Etiology and immunological cascade
The disease has a high prevalence (116 per 100,000 population in the US, 20 per 100,000 in Russia). Three factors play a role in the development of chronic inflammation: bacterial antigens (including normal biocenosis), specific features of the immune response, and genetics (the CARD15 gene, which controls the synthesis of pro-inflammatory cytokines).
Pathism / Mechanism of development:
- Bacterial antigens penetrate the lamina propria of the mucosa.
- Following antigen presentation, interleukin-23 (IL-23) plays a key role. It interacts with naive T lymphocytes, converting them into Th17 cells.
- Th17 cells produce IL-17, which mediates the chronization of inflammation and autoimmune reactions.
- Cytokine chemoattractants attract neutrophils and eosinophils. The enzyme systems of these leukocytes exert a pronounced cytotoxic effect, destroying tissues.
Pathological anatomy (Morphology)
Macroscopically, inflammation is restricted to the mucosa. The small intestine is intact (a rare exception is the involvement of a segment near the ileocecal valve, the so-called retrograde ileitis).
- Early stages: the mucosa is hyperemic, edematous, and folds are flattened. Numerous erosions and small ulcers create a "moth-eaten" appearance of the tissue.
- Late stages: large ulcers (1–1.5 cm deep) with undermined edges and a fibrin coating on the base form along the taeniae coli. At the edges of the ulcers, the regenerating stroma forms papillary projections—inflammatory polyps up to 1 cm in size. They become covered with columnar epithelium lacking goblet cells and persist even after the defect heals. Due to the limited depth of involvement, intestinal strictures do not develop as an outcome.
Microscopic picture: Neutrophils accumulate in the crypt lumens (cryptitis), leading to the formation of crypt abscesses and crypt distortion. Typical epithelium is replaced by prismatic cells with basophilic cytoplasm, goblet cells almost disappear, and Paneth cell metaplasia appears. The inflammatory infiltrate (lymphocytes, plasma cells) penetrates the muscular layer only in the area of the ulcer bases. The presence of eosinophils is a marker of high activity.
Clinical forms and complications
Based on clinical course, acute typical (debuting with purulent-hemorrhagic inflammation), chronic relapsing (seasonal exacerbations), chronic continuous (more than 6 months), and fulminant forms are distinguished.
The fulminant form leads to total involvement and toxic dilatation (toxic megacolon). Due to epithelial death, bacterial toxins penetrate into the blood and bowel wall, damaging intramural ganglia. This causes a loss of tone, marked bowel distension, and a high risk of perforation and peritonitis.
A chronic course spanning many years carries the threat of malignant transformation. The accumulation of mutations via the stage of epithelial dysplasia/neoplasia leads to colorectal cancer. High-risk factors include total involvement, disease duration of more than 10 years, and onset before the age of 18. Metabolic complications (due to malabsorption) include urolithiasis, cholelithiasis, and anemia. Amyloidosis is a rare complication.
Extraintestinal manifestations
Systemic manifestations manifest concurrently with the underlying disease. UC may be accompanied by:
- Osteoarticular pathologies: arthritis of large and small joints (without deformities), ankylosing spondylitis (may occur long before intestinal symptoms).
- Skin and mucosal lesions: erythema nodosum, pyoderma gangrenosum, pustular dermatosis, eczema, aphthous stomatitis, and lip fissures.
- Ophthalmological conditions: uveitis, iridocyclitis, scleritis, and episcleritis.
- Hepatobiliary disorders: primary sclerosing cholangitis, as well as steatohepatitis (as a consequence of malabsorption and drug toxicity), which can lead to liver cirrhosis.
Briefly: answers to topical questions
How does the macroscopic appearance of colonic involvement in UC differ from Crohn's disease?
- Pattern of involvement — In ulcerative colitis, the involvement is continuous, whereas in Crohn's disease it can be discontinuous (segmental).
- Rectal involvement — In ulcerative colitis, the rectum is always involved in 100% of cases, compared to 50% of cases in Crohn's disease.
- Character of ulcers — In ulcerative colitis, large and small V-shaped ulcers form without slit-like forms, whereas in Crohn's disease ulcers are slit-like and form a "cobblestone" pattern.
- Serosa — In ulcerative colitis, the serosa is unchanged, whereas in Crohn's disease serositis and adhesions are observed.
- Fistulae — In ulcerative colitis, fistulae are absent, whereas in Crohn's disease intestinal or cutaneous fistulae occur in 10% of cases.
- Malignant transformation — In ulcerative colitis, malignant transformation is observed after a prolonged course, whereas in Crohn's disease it is rare.
To remember the macroscopy of ulcerative colitis, the rule of three “C”s helps: only the mucosa is involved (Confined to mucosa), the inflammation is Continuous (always ascending from the rectum upward), and strictures Cannot form (since the ulcers are superficial).
Class and exam questions
How does the depth of involvement in UC differ from other inflammatory bowel diseases?
In UC, inflammation is strictly limited to the mucosal layer. The infiltrate penetrates into the muscular layer exclusively in the area of the bases of large ulcer defects.
What is a crypt abscess and is it strictly specific for UC?
This is an accumulation of leukocytes in the lumen of intestinal crypts with their subsequent destruction. A striking feature, but not pathognomonic, as it is also found in other forms of colitis.
Why does toxic colonic dilatation occur in the fulminant form?
Due to epithelial destruction, toxins enter the bowel wall, inflammation reaches the muscular layer, and damages nerve plexuses. This leads to a loss of tone and marked dilatation of the bowel.
Which cells are a marker of high inflammatory activity in UC?
The presence of eosinophilic leukocytes (along with neutrophils) in the inflammatory infiltrate of the lamina propria of the mucosa is considered a marker of high process activity.
What else to study on this topic
- Differential diagnosis of UC and Crohn's disease (granulomatous inflammation, transmural involvement).
- Mechanisms of development of malabsorption syndrome and metabolic complications (urolithiasis, cholelithiasis).
- Specific infectious colitides (shigellosis, campylobacteriosis, pseudomembranous colitis).
- Morphological criteria of epithelial dysplasia and neoplasia in long-standing UC.
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