus, malignant transformation and/or genetic predisposition may be involved in the initiation of the disease. In the following, epidemiology, symptoms, morphology and therapy of CCS are discussed. Our examinations are based on studies reported in the literature and on a case report of a female patient who developed a colon carcinoma 2 years after initial diagnosis of CCS.

Adenocarcinoma↗
PubMed1994

Pouchitis after ileal pouch-anal anastomosis: a Pouchitis Disease Activity Index.

OBJECTIVE: To develop a "Pouchitis Disease Activity Index" (PDAI) and to compare it with other diagnostic scoring systems for pouchitis. DESIGN: We compared patients who had an optimal outcome with those who had a poor result attributable to recurrent pouchitis after ileal pouch-anal anastomosis (IPAA) for ulcerative colitis at the Mayo Clinic. MATERIAL AND METHODS: We evaluated the applicability of a PDAI that quantitated clinical findings and the endoscopic and histologic features of acute inflammation in four groups of patients: (1) 10 who underwent IPAA for ulcerative colitis and had symptoms compatible with a clinical diagnosis of pouchitis, (2) 5 who underwent IPAA for ulcerative colitis and did not have pouchitis, (3) 5 who underwent IPAA for familial adenomatous polyposis and had no symptoms of pouchitis, and (4) 5 who had a Brooke ileostomy for ulcerative colitis (control group). RESULTS: The PDAI was significantly greater in patients with the clinical features of pouchitis than it was for patients in the other three groups. All 10 patients with pouchitis fulfilled the PDAI criteria for a diagnosis of pouchitis; in contrast, only 1 of these 10 patients met the diagnostic criteria for pouchitis by application of previously established scoring systems. No asymptomatic patient qualified for a diagnosis of pouchitis by the PDAI criteria. CONCLUSION: The PDAI provides simple, objective, and quantitative criteria for pouch inflammation after IPAA and is more sensitive than prior scoring systems.

Adenomatous Polyposis Coli↗
PubMed2002

Outcome after septic complications in J pouch procedures.

BACKGROUND: Despite the wide range of surgical approaches for pouch salvage, septic complications are among the main causes of pouch failure. METHODS: This study analysed the mode and outcome of various therapeutic approaches for pouch salvage and the impact of time of diagnosis, localization and form of septic complications on the risk of pouch failure in 131 patients with septic complications of a total of 706 patients undergoing a J pouch procedure. RESULTS: Septic complications consisted of 76.3 per cent fistulas, 15.3 per cent anastomotic breakdowns and 8.4 per cent pelvic abscesses. A total of 107 patients (81.7 per cent) with septic complications required a mean of 2.2 surgical procedures. The frequency of permanent defunctioning and excision of the pouch in the 131 patients with septic complications was 23.7 and 6.1 per cent respectively. The estimated cumulative 3-, 5- and 10-year rate of pouch failure in patients with septic complications was 19.6, 31.1 and 39.2 per cent respectively. The risk of pouch failure was significantly affected by the site of origin of septic complications (P = 0.02). The 5-year pouch failure rate increased in a subgroup of patients with septic complications at the pouch-anal anastomosis when the anal sphincter was involved (50.1 versus 29.2 per cent; P = 0.18). CONCLUSION: Pouch failure as a result of septic complications may occur several years after ileal pouch-anal anastomosis. For prevention of pouch failure, surgery for septic complications is required in a high percentage of patients and repeated attempts are justified. Follow-up studies are required for further analysis of pouch failure.

Abscess↗
PubMed2005

Oral contraceptives and polyp regression in familial adenomatous polyposis.

Epidemiologic and experimental reports suggest that female hormones protect against the development of colorectal cancer, but studies are limited. We describe a patient in the placebo arm of a 4-year primary chemoprevention trial who developed adenomatous polyps and then had eradication of polyps after the administration of oral contraceptives. No change in the prostaglandin levels in the colonic mucosa was noted after polyp elimination, making nonsteroidal anti-inflammatory drug ingestion unlikely as a cause. This report represents the regression of colorectal adenomas with the use of estrogen/progesterone compounds.

Adenomatous Polyposis Coli↗
PubMed1994

Dolichos biflorus agglutinin binding in hereditary bowel cancer.

Dolichos biflorus agglutinin (DBA) binds specifically to N-acetylgalactosamine (GalNAc), one of the 5 sugars contributing to the oligosaccharide component of human colorectal goblet cell mucin. DBA binds to goblet cells of the upper crypt and surface epithelium within the proximal colon and to the majority of goblet cells of the distal large bowel. DBA therefore serves as a marker of colorectal goblet cell differentiation with a distinct proximal to distal gradient effect. Previous reports indicate significant loss of DBA reactivity within morphologically normal colorectal mucosa derived from at-risk members of hereditary non-polyposis colorectal cancer (HNPCC) families. This finding could not be confirmed in the present study. Reduced binding was a relatively consistent finding in transitional mucosa, hyperplastic polyps and carcinoma, with adenomas displaying a more varied pattern of loss. Reduced binding by DBA may be explained by several mechanisms and may not necessarily reflect loss of GalNAc. The concept that lectins can be used to identify stepwise changes that occur during neoplastic evolution should not be accepted uncritically.

Adenomatous Polyposis Coli↗
PubMed1999

Familial adenomatous polyposis: a case report and histologic mucin study.

Adenocarcinoma arising at an ileostomy is uncommon, and only 29 cases have been reported in the literature. The case of a 54-year-old man who developed an adenocarcinoma at a Brooke ileostomy is reported. The ileostomy had been fashioned 21 years earlier after proctocolectomy for familial adenomatous polyposis (FAP). A wide local excision of the stoma was performed, and a new Brooke ileostomy was fashioned on the opposite side of the abdomen. Histopathologic examination revealed a well-differentiated adenocarcinoma with early invasion of the submucosa. On hematoxylin and eosin staining, the ileal mucosa adjacent to the tumor showed signs of colonic metaplasia, including loss of villous architecture and a reduced number of Paneth cells. Mucin staining using the high iron diamine-alcian blue stain demonstrated a mixture of sulfomucin and sialomucin in the ileal mucosa near the tumor, confirming colonic metaplasia. Ileostomy site carcinogenesis can be attributed to both the colonic metaplasia and the inherent nature of FAP or ulcerative colitis (UC), where colonic mucosa is susceptible to adenoma formation or dysplasia. Longstanding ileostomies in patients with FAP or UC should be followed to exclude the development of adenoma, dysplasia, or cancer.

Adenocarcinoma↗
PubMed2002

Gastrointestinal polyps and polyposis syndromes in children.

Gastrointestinal polyps are common during childhood and most often present with painless rectal bleeding. Most polyps occur as isolated colonic lesions and are not harbingers of an underlying genetic disorder, nor do they bestow a risk of gastrointestinal cancer. The astute pediatrician must be aware, however, that occasionally polyps may occur in the context of a genetic polyposis disorder characterized by an increase in the life-time risk of cancer in the gastrointestinal tract and other organ systems. This review outlines the major polyposis syndromes affecting children and highlights associated findings that might clue the alert physician to an underlying diagnosis. Recent developments in the understanding of the genetics of each disorder are emphasized.

Adenomatous Polyposis Coli↗
PubMed1985

Continence following ileo-anal anastomosis with an antiperistaltic terminal ileal segment.

The procedure of total colectomy, excision of the rectal mucosa and ileo-anal anastomosis with or without a proximal small intestinal reservoir has been described as a method of treating patients with ulcerative colitis and familial polyposis coli. The purpose of constructing a terminal ileal reservoir is to reduce the severe diarrhoea which often occurs following ileo-anal anastomosis. It is suggested that the use of a single antiperistaltic segment for this purpose would reduce the diarrhoea, and provide continence. This has been tested in the dog and the results are reported in this publication.

Anal Canal↗
PubMed1992

Rectal polyposis as a guide to duodenal polyposis in familial adenomatous polyposis.

Almost all patients with familial adenomatous polyposis (FAP) develop duodenal polyps, the severity of which is graded stage 1 (minor) to stage V (cancer). Regular endoscopy is recommended for all patients with FAP. To test whether the development of severe duodenal polyposis could be predicted in another way, rectal and duodenal polyp severity were compared in 91 patients with FAP. The fulguration ratio (number of rectal fulgurations divided by number of years since colectomy) supplied the rectal polyp severity index. Patients with stage V duodenal polyposis had significantly higher fulguration ratios (median 0.38) than did patients with stage 1 disease (median 0; P = 0.009). However, the wide scatter of results means that rectal polyp severity cannot be used as a guide to duodenal polyp severity in individual patients. The coexistence of populations with severe duodenal and rectal polyposis suggests that environmental factors are important in phenotypic expression in FAP.

Adenomatous Polyposis Coli↗
PubMed2000

Endoscopical and histological aspects of inflammatory changes in J-pouch mucosa.

The aim of the study was endoscopic and histological evaluation of mucosal inflammatory changes in the ileal reservoir after restorative proctocolectomy with ileoanal anastomosis (IPAA) because of FAP (27 patients) and ulcerative colitis (34 patients). Endoscopic symptoms of pouchitis (edema, granularity, contact bleeding, loss of vascular pattern, mucus, erosions) were found in 13 patients (4 were operated on because of FAP, 9 because of UC). A statistically significant difference (p < 0.0001) was found between endoscopic inflammatory index in UC (4.0 +/- 0.5) and in FAP (1.00 +/- 0.00). The endoscopic changes were correlated with the Moskowitz histological classification, in 12 acute score and in 6 chronic score were above 4 points. In 18 patients histological diagnosis of pouchitis was made (5 in FAP, 13 in UC). Acute pouchitis occurred in 12 patients and chronic in 6. In one patient histological changes resembled Crohn's disease. Regular endoscopic control with histological examination and verification of inflammatory lesions in the ileal reservoir is necessary.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

Neoplasias of the colorectal crypts.

Colorectal cancers are often preceded by noninvasive neoplasias arising in the surface epithelium, namely tubular, tubulovillous and villous adenomas. That neoplasias may also arise in the colorectal crypts is less well known. Between 1998 and 2002, colonoscopies, rectoscopies and colorectal surgical specimens from 8647 patients were received at this Department for histological diagnosis. The material included 502 adenomas, 865 invasive tumours and 221 cases of ulcerative colitis (UC). The following cryptal lesions were investigated: (a) neoplasias arising in the crypts, (b) neoplasias possibly arising in the crypts and (c) cryptal lesions alleged to be premalignant. Over the 5-year period, the most frequent phenotype encountered was single crypt dysplasia (in all 5 colectomies from familial adenomatous polyposis patients), followed by serrated adenomas (11.2%), hyperplastic polyps (8.4%), dysplasia in UC (6.3%), pure carcinoid tumours (1.7%), signet ring cell carcinoma (1.1%), adenocarcinoid tumours (0.2%) and de novo carcinomas (0.1%). In this survey, no case of Paneth cell adenoma or of cryptal neoplasia in lymphoid-associated mucosa (also known to originate from the crypts) was found. Hence, it was demonstrated that several neoplasia phenotypes actually arise in the colorectal crypts. The awareness that colorectal neoplasias may evolve from that particular cellular domain may cast more light on the understanding of the complex mechanisms of colorectal carcinogenesis.

Adenoma↗
PubMed1991

Extra-colonic manifestations of familial adenomatous polyposis.

Familial adenomatous polyposis (FAP) is a genetic disease created by an abnormality of chromosome number five resulting in a generalized cellular growth disorder. The growth abnormality created by the genetic defect dictates the development of benign and malignant lesions in different organs of the body. Even the term familial adenomatous polyposis does not fully describe the defect because lesions other than polyps may occur in these patients. The major organ affected is the large intestine. Adenomas occur at an earlier age than normally seen in the general population, grow more numerously and more rapidly, and become malignant at an inordinately young age.

Adenomatous Polyposis Coli↗
PubMed1990

Adenocarcinoma of the ileostomy: the latent risk of cancer after colectomy for ulcerative colitis and familial polyposis.

A case of a primary adenocarcinoma of an ileostomy is reported along with 15 other cases collected from the literature. These rare tumors are seen on the average 24 years after colectomy with ileostomy and in all cases are associated with a past history of ulcerative colitis or familial polyposis. Most of the reported cases of these tumors have appeared in the literature within the past 5 years, suggesting that there is a rising incidence of this disease corresponding to completion of a biologic latency period that began when the Brooke ileostomy was introduced for ulcerative colitis in 1951. In our case a mucinous adenocarcinoma occurred at the ileostomy site 34 years after colectomy. Adjacent to the tumor was mucosa showing colonic metaplasia and focal dysplasia. Subsequent biopsy specimens of the revised stoma showed inflammatory lesions morphologically suggestive of inflammatory (pseudo) polyps. The clinical and morphologic features in this case suggest that there is transition from ileal mucosa to colonic mucosa to colonic dysplasia to adenocarcinoma. Annual evaluation of the ileostomy for colonic metaplasia, inflammatory lesions consistent with ulcerative colitis and dysplasia, is recommended. In the presence of dysplasia, stomal revision is advised. Wide local excision is advised for adenocarcinoma.

Adenocarcinoma↗