Harvey's Garden

Ulcerative colitis

4 min read

Epidemiology

  • Higher in White populations than in Black, Hispanic, or Asian populations
  • Highest among individuals of Ashkenazi Jewish descent
  • 15–35 years of age

Tip

Compared with Crohn disease, which is bimodal distribution with one peak at 15–35 years and another one at 55–70 years

Etiology

  • Genetic predisposition (e.g., HLA-B27 association)
  • Ethnicity (White populations, individuals of Ashkenazi Jewish descent)
  • Protective factors: smoking
    • The pathophysiology is not fully understood, as smoking has negative effects on other inflammatory diseases (e.g., Crohn disease).

Pathophysiology

  • Dysregulation of intestinal epithelium: increased permeability for luminal bacteria → activation of macrophages and dendritic cells → antigen presentation to macrophages and naive CD4+ cells
  • Dysregulation of the immune system: upregulation of lymphatic cell activity (T cells, B cells, plasma cells) in bowel walls → enhanced immune reaction and cytotoxic effect on colonic epithelium → inflammation with local tissue damage (ulcerations, erosions, necrosis) in the submucosa and mucosa
    • Autoantibodies (pANCA) against cells of the intestinal epithelium
  • Pattern of involvement
    • Ascending inflammation that begins in the rectum and spreads continuously proximally throughout the colon
    • Inflammation is limited to the mucosa and submucosa.

Crohn disease is characterized by transmural inflammation.

Unlike ulcerative colitis,

Tip

The rectum is always involved in ulcerative colitis.

Clinical features

  • Intestinal symptoms
    • Bloody diarrhea with mucus
    • Fecal urgency
    • Abdominal pain and cramps
    • Tenesmus
  • Extraintestinal symptoms of ulcerative colitis

Tip

PSC is often associated with inflammatory bowel disease, especially ulcerative colitis. However, only approximately 4% of patients with inflammatory bowel disease develop PSC.

Diagnostics

Ileocolonoscopy

Recommended method for diagnosis and disease monitoring

Early stages

  • Inflamed, erythematous, edematous mucosa
  • Friable mucosa with bleeding on contact with endoscope A fibrin-covered ulceration (blue overlay) and several pseudopolyps (indicated by dashed lines) are visible.
  • Fibrin-covered ulcers

Chronic disease

  • Loss of haustra
  • Pseudopolyps
    • Raised areas of normal mucosal tissue that result from repeated cycles of ulceration and healing
    • Ulceration → formation of granulation tissue → deposition of granulation tissue → epithelialization

Treatment

Ulcerative Colitis (UC) Treatment

  • Goal: Induce and maintain remission; surgery (proctocolectomy) is curative.
  • Mild-to-Moderate Colitis:
    • Induction/Maintenance: 5-ASA (Mesalamine) is first-line, given orally and/or rectally. If no response, add oral/rectal corticosteroids.
  • Moderate-to-Severe Colitis:
    • Induction: Oral corticosteroids (e.g., Prednisone). For refractory cases, use Biologics (e.g., Infliximab, Vedolizumab).
    • Maintenance: Immunomodulators (Azathioprine/6-MP) or Biologics to remain steroid-free.
  • Severe/Fulminant Colitis:
    • Tx: Hospitalize, give IV corticosteroids. If no response after 3-5 days, use rescue therapy (IV Infliximab) or proceed to surgery.

Crohn Disease (CD) Treatment

  • Goal: Induce and maintain remission; surgery is not curative and reserved for complications.
  • Mild-to-Moderate Disease:
    • Induction: Corticosteroids are first-line for flares (Budesonide preferred for ileocecal disease to limit systemic effects).
    • Maintenance: May not require therapy if remission is stable. Use Azathioprine/6-MP for recurrent disease.
  • Moderate-to-Severe Disease:
    • Induction: Biologics (e.g., Infliximab, Adalimumab) are often used early, with or without corticosteroids.
    • Maintenance: Biologics and/or immunomodulators are the standard.
  • Fistulizing Disease:
    • Tx: Anti-TNF biologics (e.g., Infliximab) are the most effective treatment.

Key Drug Classes

  • 5-ASA (Mesalamine): Mainstay for mild-moderate UC. Less effective in CD.
  • Corticosteroids (Prednisone, Budesonide): For acute flares only (induction). Not for maintenance.
  • Immunomodulators (Azathioprine, Methotrexate): Steroid-sparing agents for maintenance in both UC & CD.
  • Biologics (Anti-TNF, etc.): For moderate-to-severe or refractory disease in both UC & CD. Crucial for fistulizing Crohn’s.

Complications

  • ↑ Risk of cancer
    • chronic inflammation → hyperplasia → non-polypoid dysplasia → neoplasia
  • Toxic megacolon
  • Fulminant colitis
  • Gastrointestinal bleeding (both acute and chronic)
  • Perforation

Graph View

Backlinks