Ji Keon LOOI
Monash University Sunway Campus
Introduction
•A.k.a. Gluten-sensitive enteropathy
•an autoimmune inflammatory disease of the small intestine
•Precipitated by the ingestion of gluten
•genetically susceptible persons
Oral tolerance
•Ingested protein does not normally provoke an immune response - "oral tolerance"
Oral intolerance / true allergy to an ingested protein (milk or soy protein)
•a typical IgE-mediated response
–urticaria,
–angioedema, and
–bronchoreactivity
Pathophysiology (1)
•involves plasma cells - IgA and IgG
•little or no IgE involvement
Current theory
•Ingested alpha-gliadin and related peptides bind with tissue transglutaminase in enterocytes
•The alpha-gliadin is rich in glutamine; transglutaminase deamidates glutamine residues, forming glutamic acid.
•Deamidation enhances the immunogenicity of alpha-gliadin by creating epitopes that are recognized as foreign by host cellmediated immunity
Pathophysiology (2)
•IgA and IgG (by plasma cells) direct against a variety of antigens
–transglutaminase, endomysium, gliadin, and reticulin.
•Locally elaborated lymphokines attract inflammatory cells à villous flattening appearance
•Followed by malabsorption of micronutrients and macronutrients
•Small-bowel involvement is most prominent proximally and may be "patchy," especially in patients with "silent" celiac disease (i.e., minimal or no symptoms) and those with dermatitis herpetiformis.
My Task
•To explain the histologic charateristics of Coeliac Disease
Note: These slides were provided by Dr Rakesh Naidu on Monday's PCL.Histologic Findings of Coeliac Disease
Histology
•In untreated coeliac disease
•inflammed lining of the intestine becomes inflamed
•villous atrophy
–flat appearance
•reduced surface area à nutritional deficiencies
Histological Description of CD
•Disease causality was established when the characteristic features of
–villous flattening,
–crypt hyperplasia, and
–increased intraepithelial lymphocytes
Before - After
A At time of diagnosis. There is severe villous abnormality associated with marked enterocyte damage (black arrows), in keeping with untreated coeliac disease.
B After 6 months of gluten-free diet. There is partial improvement of the previous villous abnormality, but a moderate villous abnormality with associated crypt hyperplasia remains
Remember……
•Exclusion of dietary gluten results in healing of the mucosa, resolution of the malabsorptive state, and reversal of most, if not all, effects of celiac disease.
Thank you!
•http://www.aafp.org/afp/20021215/2259.html
•http://content.answers.com/main/content/wp/en/6/60/CoeliacDisease.png
Histology
•In untreated coeliac disease
•inflammed lining of the intestine becomes inflamed
•villous atrophy
–flat appearance
•reduced surface area à nutritional deficiencies
Histological Description of CD
•Disease causality was established when the characteristic features of
–villous flattening,
–crypt hyperplasia, and
–increased intraepithelial lymphocytes
Before - After
A At time of diagnosis. There is severe villous abnormality associated with marked enterocyte damage (black arrows), in keeping with untreated coeliac disease.
B After 6 months of gluten-free diet. There is partial improvement of the previous villous abnormality, but a moderate villous abnormality with associated crypt hyperplasia remains
Remember……
•Exclusion of dietary gluten results in healing of the mucosa, resolution of the malabsorptive state, and reversal of most, if not all, effects of celiac disease.
Thank you!
•http://www.aafp.org/afp/20021215/2259.html
•http://content.answers.com/main/content/wp/en/6/60/CoeliacDisease.png
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