Ulcerative Colitis

Gastrointestinal

Description

Ulcerative colitis is a chronic, idiopathic inflammatory bowel disease in which immune-mediated injury produces continuous, superficial ulceration of the colonic mucosa beginning in the rectum and extending proximally in an unbroken pattern; it spares the small bowel except in rare back-wash ileitis. The disease follows a relapsing-remitting course marked by symptomatic flares and endoscopic healing phases, affects roughly 600 000–900 000 people in the United States, and—unlike Crohn’s disease—remains confined to the colon, making it both the prototypical cause of bloody diarrhea in young adults and a major driver of colitis-associated colorectal cancer.

Symptoms

Typical flares feature insidious onset of bloody or mucus-tinged diarrhea, nocturnal stools, urgency, tenesmus, and crampy left-lower-quadrant abdominal pain accompanied by low-grade fever, fatigue, and weight loss; severity correlates with disease extent. Extraintestinal manifestations—including peripheral arthritis, erythema nodosum, aphthous ulcers, episcleritis, and primary sclerosing cholangitis—reflect circulating immune complexes and may parallel or diverge from colonic activity.

Risk Factors

Disease incidence peaks between ages fifteen and thirty and again after age sixty, is higher in Ashkenazi Jewish and Northern European populations, and rises four-fold with a first-degree family history. Former—though not current—tobacco use, oral contraceptives, non-steroidal anti-inflammatory drugs, high intake of linoleic acid, and a history of respiratory or gastrointestinal infections modestly increase risk, whereas appendectomy before age twenty and active smoking are paradoxically protective. Co-existing immune-mediated conditions such as primary sclerosing cholangitis, psoriasis, or autoimmune thyroid disease often coexist and predict more extensive colitis.

Diagnosis

Colonoscopy with segmental biopsies is the gold standard, revealing diffuse, continuous erythema, loss of vascular pattern, friability, and superficial ulceration; histology shows crypt architectural distortion, basal plasmacytosis, and mucosal neutrophils. Baseline labs demonstrate anemia of chronic disease, hypoalbuminemia, C-reactive-protein elevation, and fecal calprotectin > 150 µg/g. Stool cultures, Clostridioides difficile toxin PCR, and ova-and-parasite evaluation exclude infection. MR enterography or CT enterography screens for proximal small-bowel involvement when indeterminate. Disease activity is graded endoscopically by the Mayo score, while the Truelove and Witts criteria stratify clinical severity in acute flares.

Treatment

Management follows a step-up algorithm tailored to severity and distribution. Mild to moderate proctitis or left-sided disease responds to rectal and oral 5-aminosalicylates (mesalamine ≥ 2 g/day) with topical corticosteroid foams as adjuncts. Moderate to extensive colitis unresponsive to 5-ASA requires a brief oral prednisone taper or budesonide MMX, after which steroid-sparing immunomodulators such as azathioprine or 6-mercaptopurine maintain remission. Biologic therapy—anti-TNF agents (infliximab, adalimumab, golimumab), anti-integrin vedolizumab, anti-IL-12/23 ustekinumab, or the IL-23-specific risankizumab—and small-molecule Janus-kinase inhibitors (tofacitinib, upadacitinib) or S1P modulator etrasimod treat moderate-to-severe refractory disease. Acute severe colitis mandates hospitalization, bowel rest, high-dose IV methylprednisolone, venous-thromboembolism prophylaxis, and rescue with infliximab or cyclosporine if no response within three days. Subtotal colectomy with ileal pouch–anal anastomosis cures colitis but carries risks of pouchitis and infertility.

Outlook

With contemporary 5-ASA and biologic strategies, one-year corticosteroid-free remission approaches 45 % and ten-year colectomy rates have fallen below 15 %. Nevertheless, chronic inflammation confers a cumulative colorectal-cancer risk of roughly 2 % at twenty years and 8 % at thirty years, highest in pancolitis, early-onset disease, or concomitant primary sclerosing cholangitis, necessitating surveillance colonoscopy every one to three years beginning eight years after diagnosis. Overall mortality mirrors the general population except in fulminant colitis or cancer, and quality-of-life studies show near-normal work productivity during remission.

Complications

Chronic uncontrolled inflammation predisposes to massive lower-gastrointestinal hemorrhage, toxic megacolon with perforation, stricture formation, colorectal adenocarcinoma, primary sclerosing cholangitis, cholangiocarcinoma, osteoporosis from corticosteroids, venous thromboembolism, growth failure in pediatric cases, and extraintestinal immune complications such as uveitis and axial spondyloarthritis.

Prevention

No intervention reliably prevents disease onset, yet maintaining a high-fiber, low saturated-fat diet, limiting antibiotic overuse, and preserving gut microbial diversity through breast-feeding and fermented foods are areas of active research. For those already diagnosed, chemoprevention with daily mesalamine appears to reduce colorectal-cancer risk, while scheduled colonoscopic surveillance with chromoendoscopy enables detection of dysplasia at a curable stage.

Support

Sustained remission depends on strict adherence to maintenance drugs, avoidance of NSAIDs and high-sugar diets, smoking cessation despite its protective epidemiology, age-appropriate immunizations, and scheduled surveillance colonoscopies. Patients benefit from individualized nutrition plans rich in calcium and vitamin D, stress-reduction techniques, regular aerobic exercise, and engagement with Crohn’s & Colitis Foundation support networks; caregivers can assist with medication reminders, symptom diaries, and recognizing early flare signals.