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Pathology of Ulcerative Colitis

A brief outline of some important features:

Dr Sampurna Roy MD

 

 

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Extent of the disease:

Ulcerative Colitis starts from the rectosigmoid area.

May remain localized to the rectum (ulcerative proctitis).

Spread  proximally, involving variable length of the colon.

May involve the entire colon - pancolitis.

Pancolitis usually stops abruptly at the ileocaecal valve.

Ileum is involved in almost one third of the cases - backwash ileitis (Superficial lesion ; in continuity with the colonic disease; usually limited to10 cm from the ileocaecal junction; accompanied by dilatation of the lumen ; in Crohn's disease there is stenosis)

Left sided involvement of the colon and involvement of the caecum (caecal patch) or appendix.

The affected sites are separated by normal mucosa.

Appendix involvement (20%-60% of cases) may occur in continuity with adjacent involved caecum or as a skip lesion.

Diffuse duodenitis and extensive involvement of the upper small bowel can occur rarely in severely ill patients.

Anal lesions (10% of cases)- In the anal canal there may be involvement of glandular epithelium and hyperplastic changes of the transitional mucosa.

Anal lesions include midline dorsal fissures, skin excoriations, acute perianal and ischiorectal abscesses or rectovaginal fistula.

Other manifestations:

Involvement of liver- Fatty infiltration, abscess, cirrhosis, sclerosing cholangitis, pericholangitis and biliary carcinoma.

Arthritis, uveitis, pyoderma gangrenosum & limited forms of Wegener's granulomatosis.

These lesions usually occur severe cases of Ulcerative Colitis with extensive colonic involvement.  

Late complications: Inflammation may extend towards the submucosa.

In such cases, the wall is thin and perforation can occur together with peritonitis and abscess.

In severe, active forms, the entire colon, or a segment, may become dilated (toxic megacolon).

Other complications include venous thrombosis (iliac vein) and carcinoma.   

 

  

Macroscopic features:

Gross appearance varies with the stage of the disease.

Inflammation and ulceration are usually limited to the mucosa ; involvement of deeper parts of bowel wall is seen in one-third of surgical resections and in toxic megacolon.

Serosal surface appears congested often to a larger extent than the mucosal lesions.

Acute form:

Mucosal surface is wet and glaring from blood and mucus with numerous petechial hemorrhages.

Ulcers are of different sizes and are small, round, superficial or of more irregular configuration.

Fissuring ulcers are usually not present , except in toxic megacolon.

Ulcers can become more extensive and undermine the mucosa so that mucosal bridges with an underlying inflammatory infiltrate develop.

Multiple confluent ulcers may cause denudation of the mucosa.

Elevated sessile reddish nodules (small and multiple) appear on the flat surface -pseudopolyps.

These may have a filiform configuration.  

Advanced stage:

Bowel becomes fibrotic, narrowed and shortened. Cicatrical stenosis associated with inflammatory mass may be mistaken for carcinoma.

Quiescent stage: 

 

Ulceration is absent ; mucosa is atrophic ( in some cases mucosa appear normal ) ; extensive submucosal fat deposition.

During remission, the mucosa may become normal again.

Healing often occurs in an irregular way leading to a discontinuous, heterogeneous mucosal lesion , which can be confused with CD. 

Treatment may increase the heterogeneous nature of the lesions.

In children, lesions may initially be heterogeneous.

Topical treatment of the rectum can induce complete rectal healing.

Ulcerative colitis with rectal sparing, although rare, must therefore not be confused with CD.

Note:  Pseudopolyps are common in the sigmoid and descending colon and rare in the  rectum. 

 

Microscopic features:

In ulcerative colitis the microscopic features are noted in the mucosa and submucosa.

Cellular infiltrate:

Increased intensity of the cellular infiltrate in the lamina propria with alterations of the composition.

Infiltrate is more extensive and extends diffusely towards the deeper part (transmucosal) - In normal lamina propria and infectious colitis infiltrate is located in the upper part of the mucosa.

Accumulation of plasma cells near the mucosal base, in-between the crypt base and the muscularis mucosae (basal plasmacytosis).

Starts as focal and later develops into diffuse plasmacytosis.

Presence of neutrophils together with unequivocal epithelial cell damage indicates disease activity.

Neutrophils within epithelial structures, such as the crypt wall (cryptitis), or the crypt lumen and wall (crypt abscesses) or in association with crypt damage (crypt destruction) are helpful for the diagnosis. Cryptitis and crypt abscesses can also be seen in infectious colitis, Crohn's colitis and diversion colitis.

Eosinophils may be numerous- in chronic disease or when the disease is quiescent. (may also suggest eosinophilic colitis).   

Structural changes:

An irregular surface or a villiform surface and a disturbed crypt architecture. Low power examination is important (may be seen after surgery, in drug-induced lesions and chronic infectious colitis such as chronic Shigella dysentery.)

Mucosal atrophy characterized by a combination of crypt drop-out and shortening of crypts.

Other features:

Mucosal ulcerations and erosions, mucin depletion, Paneth-cell metaplasia and diffuse thickening of the muscularis mucosae.

Paneth cells in crypts distal to the ascending colon suggest IBD, usually UC.
Mast cells may accumulate at the line of demarcation between normal and abnormal mucosa.
Granulomas are not present in UC but isolated giant cells or a histiocytic reaction around a ruptured crypt may be seen - ('Cryptolytic lesions' or pericryptal granulomas)   

UC is also characterized by a special distribution of inflammation and architectural distortion with increasing intensity from the proximal towards the distal colon.

For proper assessment of this feature, examination of multiple biopsies obtained in different segments is needed.

Activity of the disease:

Histology is an important tool for measurement of disease activity.

Active disease is defined by the presence of neutrophils in association with epithelial cell damage.

Inactive chronic disease is defined as the presence of architectural changes and an increase of lamina propria mononuclear cells.

Quiescent disease means the presence of structural changes without alterations in intensity and composition of the lamina propria infiltrate.

(In inactive and quiescent disease there is presence or persistence of severe crypt architectural abnormalities - branching and irregular glands rather than parallel evenly spaced glands, while mucin secretion returns to normal.)

In a more chronic stage lymphoid aggregates and follicles, mainly situated in the deeper part of the mucosa, will develop or increase in number.

Activity scores may be used to either document disease evolution, or to assess clinical efficacy in therapeutic trials.

Persistent active inflammation and basal plasmacytosis are associated with an increased frequency of relapse.

In fulminant disease, mucosal inflammation may extend towards the submucosa and focally even towards the muscularis propria.

A significant association between disease activity and numbers of immunoglobulin-containing cells in the lamina propria has been demonstrated.

  

 

Summary of Microscopic features suggestive for a diagnosis of ulcerative colitis:

Architecture:
Severe crypt architectural distortion
Severe widespread decreased crypt density
Frankly villous surface

Inflammatory:
Heavy diffuse transmucosal lamina propria cell increase
Diffuse basal plasmacytosis

Miscellaneous:
Increased intensity of the alterations towards the distal colon
Severe mucin depletion
Paneth-cell metaplasia distal to the hepatic flexure

 

 

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Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)


 

 

 

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