Inflammatory Bowel Disease

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Basics

Description

  • Idiopathic, chronic inflammatory diseases of intestines, which can involve extraintestinal sites as well
  • Differentiation between ulcerative colitis (UC) and Crohn disease is not always clear; intermediate forms of inflammatory bowel disease (IBD) exist
  • May present as initial onset of disease or exacerbation of existing disease
  • Maintain high index of suspicion owing to frequent, subtle presentation of Crohn disease
  • Pediatric considerations:
    • Can occur in first few years of life
    • Extraintestinal manifestations may predominate
  • Differences between Crohn and UC:
    • Rectum almost always involved in UC with continuous inflammation proximally
    • Small intestine is not involved in UC
    • Crohn can occur anywhere from mouth to anus, often with normal GI tract segments between affected areas
    • Crohn involves transmural inflammation, whereas UC is confined to submucosa
  • Similarities between Crohn and UC:
    • Higher rate of colon cancer with disease >10 yr
    • Bimodal age distribution, with early peak between teens and early 30s and second peak about age 60 yr
  • Crohn disease clinical pattern:
    • Ileocecal: ∼40%
    • Small bowel: ∼30%
    • Colon: ∼25%
    • Other: ∼5%
  • UC clinical pattern on presentation:
    • Pancolitis: 30%
      • Most severe clinical course
  • Proctitis or proctosigmoiditis: 30%
    • Relatively mild clinical course
  • Left-sided colitis (up to splenic flexure): 40%
    • Moderate clinical course

Etiology

  • Unknown
  • Crohn disease and UC are separate entities with common genetic predisposition
  • A positive family history is very common
  • Multifactorial origin involving interplay among the following factors:
    • Genetic
    • Environmental
    • Immune
  • Pathogenesis:
    • Gut wall becomes unable to downregulate its immune responses, ultimately resulting in chronic inflammation
  • There is no definitive evidence for the etiologic role of infectious agents
  • Psychogenic factors may play a role in some symptomatic exacerbations

-- To view the remaining sections of this topic, please or --

Basics

Description

  • Idiopathic, chronic inflammatory diseases of intestines, which can involve extraintestinal sites as well
  • Differentiation between ulcerative colitis (UC) and Crohn disease is not always clear; intermediate forms of inflammatory bowel disease (IBD) exist
  • May present as initial onset of disease or exacerbation of existing disease
  • Maintain high index of suspicion owing to frequent, subtle presentation of Crohn disease
  • Pediatric considerations:
    • Can occur in first few years of life
    • Extraintestinal manifestations may predominate
  • Differences between Crohn and UC:
    • Rectum almost always involved in UC with continuous inflammation proximally
    • Small intestine is not involved in UC
    • Crohn can occur anywhere from mouth to anus, often with normal GI tract segments between affected areas
    • Crohn involves transmural inflammation, whereas UC is confined to submucosa
  • Similarities between Crohn and UC:
    • Higher rate of colon cancer with disease >10 yr
    • Bimodal age distribution, with early peak between teens and early 30s and second peak about age 60 yr
  • Crohn disease clinical pattern:
    • Ileocecal: ∼40%
    • Small bowel: ∼30%
    • Colon: ∼25%
    • Other: ∼5%
  • UC clinical pattern on presentation:
    • Pancolitis: 30%
      • Most severe clinical course
  • Proctitis or proctosigmoiditis: 30%
    • Relatively mild clinical course
  • Left-sided colitis (up to splenic flexure): 40%
    • Moderate clinical course

Etiology

  • Unknown
  • Crohn disease and UC are separate entities with common genetic predisposition
  • A positive family history is very common
  • Multifactorial origin involving interplay among the following factors:
    • Genetic
    • Environmental
    • Immune
  • Pathogenesis:
    • Gut wall becomes unable to downregulate its immune responses, ultimately resulting in chronic inflammation
  • There is no definitive evidence for the etiologic role of infectious agents
  • Psychogenic factors may play a role in some symptomatic exacerbations

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