• The dysplastic cells have crowded enlarged hyperchromatic nuclei

• There is loss of function evidenced by decreased mucin production

• The marked architectural disarray with prominent palisading of nuclei is the basis for classifying this as severe dysplasia

•Unknown

•The prominence of both humoral and cellular immune activity has suggested an immunologic basis for the disease but to what degree this is an epiphenomenon is unknown

•A disease of young adults with peak incidence 25-30 years

•Higher incidence in the U.S., England, and northern Europe

•Women>men, Jews>non-Jews, white>black

•An increased familial incidence exists and twin studies support a slight genetic basis

•The major symptoms of ulcerative colitis are bloody diarrhea often with mucous. Vague abdominal pain may be present but is not the most prominent symptom

•Most patients have intermittent acute attacks of variable intensity but are able to be fully functional between attacks

•Severe acute explosive episodes occur in a minority of patients and may require colectomy

•The development of dysplasia with its attendant risk for development of carcinoma occurs most frequently in patients with extensive disease which is defined as involvement proximal to the mid transverse colon

•Extraintestinal manifestations may include skin (erythema nodosum), joints (acute arthropathy), Mouth (aphthous ulcers) and liver

•Ulcerative colitis is a disease of the rectum spreading proximally in continuous fashion with involvement of the terminal ileum in about 10% of cases

•The disease is limited to the rectum and rectosigmoid in 40-50% of cases with only 20% of cases involving the entire colon

•Mild cases may show only erythema, with increasing activity evidenced by edema, mucosal granularity, friability, bleeding and ulceration

•The ulcers are broad based and may show extensive denuding of the mucosa in some cases

•Extensive ulceration may leave projecting islands of regenerating inflamed mucosa which form "pseudopolyps"

•The affected mucosa is involved continuously without skip areas of normal mucosa as is seen in Crohn^s Disease

•Ulcerative colitis involves the mucosa and submucosa almost exclusively so that thickening of the bowel wall is not seen, and in severe cases with toxic dilatation, significant thinning may occur

•During periods of inactivity the colon may appear relatively normal

•Microscopic findings are limited almost exclusively to the mucosa without areas of normal mucosa in the segments affected

•A diffuse infiltrate of lymphocytes, plasma cells and histiocytes is present in the lamina propria

•The hallmark of active disease is a neutrophilic infiltrate in the lamina propria, walls of crypts (cryptitis) and crypt lumen (crypt abscesses)

•Crypt abscesses are accompanied by mucin depletion, and degeneration of the crypt epithelium

•The mucosa shows intense vascular engorgement and in more active cases mucosal ulceration

•Involvement of crypts leads to distortion of crypt architecture with loss of crypts, irregular crypt shape and regenerative changes such as abnormal branching of crypts. These features can be seen in periods of inactive disease

•Progressively with time and extent of disease, microscopic evidence of dysplasia can be seen

•The onset of definite dysplasia is associated with a progressive incidence over time of invasive carcinoma

•The carcinoma associated with ulcerative colitis occurs in flat mucosa as opposed to the usual colorectal carcinoma which is a raised lesion

• Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 804-807

• Sleisenger MH, Fordtran JS. Gastrointestinal disease. 5th ed. Philadelphia: Saunders, 1993, pp. 1305-1330

• Current literature from PubMed at National Library of Medicine