Ulcerative colitis (Colitis ulcerosa, UC) is a form of inflammatory bowel disease (IBD). Ulcerative colitis is a form of colitis, a disease of the intestine, specifically the large intestine or colon, that includes characteristic ulcers, or open sores, in the colon with rising incidence worldwide, including in the US where prevalence is about 1.253 million people.. The main symptom of active disease is usually diarrhea mixed with blood, of gradual onset. Ulcerative colitis is, however, a systemic disease that affects many parts of the body outside the intestine. Because of the name, IBD is often confused with irritable bowel syndrome (“IBS”), a troublesome, but much less serious condition. Ulcerative colitis has similarities to Crohn’s disease, another form of IBD. Ulcerative colitis is an elapsing and remitting condition, with symptoms such as rectal bleeding, urgency, and tenesmus.

Ulcerative colitis (UC) moved from isolated 19th-century case reports to one of the two defined forms of inflammatory bowel disease (IBD) over roughly 150 years.^[1] Samuel Wilks reported the first case of non-infectious colitis in 1859. Most historical reviews credit William Hale White’s 1888 case series with establishing the term ulcerative colitis.^[1][2] Before the 1932 description of regional ileitis by Crohn, Ginzburg, and Oppenheimer, colonic Crohn’s disease and UC were often confused with each other. This means 19th-century physicians could not have distinguished UC from Crohn’s disease.^[1][3] Corticosteroids, introduced in the mid-1950s, sharply reduced the historically high mortality of severe UC. Anti-TNF therapy, starting in 2005, opened the era of biologic and small-molecule therapy.^[4][2]

Ulcerative colitis (UC) is classified along two complementary axes that together drive treatment selection: anatomic extent, described by the Montreal classification as proctitis (E1), left-sided colitis (E2), or extensive colitis (E3), and disease activity/severity.^[5][6] Current definitions of severity integrate patient-reported outcomes, endoscopic scores (Mayo Endoscopic Score or UCEIS), biomarkers, disease course, and disease impact, rather than symptoms alone.^[5] Validated indices include the Truelove and Witts criteria, the Mayo Score and its modified versions, and endoscopic indices. In clinical practice, patients are grouped into three treatment-relevant tiers: mild to moderate, moderate to severe, and acute severe ulcerative colitis (ASUC). ASUC has replaced the older term “fulminant colitis”.^[6][7]

Ulcerative colitis (UC) arises from a gene–environment interaction. In a genetically susceptible host, environmental exposures lead to a defective epithelial barrier, gut microbial dysbiosis, and a dysregulated mucosal immune response. Together these start and sustain continuous mucosal inflammation of the colon.^[6][8] There is no single causative agent. Genetics, barrier failure, dysbiosis, and immune dysregulation each contribute, but none is sufficient on its own.^[9] The adaptive immune response in UC is classically an atypical Th2 response driven by NKT cells through IL-13. This contrasts with the Th1 pattern of Crohn’s disease, and both diseases share a Th17/IL-23 axis.^[10][11] Each mechanistic node maps to an approved drug class: anti-TNF, anti-integrin, anti-IL-12/23 or IL-23, JAK inhibitors, and sphingosine-1-phosphate (S1P) receptor modulators. This mapping is the main clinical value of understanding UC pathogenesis.^[6]

No single cause of ulcerative colitis (UC) has been identified. The current model is that UC results from a dysregulated innate and adaptive mucosal immune response against the commensal gut microbiota. This response occurs in genetically susceptible individuals and is triggered or shaped by environmental exposures and a defective epithelial barrier.^[8][6][12] Genetic risk is polygenic and explains only a small fraction of disease variance. Family history is the strongest individual risk factor. Environmental associations include an inverse association with current smoking and appendectomy, and positive associations with former smoking, enteric infection, antibiotic exposure, and Westernized diet. Dysbiosis is consistently present, but it is both a cause and a consequence of inflammation.

Ulcerative colitis should be differentiated from other causes of diarrhea. It is very important to differentiate it from Crohn’s disease as the management of both conditions is different though the initial presentation may be confused for any of these disorders.^[13][14]

Ulcerative colitis (UC) is most common in early-industrialized regions such as North America, Northern and Western Europe, and Oceania. In these regions incidence has stabilized or declined since 1990, while prevalence continues to rise.^[15][1] Incidence is now rising rapidly in newly industrialized countries of Asia, Latin America, and the Middle East. UC therefore can no longer be regarded as a disease confined to Western populations.^[16] In the United States, UC prevalence is approximately 378 per 100,000 population, or about 1.25 million people.^[17] UC is most often diagnosed in the second to fourth decades of life, but elderly-onset disease accounts for a growing share of new diagnoses. There is no consistent sex predominance.^[8]

Ulcerative colitis (UC) develops from the interaction of genetic susceptibility, environmental exposures, gut dysbiosis, and dysregulated mucosal immunity; no single risk factor is necessary or sufficient.^[18][9] A family history of inflammatory bowel disease (IBD) is the strongest known risk factor, conferring roughly 4–10 times the background risk in first-degree relatives.^[19][20] UC risk is characteristically increased in former smokers and reduced in current smokers and after appendectomy for appendicitis in early life, the inverse of the pattern seen in Crohn’s disease.^[10][4] Most environmental associations derive from observational, largely retrospective data subject to recall bias and reverse causation, and should be interpreted as risk markers rather than proven causal or modifiable targets.^[21]

Patients with ulcerative colitis (UC) extending beyond the rectum have an increased risk of colitis-associated colorectal cancer (CRC), driven mainly by disease duration, extent, and cumulative inflammation, with the highest risk in patients with concomitant primary sclerosing cholangitis (PSC). Contemporary population-based data show a relative risk of approximately 1.4–1.7 compared with the general population, substantially lower than historical estimates but still above the threshold at which colonoscopic surveillance is recommended.^[22][23] All major societies recommend an index (baseline) colonoscopy approximately 8 years after symptom onset to re-stage disease extent and stratify risk, with immediate and annual surveillance for patients with PSC.^[22][24][25] Subsequent surveillance intervals (1, 3, or up to 5–10 years) are individualized according to inflammatory activity, extent, PSC, prior dysplasia, strictures, post-inflammatory polyps, and family history of CRC. Surveillance should be performed in remission, with high-definition colonoscopy, preferably with dye-based chromoendoscopy, by endoscopists trained in IBD surveillance. Random biopsies are now reserved for high-risk patients or for white-light-only examinations. Proctitis alone does not warrant IBD-specific surveillance.^[22]

Ulcerative colitis (UC) is a lifelong relapsing–remitting disease with no reliable medical cure; proctocolectomy is the only definitive cure.^[26] In population-based cohorts, the cumulative risk of relapse is approximately 70–80% at 10 years, about 10–15% of patients follow an aggressive course, nearly half require at least one UC-related hospitalization, and the 5- and 10-year cumulative risk of colectomy is approximately 10–15%.^[27] Major complications include acute severe ulcerative colitis with toxic megacolon, perforation or massive hemorrhage, venous thromboembolism, extraintestinal manifestations, and colitis-associated colorectal cancer (CRC).^[3] Contemporary CRC risk is substantially lower than historical referral-center estimates, and surveillance colonoscopy is risk-stratified, beginning 8 years after symptom onset or at diagnosis of primary sclerosing cholangitis (PSC).^[6][24] Large nationwide cohorts show a modest excess all-cause mortality (adjusted HR ~1.4 in Sweden), although relative mortality has declined over time.^[28]

Patients with ulcerative colitis present with a history of bloody diarrhea mixed with mucus, of gradual onset. Some patients may present with a sudden attack of diarrhea, fever and abdominal pain. The extra intestinal symptoms may include joint swelling and pain, inflammation of the eye and skin involvement.^[29]

Ulcerative colitis shows intestinal and extra intestinal findings on physical examination. These include abdominal tenderness, fever, pallor, inflammation of the iris and uvea, skin rash, inflammation of the joints, aphthous ulcers and clubbing of the fingers.^[29][30]

The laboratory findings in a patient with ulcerative colitis include anemia, low albumin, elevated ESR, elevated serum alkaline phosphatase, deranged LFTs and electrolyte abnormalities.^[31][32]

Xray of the abdomen is not required for the diagnosis of ulcerative colitis. Xray may sometimes be one in case colitis is suspected. Xray is normal in mild to moderate disease and can show dilation and/or “thumb printing sign” in fulminant cases.^[33]

CT scan can b helpful in the diagnosis of severe ulcerative colitis and in differentiating ulcerative colitis from Crohn’s disease. Initial changes in the mucosa may not be detected by a CT scan.^[33]

MRI can b helpful in the diagnosis of severe ulcerative colitis and in differentiating ulcerative colitis from Crohn’s disease. Initial changes in the mucosa may not be detected by a CT scan.^[33][34]

Other imaging findings for ulcerative colitis can be seen by the help of barium enema. Barium enema may show micro ulcerations. barium enema must be avoided in severe cases as it can lead to the manifestation of toxic megacolon.^[34]

Other diagnostic studies like upper endoscopy, colonoscopy, tissue biopsy and histological analysis can help with the diagnosis of ulcerative colitis.^[35][30]

Medical therapy of ulcerative colitis (UC) follows a two-phase paradigm: induction of remission followed by maintenance of remission. The agent and route are selected according to disease extent (proctitis, left-sided colitis, or extensive colitis) and disease activity (mild-to-moderate, moderate-to-severe, or acute severe).^[5] The current treatment target is corticosteroid-free remission with endoscopic (mucosal) healing rather than symptom control alone.^[6][8] 5-aminosalicylic acid (5-ASA) is first-line for mild-to-moderate disease. Moderate-to-severe disease is managed with early initiation of an advanced therapy (biologic or oral small molecule), with corticosteroids used only as a short-term bridge.^[5][36] Acute severe UC requires hospitalization, intravenous corticosteroids, and an early decision about rescue therapy or colectomy.^[37]

Because ulcerative colitis (UC) is confined to the colon and rectum, proctocolectomy removes the target organ and cures the intestinal disease.^[38]

Indications for surgery fall into three tiers: emergent, urgent, and elective. Emergent indications are perforation, uncontrolled hemorrhage, and refractory toxic megacolon. The main urgent indication is acute severe UC (ASUC) that fails intravenous corticosteroids or medical rescue therapy. Elective indications include medically refractory disease, intolerable drug toxicity, and dysplasia or colorectal cancer that cannot be managed endoscopically.^[5][39]

For most patients who want to avoid a permanent stoma, restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) is the procedure of choice. Total proctocolectomy with end ileostomy remains a curative alternative with equivalent quality of life.^[38] The most common long-term complication of IPAA is pouchitis, which is managed along a chronicity spectrum.^[40]

Limited evidence exists for the efficacy of alternative treatments for ulcerative colitis. Dietary modification, fish oil supplements, short chain fatty acid enema, herbal therapy, helminth therapy, probiotics, are the most common homepathic remedies used in ulcerative colitis. Data is lacking in regards to the efficacy of these therapies. Using these treatment modalities should not preclude physician-recommended, evidence-based interventions.

The cause of ulcerative colitis is unknown, therefore primary preventive strategies are also unknown. Nonsteroidal anti-inflammatory drugs (NSAIDs) may make symptoms worse.

Due to the risk of colon cancer associated with ulcerative colitis. screening with colonoscopy is recommended for secondary prevention of ulcerative colitis. Adherence to maintenance therapy is recommended for secondary prevention of acute exacerbation of colitis.