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Ulcerative Colitis

Q: How do macroscopic colonic lesions in UC differ from Crohn disease?

Pattern of involvement — In ulcerative colitis, involvement is continuous, whereas in Crohn disease, lesions may be segmental (skip lesions).Rectal involvement — In ulcerative colitis, the rectum is involved in 100% of cases; in Crohn disease, rectal sparing is common.Ulcer morphology — Ulcerative colitis features broad-based shallow ulcers without deep fissures, whereas Crohn disease produces deep, slit-like ulcers creating a "cobblestone" mucosal relief.Serosa — In ulcerative colitis, the serosa is unaffected; in Crohn disease, serositis and adhesions are observed.Fistulas — In ulcerative colitis, fistulas are absent; in Crohn disease, enterocutaneous or enteroenteric fistulas occur in up to 10% of cases.Malignancy — In ulcerative colitis, malignant transformation is common in long-standing disease; in Crohn disease, it is less frequent.

Colitis ulcerosa

For medical students2 min readUpdated 2026-10-10

Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease of unclear etiology. The pathological process always originates in the rectum and involves exclusively the mucosa, leading to ulceration and inflammatory polyps.

Depth of involvementMucosa only. Infiltration extends into the muscular layer only at the base of large ulcers.

LocalizationThe rectum is always involved, with the process extending proximally.

GeneticsAssociated with polymorphisms of the CARD15 gene on chromosome 16.

ComplicationsHigh risk of colorectal carcinoma when disease duration exceeds 10 years.

Etiology and Immunological Cascade

The disease has a significant global prevalence. The development of chronic inflammation involves three main factors: bacterial antigens (including normal microbiota), specific immune response features, and genetics (CARD15 gene, which controls pro-inflammatory cytokine synthesis).

Pathogenetic Mechanism:

Bacterial antigens penetrate the lamina propria of the mucosa.
Following antigen presentation, interleukin-23 (IL-23) plays a pivotal role, interacting with naive T lymphocytes to differentiate them into Th17 cells.
Th17 cells produce IL-17, which mediates chronicity of inflammation and autoimmune reactions.
Chemoattractant cytokines recruit neutrophils and eosinophils. Leukocyte enzyme systems exert pronounced cytotoxic effects, destroying tissue.

Pathological Anatomy (Morphology)

Macroscopically, inflammation is restricted to the mucosa. The small intestine remains intact (rare exceptions include involvement near the ileocecal valve, termed retrograde ileitis).

Early stages: The mucosa is hyperemic and edematous, with flattened folds. Numerous erosions and small ulcers create a "moth-eaten" appearance.
Late stages: Large ulcers (1–1.5 cm deep) with undermined edges and a fibrinous base form along the lines of the taeniae coli. At the margins of the ulcers, regenerating stroma forms papillary projections—inflammatory polyps up to 1 cm in size. These become covered by columnar epithelium lacking goblet cells and persist even after the mucosal defect heals. Because the lesions are superficial, intestinal strictures do not form as a sequela.

Microscopic Findings: Neutrophils accumulate within 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 nearly disappear, and Paneth cell metaplasia occurs. Inflammatory infiltrates (lymphocytes, plasma cells) penetrate the muscular layer only in the floors of deep ulcers. The presence of eosinophils serves as a marker of high activity.

Clinical Forms and Complications

Clinical courses include acute typical (debut with purulent-hemorrhagic inflammation), chronic relapsing (seasonal flares), chronic continuous (>6 months), and fulminant forms.

Fulminant colitis leads to total involvement and toxic dilation (toxic megacolon). Due to epithelial destruction, bacterial toxins penetrate the bloodstream and bowel wall, damaging intramural ganglia. This causes loss of tone, marked colonic distension, and a high risk of perforation and peritonitis.

Long-standing chronic disease carries a risk of malignant transformation. The accumulation of mutations via epithelial dysplasia/neoplasia leads to colorectal carcinoma. High-risk factors include total colonic involvement, disease duration over 10 years, and onset before age 18. Metabolic complications (secondary to malabsorption) include urolithiasis, cholelithiasis, and anemia. Amyloidosis is a rare complication.

Extraintestinal Manifestations

Systemic manifestations often develop concurrently with the primary intestinal disease. UC may be accompanied by:

Musculoskeletal disorders: Arthritis of large and small joints (non-deforming), ankylosing spondylitis (which may precede 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 and steatohepatitis (secondary to malabsorption and drug toxicity), which may progress to cirrhosis.

Mnemonic

To remember the macroscopic features of ulcerative colitis, use the rule of three "C's": restricted to the Continuous mucosa (always starting from the rectum upwards), Continuous inflammation, and Cno strictures (since ulcers are superficial).

Frequently asked questions

How do macroscopic colonic lesions in UC differ from Crohn disease?

Pattern of involvement — In ulcerative colitis, involvement is continuous, whereas in Crohn disease, lesions may be segmental (skip lesions).
Rectal involvement — In ulcerative colitis, the rectum is involved in 100% of cases; in Crohn disease, rectal sparing is common.
Ulcer morphology — Ulcerative colitis features broad-based shallow ulcers without deep fissures, whereas Crohn disease produces deep, slit-like ulcers creating a "cobblestone" mucosal relief.
Serosa — In ulcerative colitis, the serosa is unaffected; in Crohn disease, serositis and adhesions are observed.
Fistulas — In ulcerative colitis, fistulas are absent; in Crohn disease, enterocutaneous or enteroenteric fistulas occur in up to 10% of cases.
Malignancy — In ulcerative colitis, malignant transformation is common in long-standing disease; in Crohn disease, it is less frequent.

How does the depth of tissue involvement in UC differ from other inflammatory bowel diseases?

In UC, inflammation is strictly limited to the mucosa. Infiltration extends into the muscular layer exclusively at the base of large ulcerated defects.

What is a crypt abscess, and is it strictly specific to UC?

It is an accumulation of leukocytes within the lumens of intestinal crypts leading to their destruction. It is a striking finding, but not pathognomonic, as it also occurs in other forms of colitis.

Why does toxic megacolon occur in the fulminant form of UC?

Due to epithelial destruction, toxins penetrate the bowel wall, and inflammation extends to the muscular layer, damaging nerve plexuses. This results in a loss of tone and marked dilation of the colon.

Which cells serve as a marker of high inflammatory activity in UC?

The presence of eosinophils (along with neutrophils) in the inflammatory infiltrate of the lamina propria is considered a marker of high disease activity.

Go deeper

Differential diagnosis between ulcerative colitis and Crohn disease (granulomatous inflammation, transmural involvement).
Mechanisms of malabsorption syndrome and metabolic complications (urolithiasis, cholelithiasis).
Specific infectious colitides (shigellosis, campylobacteriosis, pseudomembranous colitis).
Morphological criteria for epithelial dysplasia and neoplasia in long-standing ulcerative colitis.