Jafri, S M

English

eCommons@AKU

eCommons@AKUSection of Gastroenterology Department of MedicineSeptember 1994Dysplasia and surveillance in ulcerative colitisS M. JafriAga Khan UniversityFollow this and additional works at: https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterolPart of the Gastroenterology CommonsRecommended CitationJafri, S. M. (1994). Dysplasia and surveillance in ulcerative colitis. Journal of Pakistan Medical Association, 44(9), 223-224.Available at: https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterol/175Dysplasia and Surveillance in Ulcerative ColitisPages with reference to book, From 223 To 224 S. M. Wasim Jafri ( Department of Medicine, The Aga Khan University Hospital, Karachi. ) Chronic ulcerative colitis is a premalignant condition and predisposes to adenocarcinoma of the colon.The association between ulcerative colitis and colorectal cancer was first reported in 1920. Severalsubsequent studies2-5 have since confirmed ulcerative colitis as a predisposing cause of large bowelcancer. The management of ulcerative colitis is never complete unless an appropriate surveillanceprotocol is established6. The concept of screening high risk group for colon cancer is based on the factthat cancers discovered and removed before they cause symptoms are more likely to be cured. Becausethe prognosis after surgical treatment in colon cancer complicating ulcerative colitis is Duke’s stagedependent, survival would be improved if colitis - cancer is diagnosed earlier7. Ulcerative colitis isbeing more commonly diagnosed in our country and the period of follow-up is also increasing8. InPakistan true prevalence of this disease is unknown. In a large referral centre the incidence of ulcerativecolitis in patients presenting with rectal bleeding was reported to be as high as 25%9.The risk of cancerin ulcerative colitis has been calculated to be 3-30 times that of the general population3,10. Duration ofcolitis and extent of disease are major risk factors influencing risk of cancer4. Early age of onset, asevere first attack and continuous activity of disease are other important risk factors11. Age and extentof disease at diagnosis are strong and independent risk factors for colorectal cancer; the absolute risk ofcolorectal cancer 35 years after diagnosis was 30% for patients with pancolitis and 40% for those giventhis diagnosis at less than 15 years of age12. Several studies have reported that patients with left sidedcolitis or proctitis have a relatively lower risk of colorectal cancer than those with pancolitis13,14. Inyounger groups, however, and especially among patients 15 to 29 years of age at the time of diagnosis,left sided colitis entailed a relative risk of colorectal cancer that was close to that for pancolitis. In oldergroup the relative risk was close to 1.012. We have a close system of follow-up at our institution andpatients with history of active chronic ulcerative colitis of 5 years or more are closely followedregarding activity of disease. Traditional screening methods used for other high risk groups are notapplicable to patients with ulcerative colitis. Tests for occult blood in the stool are useless becauseblood is commonly present in the stool of ulcerative colitis patient16. Serum levels of CEA (carcinomaembryonic antigen) are also often elevated in these patients15. Barium enema is not suitable forsurveillance because the meticulous technique needed to detect small abnormalities are generally notavailable17. Dysplasia is present in over 80% of colectomy specimen in which a carcinoma is found18.Colonoscopy has emerged as a major technique providing a magnified view and tissue samplingcapability for the entire colon19. In a review by Dobbins dysplasia was found in 88% of 108 colectomyspecimens containing cancers while dysplasia was noted in the rectum in 66% of these cases20.Histologically dysplasia is classified as negative, indefinite and positive with positives divided into lowand high grade classes. Dysplasia appears to be apre-neoplastic abnormality but the timing of itsevolution and possible regression remain to be elucidated21. The reported incidence of dysplasia andcancer complicating ulcerative colitis in Pakistan is low mainly because of shorter duration of followup and possibly due to a higher incidence of left sided colitis22. Biopsies should be performed onsuspicious pseudopolyps and adenomatous polyps should be removed. In seeking dysplasia which isfound most often in flat mucosa, about 12 biopsies should be taken systematically through the colon at10 cms intervals. The most common approach is to take biopsies from caecum, ascending colon,hepatic flexure, transverse colon, splenic flexure, descending colon, sigmoid colon and rectum.Biopsies from areas not actually inflamed are more easily interpreted for dysplasia2’. Based onmultiple studies about one-third to one-half of patients with high grade dysplasia have a synchronousoccult cancer23. Risk of cancer will not be affected by surveillance but early diagnosis would makethem more amenable to treatment. The design of most surveillance programmes is essentially similarwith variation in recommended frequency of colonoscopy and sigmoidos copy with mucosal biopsies.Surveillance need not be instituted before 7-8 years in pancolitis and 15 years in disease limited to leftcolon. Ileoproctostomy for severe pancolitis should be included in a surveillance programme.Pathologist experienced in interpreting dysplasias is essential for such a programem. Optimal timingsare far from established. In many programmes colonoscopy every 2-3 years with annual sigmoidoscopyis recommended, others prefer annual colonoscopy. High grade dysplasia or any dysplasia associatedwith a lesion such as mass or stricture is a strong indication for colectomy and should be confirmed byrepeat biopsy20,21. A difficult area is follow-up of low grade dysplasia in flat mucosa20. It needsfrequent examination and aggressive treatment. A repeat procedure in the first 3-6 months is warrantedsince low grade dysplasias in flat mucosa may be accompanied by invasive carcinomas either at the siteor elsewhere in 10-15% of these individuals20. It is felt that wider awareness amongst doctors workingwith inflammatory bowel diseases would help to sort out some of these contentious issues.References 1. Bargen, J.A. Chronic uloeratiive colitis associated with malignant disease. Arch. Surg.,1928;17:5611-76.2. Bonnevie, 0., Binder, V., Anthomsen, P eta!. The prognosis of ulcerative colitis. Scand J.Gastroentecol., 1974;9:81-91.3. Edwards, FC. and Truelove, S.C. The comae and prognosis of ulcerative colitis. (Jut., 1964,2:15-22.4. Gsccnstthn,AJ., Sachsr, D.B., Smith, H. eta!. Cancerin universal and left sided ulcerative colitis;factors determining risk Gastroenterotogy, 1979;77:290-4.5. Collins, RH. Jr., Feldman, M., Fordiran, J.S. Colon cancer, dysplasia and surveillance in patientswithulcerative colitis: a critical review. N. Engl. J. Med., 1987;316:1654-8.6. Jafri, W. Management of inflammatory bowe disease. J. PaIc. Mccl Assoc., 1990;40: 162-1677. Parks, AC)., Nicholls, RI. and Belliveau, P. Proctocolectomy with ileal reservior and sisalsnastonsosis. Br. I. Surg., 1980;67:533-38.8. Qureshi, H., Zssbeti, S.J., Banatwala, N., et al. Ulcerative colitis in Karachi J. GastroenterolHepatot., 1989;4:313-1 6.9. Jafri, W. Inflammatory bowel disease: an important cause of rectal bleeding - a review of 100 rectalbleeders. Gut., 1989;30:1466(Abs).10. Slancy, G. andBrooke, B.N. Cancerinulcerarivecolitis. Lancet, 1959;2:694-698.11. Sales, D.J. The prognosis of inflammatory bowel disease. Arch Intern Med., 1983;143:294.12. Ekbon, A, Helmick, C., Zsck. M., et aL Ulcerative colitis and colorectal cancer A population basedstudy. N. Eng. J. Med., 1990,223:1288-33.13. Gilat, T., Fireman, Z., Grossman, A eta!. Colorectal cancer in patients with ulcerative colitis: apopulation study in central Israel. Gastroenterology, 1988;94:870-77.14. Gyde, SN., Psior P., Allan, RN. eta!. Colorectal cancer inulcerative colitis: a cohost studyofprisnaryretënsla fromthreecentres. Gut, 1988,29:206.17.15. Winawer, Si., Enker, WE., Lightdale, C.J. Malignant Turnouts of the colon and rectum. In Bockus.Gastroenterology edited by JE Berk. Philadelphia W.B. Saunders, 1985.16. Rule A.H., Reilly, CO., Sacher, D.B. eta!. Circulating carcinoembryonic antigen (CEA).relationship to clinical status in patients with inflammatory bowel disease. GUT, 1973;14:880-84.17. Frank, R., Riddel, R, Feczko, P. et a!. Radiological detection of colonic dysplasia (pre-carcinorna)in chronic ulcerative colitis. Gsstrointest. Radiol., 1978;3:20918. Hulten, L., Keswener, J. and Ahern, C. Pre cancer and csrcinomainchronic ulcerative colitis: ahistopathological and clinical investigation. Scand J. Clsstroenterol., 1972;7:663-64.19. Waye, ID. Colitis, cancer and colonoscopy. Med. Chin. North Am., 1978;62:211-24.20. Dobbins, WO. III. Ctsnentststus of the pre cancer lesioninulcerative colitis. Gastroenterology,1977;73: 1431-33.21. Riddel, R Dysplasia in inflammatory bowel disease: Standardized classification with provisionalclinical application. Hum Pathol., 1983;14:931.22. Sheikh, H., Husaainy, A. and Jafri, W. Ulcerativecolitis: a histopathological etudycomparingWestem and Pakistani idiopathic ulcerative colitis. Pak. I. Pathol., 1991:2:23-28.23. Lenmard Jones, J., ED. Ritchie, 3K., Moraon, Beta!. Cancersurveillanceinulcerative colitis. Lancet,1983,2:149-53.

Dysplasia and surveillance in ulcerative colitis

https://ecommons.aku.edu/cgi/viewcontent.cgi?article=1174&amp;context=pakistan_fhs_mc_med_gastroenterol

Dysplasia and surveillance in ulcerative colitis

Abstract

Similar works

Full text

Available Versions

eCommons@AKU