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Ulcerative colitis (UC)

  • Relapsing and remitting inflammatory bowel disease (IBD) of the colonic mucosa.
    • May just affect the rectum (proctitis); extend to involve part of the colon (left-sided colitis); or the entire colon (pancolitis)

Epidemiology

  • MC in developed countries – in Caucasians, Ashkenazi Jews
  • All ages susceptible but MC in pts <30yr
  • MC in non smokers

Etiology

  • Unknown – environmental and genetic components – HLA-B27 association
  • Family history of IBD is risk

Pathology

  • UC develops as a result of an environmental trigger in a genetically susceptible person
  • Starts in the rectum and spreads proximally – rectum is involved in all circumstances
  • UC is a diffuse inflam disease, primarily affecting the mucosa + submucosa
    • Only in severe cases are the deeper layers of the intestinal wall affected
  • Multiple minute ulcers
  • Chronic cases – inflammatory polyps (pseudopolyps)
  • Severe fulminant colitis – section of the colon (MC transverse colon) becomes acutely dilated with risk of perforation (toxic megacolon)
  • Histology – ↑inflam cells in lamina propria (TNF-a, IL-12, IL-18). Walls of the crypts are infiltrated by inflam cells (crypt abscess)
    • Depletion of goblet cell mucin. With time precancerous changes can develop

Clinical features

  • Episodic or chronic diarrhoea – with or without blood + mucus
  • Crampy abdominal discomfort
  • Relapsing and remitting course
  • Urgency/tenesmus
  • Systemic features – fever, malaise, anorexia, WL
  • Extra-intestinal signs
    • Clubbing, aphthous oral ulcers, erythema nodosum, pyoderma gangrenosum, conjunctivitis, arthritis
  • Emotional stress, infections, gastroenteritis, antibiotics, NSAIDs can provoke a relapse

Investigations

  • Blood – FBC, ESR, CRP, U+E, blood culture,
  • Stool – to exclude Campylobacter, C.difficile, Salmonella, Shigella, E.coli
    • Calprotectin – accurate marker for GIT inflammation

  • AXR – no faecal shadows, mucosal thickening, colonic dilation
  • Erect CXR – perforation
  • Barium enema – never perform during acute attacks
  • Colonoscopy shows disease extent and allows biopsy – look for inflammatory infiltrate, goblet cell depletion, glandular distortion, crypt abscesses
  • Backwash ileitis

Treatment

  • Sulfasalazine or mesalamine (5-ASA) – first line. [2-4g/day]
    • Remission induction. Inhibits PG E1+E2 to reduce inflam
  • Oral presnisolone – for refractory cases
    • [40mg daily, tapered by 5mg/week over an 8 week period]
  • Venous thrombus prophylaxis
    • Heparin [5K/12hrs]
    • Fondaparinux [2.5mg/day]
  • Severe cases
    • Thrombo prophylaxis, I.V hydration, nil-by-mouth, hydrocortisone [100mg/6hrs I.V]
    • Rescue therapy – infliximab, cyclosporin

Surgery – often curative (unlike CD),

  • Involves total colectomy with ileo-anal anastomosis and a pouch (acts as a reservoir for stool)
  • Indications for surgery
    • Severe, debilitating, refractive disease unresponsive to medical therapy
    • Toxic megacolon (risk of perforation), obstruction due to stricture, severe haemorrhage, perforation
    • Fulminant exacerbation that doesn’t respond to steroids
    • Evidence of increased risk of colon cancer
    • Growth failure or failure to thrive

Complications

  • Perforation and bleeding
  • Toxic megacolon
  • Venous thrombosis
  • Colonic cancer – risk is 15% with pancolitis for 20 years
  • Strictures – benign and malignant
  • Cholangiocarcinoma – half of all bile duct cancers assoc with UC

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