- Clinical science
Ulcerative colitis (UC) is an inflammatory bowel disease (IBD) characterized by chronic mucosal inflammation of the colon and cecum. Common symptoms include bloody diarrhea, abdominal pain, and fever. Laboratory findings typically show elevated inflammatory markers and the presence of autoantibodies (pANCA). Definitive diagnosis requires biopsies showing abnormal colonic mucosa and characteristic histopathology. Aminosalicylic acid derivatives are the mainstay of treatment, although severe episodes typically require corticosteroids and immunosuppressants to achieve remission. In the case of distal colitis, some drugs may be administered topically (e.g., via enema), whereas more proximal inflammation requires systemic treatment. Proctocolectomy is curative and indicated for complicated UC or dysplasia. Individuals with UC are predisposed to colorectal cancer and should thus undergo regular surveillance colonoscopy.
- Approx. 600,000 adults in the U.S. are affected by UC 
- Higher in the white than in the black, Hispanic, or Asian populations
- Highest among individuals of Ashkenazi Jewish descent.
- Slightly higher in men than women 
- 15–35 years 
- Another smaller peak may be observed in individuals > 55 years 
Epidemiological data refers to the US, unless otherwise specified.
|Bowel movements/day||< 4||4–6||> 6|
|Blood in stools||Intermittent||Frequent||Continuous|
|Temperature||< 37.5°C (99.5°F)||≤ 37.8°C (99.68°F)||> 37.8°C (100.4°F)|
|Heart rate||< 90/min||≤ 90/min||> 90/min|
|Hemoglobin||> 11.5 g/dL||≥ 10.5 g/dL||< 10.5 g/dL|
|ESR||< 20 mm/h||≤ 30 mm/h||> 30 mm/h|
The exact mechanism is unknown but studies suggest that ulcerative colitis is the result of abnormal interactions between host immune cells and commensal bacteria. 
- Dysregulation of intestinal epithelium: increased permeability for luminal bacteria → activation of macrophages and dendritic cells → antigen presentation to macrophages and naive CD4+ cells leads to
- Dysregulation of the immune system: upregulation of lymphatic cell activity in bowel walls (T cells, B cells, plasma cells) → enhanced immune reaction and cytotoxic effect on colonic epithelium → inflammation with local tissue damage (ulcerations, erosions, necrosis) in the submucosa and mucosa
Pattern of involvement
- Ascending inflammation beginning in the rectum and spreading continuously proximally throughout the colon
- Mucosal and submucosal inflammation
The rectum is always involved in UC!
Risk factors 
- Genetic predisposition (e.g., )
- Ethnicity (white populations, individuals of Ashkenazi Jewish descent)
- Family history of inflammatory bowel disease
- Episodes of previous intestinal infection
- Increased fat intake (esp. saturated fat and animal fat)
- Oral contraceptive intake
- NSAIDs may exacerbate UC
Protective factors 
- Smoking has a protective effect
- Skeletal: (most common extraintestinal manifestation of ulcerative colitis): sacroiliitis, , 
- Ocular: ; , episcleritis, iritis
- Biliary: primary sclerosing cholangitis ( )
- Cutaneous: aphthous stomatitis,, ,
- General: fatigue, fever
- In children/adolescents: growth retardation and delayed puberty
- ↑ ESR, ↑ CRP, leukocytosis
- Thrombocytosis in some cases
- ↑ Perinuclear ANCA (pANCA)
- In case of concurrent gamma-glutamyl transferase: elevated
- Test for bacteria to rule out infectious causes. 
- Calprotectin and lactoferrin are indicators of mucosal inflammation.
Endoscopy (e.g., colonoscopy) with histological examination is considered the best test to definitively diagnose UC.
- Typical findings: see “Gross pathology” below
Pattern of disease involvement 
- Proctosigmoiditis: limited to the rectum, with possible sigmoid involvement
- Left-sided colitis: extends distally to the splenic flexure
- Extensive colitis: extends beyond the splenic flexure
- Recommendations 
Observe caution in taking biopsies from patients with severe disease, as the risk of perforation is high.
Imaging studies may serve as useful adjunct diagnostic procedures for UC, particularly when it comes to detecting complications.
- Typically normal in mild to moderate disease
- Loss of colonic haustra (“lead pipe” appearance) may be seen in severe cases
- Massive distention in cases of toxic megacolon
- Pneumoperitoneum in cases of perforation
Barium enema radiography
- Able to detect very early changes
- Granular appearance of the mucosa
- Deep ulcerations
- Loss of haustra
- Pseudopolyps that appear as filling defects
- Plain radiography
- CT: Detection of bowel wall thickening is possible in severe disease.
- MRI: can be helpful in assessing disease severity and extent of bowel wall involvement
- Ultrasound: can detect bowel wall thickening (manifests with absent hyperechoic reflection from the lumen)
- Early stages
- Loss of mucosal folds
- Loss of haustra
- Raised areas of normal mucosal tissue that result from repeated cycles of ulceration and healing
- Ulceration → formation of granulation tissue → deposition of granulation tissue → epithelization
- Morphologically resemble polyps but do not undergo neoplastic transformation
- Found in advanced disease
In ulcerative colitis, the extent of intestinal inflammation is limited to the mucosa and submucosa. In contrast, Crohn disease shows a transmural pattern of intestinal involvement.
- Early stages
- Chronic disease
Noncaseating granulomas are seen in Crohn disease but are not a feature of ulcerative colitis!
Initially, UC is treated conservatively with drugs to induce and maintain disease remission. Curative proctocolectomy is generally indicated if medical therapy fails or complications arise.
- Supplementation of nutritional deficiencies (e.g., iron)
- Supplementation of nutrition: severe cases may warrant consideration of a feeding tube or parenteral nutrition.
Medical therapy 
- Antidiarrheal agents (e.g., loperamide)
- Anticholinergic medication (e.g., propantheline, dicyclomine): relieves abdominal cramping
- NSAIDs, opioids, and anticholinergics should be avoided in severe disease.
Recommended medical therapy by the severity of disease 
- 5-aminosalicylic acid derivatives (5-ASAs)
- If no improvement or 5-ASA agents are not tolerated
- Oral and topical 5-ASAs
- Topical corticosteroids (e.g., budesonide) → systemic corticosteroids only if no response
- Anti-TNF therapy; (adalimumab, golimumab, or infliximab)
Severe or refractory disease
- High‑dose oral and topical 5-ASAs
- Systemic corticosteroids
- Anti-TNF therapy; (e.g., adalimumab, golimumab, or infliximab)
- Calcineurin antagonists (e.g., cyclosporine, tacrolimus)
- Thiopurines (e.g., azathioprine) may be considered but are no longer recommended as monotherapy due to lack of efficacy 
- Referral for surgical proctocolectomy (see below)
Systemic corticosteroids should only be used for the treatment of an active flare and are not recommended as a maintenance medication for ulcerative colitis!
- Procedure: proctocolectomy with an ileal pouch-anal anastomosis (IPAA or J pouch)
In contrast to Crohn disease, ulcerative colitis can be cured surgically (proctocolectomy)!
- (both acute and chronic)
- Perforation → peritonitis
- Fulminant colitis
↑ Risk of cancer (see
- Risk increases with increased duration and/or extent of disease
- Risk is not significantly increased in patients with mild UC
- Prevention: Screening colonoscopy with biopsies every 1–3 years starting 8 years after the initial diagnosis to screen for colorectal cancer 
We list the most important complications. The selection is not exhaustive.
On average, the life expectancy of patients with UC is normal.