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IBD IMC, Nazmul .pdf



Original filename: IBD-IMC, Nazmul.pdf
Title: Inflammatory Bowel Disease
Author: redqueen

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Inflammatory Bowel Disease

Inflammatory Bowel Disease
Def: Inflammatory bowel disease (IBD) is an idiopathic
disease caused by a dysregulated immune response to
host intestinal microflora.
Two major types of IBD.
•Ulcerative colitis (UC)
•Crohn’s disease (CD)

Ulcerative Colitis (UC):
• It is an inflammatory disorder of the colonic
mucosa characterized by relapses and remissions.
• Rectal mucosa is always involved and the disease
extends proximally.

Crohn’s disease (CD):
It is a chronic inflammatory disorder of the
gastro intestinal tract of unknown etiology.
It can affect any part of the GIT from mouth to
anus.

Epidemiology:
Incidence: More in western population
and lower in Asian and African countries.
•Jewish suffer more especially in Ashkenazi Jews.
• High socioeconomic classes have a higher
prevalence than lower socioeconomic classes.

Epidemiology: contd.
• The peak age of onset of UC and CD is between
15 and 30 years.
• A second peak occurs between the ages of 50
and 60 yrs.
• The male to female ratio for UC is 1:1 and for CD
is 1.1 to 1.8:1.

Predispositions of IBD:
Environmental Predispositions:
Smoking :
• UC is more common in non smokers and ex smoker.
• In CD - -most patients are smokers (relative risk = 3).
Oral Contraceptives:
• Oral contraceptives are also linked to CD.

Appendecectomy:
•Appendectomy appears to be protective against UC.
Diet:
•Associated with low residue and high refined sugar diet.

Predispositions:
Genetic predisposition:
• More common in Ashkenazi Jews.
• 10% have 1st degree relative or close relative with IBD.
• HLADR103 is associated with severe UC.
• UC and CD patients with HLAB27 are commonly associated
with Ankylosing spodylitis.
• Linkage with mutation in CARD 15/NOD-2 gene on
chromosome 16 (IBD-1 locus).
• Other regions of linkage on chromosome 12,6,14 (IBD 2-4).

IBD Etiology:

Over 100 years, its etiology and pathogenesis have not
been defined. A consensus hypothesis is that in
genetically predisposed individuals, both exogenous
factors (e.g., infectious agents, normal luminal flora) and
host factors (e.g., intestinal epithelial cell barrier
function, vascular supply, neuronal activity) cause a

chronic state of dysregulated mucosal immune function
that is further modified by specific environmental
factors (e.g., smoking).


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