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      Alternative treatments for prophylaxis of colorectal cancer in familial adenomatous polyposis

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          Abstract

          Familial adenomatous polyposis (FAP) is a rare, hereditary disease characterized by the presence of 100 or more adenomas distributed throughout the colon and rectum. If untreated, colorectal cancer develops in almost 100% of FAP patients. As prophylactic treatment, proctocolectomy with ileal pouch-anal anastomosis remains the surgical treatment of choice. High rates of postoperative complications, however, have been reported with this procedure, including bowel dysfunction, incontinence, and reduced female fecundity. Some novel strategies for preventing hereditary colon cancers have been reported. This review summarizes alternative treatments, including the laparoscopic approach, chemoprevention, endoscopic management, and subtotal colectomy combined with endoscopic treatment, for prophylaxis of colorectal cancer in FAP patients.

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          Familial adenomatous polyposis.

          Polymnia Galiatsatos, William Foulkes (2006)
          Familial adenomatous polyposis (FAP) is an autosomal-dominant colorectal cancer syndrome, caused by a germline mutation in the adenomatous polyposis coli (APC) gene, on chromosome 5q21. It is characterized by hundreds of adenomatous colorectal polyps, with an almost inevitable progression to colorectal cancer at an average age of 35 to 40 yr. Associated features include upper gastrointestinal tract polyps, congenital hypertrophy of the retinal pigment epithelium, desmoid tumors, and other extracolonic malignancies. Gardner syndrome is more of a historical subdivision of FAP, characterized by osteomas, dental anomalies, epidermal cysts, and soft tissue tumors. Other specified variants include Turcot syndrome (associated with central nervous system malignancies) and hereditary desmoid disease. Several genotype-phenotype correlations have been observed. Attenuated FAP is a phenotypically distinct entity, presenting with fewer than 100 adenomas. Multiple colorectal adenomas can also be caused by mutations in the human MutY homologue (MYH) gene, in an autosomal recessive condition referred to as MYH associated polyposis (MAP). Endoscopic screening of FAP probands and relatives is advocated as early as the ages of 10-12 yr, with the objective of reducing the occurrence of colorectal cancer. Colectomy remains the optimal prophylactic treatment, while the choice of procedure (subtotal vs proctocolectomy) is still controversial. Along with identifying better chemopreventive agents, optimizing screening of extracolonic cancers and applying new radiological and endoscopic technology to the diagnosis and management of extracolonic features are the major challenges for the future.
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            Sulindac causes regression of rectal polyps in familial adenomatous polyposis.

            F. Drouhin, M Trousset, O Duhamel … (1991)
            In familial adenomatous polyposis, sulindac-induced polyp regression has been reported by several authors. In this study, the goal was to confirm these results by a randomized, placebo-controlled, double-blind crossover study in 10 patients with rectal polyps that had been previously treated by colectomy and ileorectal anastomosis. Patients received sulindac, 300 mg/day, or placebo during two 4-month periods separated by a 1-month wash-out phase. One patient was not compliant and was excluded. With sulindac, the authors observed a complete (6 patients) or almost complete (3 patients) regression of the polyps. With placebo, the authors observed an increase (5 patients), no change (2 patients), and a relative decrease (2 patients) in the number of polyps. The difference between sulindac and placebo was statistically significant (P less than 0.01). In biopsy specimens of polyps and normal rectal mucosa of 6 patients, the authors conducted an immunohistochemical study of the cellular proliferation index using the Ki 67 monoclonal antibody (Ki 67 index), at the beginning and at the end of each treatment period. They were not able to show a sulindac-induced modification of the Ki 67 index. The authors conclude that sulindac is effective in inducing the regression of rectal polyps in familial adenomatous polyposis.
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              Primary chemoprevention of familial adenomatous polyposis with sulindac.

              Francis Giardiello, Jill D Trimbath, W. Hubbard … (2002)
              Familial adenomatous polyposis is caused by a germ-line mutation in the adenomatous polyposis coli gene and is characterized by the development of hundreds of colorectal adenomas and, eventually, colorectal cancer. Nonsteroidal antiinflammatory drugs can cause regression of adenomas, but whether they can prevent adenomas is unknown. We conducted a randomized, double-blind, placebo-controlled study of 41 young subjects (age range, 8 to 25 years) who were genotypically affected with familial adenomatous polyposis but phenotypically unaffected. The subjects received either 75 or 150 mg of sulindac orally twice a day or identical-appearing placebo tablets for 48 months. The number and size of new adenomas and side effects of therapy were evaluated every four months for four years, and the levels of five major prostaglandins were serially measured in biopsy specimens of normal-appearing colorectal mucosa. After four years of treatment, the average rate of compliance exceeded 76 percent in the sulindac group, and mucosal prostaglandin levels were lower in this group than in the placebo group. During the course of the study, adenomas developed in 9 of 21 subjects (43 percent) in the sulindac group and 11 of 20 subjects in the placebo group (55 percent) (P=0.54). There were no significant differences in the mean number (P=0.69) or size (P=0.17) of polyps between the groups. Sulindac did not slow the development of adenomas, according to an evaluation involving linear longitudinal methods. Standard doses of sulindac did not prevent the development of adenomas in subjects with familial adenomatous polyposis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Anus Rectum Colon
                Journal ID (iso-abbrev): J Anus Rectum Colon
                Title: Journal of the Anus, Rectum and Colon
                Publisher: The Japan Society of Coloproctology
                ISSN (Electronic): 2432-3853
                Publication date Collection: 2017
                Publication date (Electronic): 25 May 2018
                Volume: 1
                Issue: 3
                Pages: 74-77
                Affiliations
                [1 ]Department of Surgery, Toho University Ohashi Medical Center, Tokyo, Japan
                Author notes

                Corresponding author: Yoshihisa Saida, yoshisaida@ 123456nifty.com

                Article
                DOI: 10.23922/jarc.2017-007
                PMC ID: 6768673
                SO-VID: ff8933b7-97fa-4c89-b5a2-91a0b3cc2f95
                Copyright © Copyright © 2017 by The Japan Society of Coloproctology
                License:

                Journal of the Anus, Rectum and Colon is an Open Access article distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. To view the details of this license, please visit ( https://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 9 February 2017
                Date accepted : 4 April 2017
                Categories
                Subject: Review Article

                Keywords: familial adenomatous polyposis,total proctocolectomy,ileal pouch-anal anastomosis (ipaa),ileorectal anastomosis (ira),chemoprevention,endoscopic management
                Data availability:
                Keywords: familial adenomatous polyposis, total proctocolectomy, ileal pouch-anal anastomosis (ipaa), ileorectal anastomosis (ira), chemoprevention, endoscopic management

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