Celiac Disease
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Transcript Celiac Disease
CELIAC DISEASE
PRESENTED BY: DALLAS MONTAG
DATE: 12/6/16
WHAT IS CELIAC DISEASE (CD)? 3,4,6
Intestinal inflammatory autoimmune
disease in response to gluten
Destroys the villi, lining of the small intestine
Other names for the disease:
Celiac Sprue
Gluten-Sensitive Enteropathy
Sprue
https://medivizor.com/blog/2016/10/19/celiac-disease/
COMMON SOURCES OF GLUTEN 5,8
Beer
Cookies
Bread
Pasta/Noodles
Bagels
Pastries/Pies
Cakes
Rolls
Cereal
Salad Dressings
CELIAC DISEASE OCCURS PRINCIPALLY IN INDIVIDUALS OF
EUROPEAN DESCENT 3,4,5
Other epidemiology's include:
Occurrence: 1 in 250 individuals
20% of first degree relatives are
affected
Females > Males
Age of diagnosis
http://www.whattoexpect.com/first-year/celiac-disease-in-children.aspx
CELIAC DISEASE HAS A STRONG GENETIC COMPONENT 3,5,6
Genetic Factors
Environmental Factors
HLA-DQ locus
Foods containing GLUTEN
Majority: DQ2 (DQA1*05/DQB1*02)
Infant Feeding
Minority: DQ8 (DQA1*03/DQB1*0302)
Drug exposures
Females create a larger risk factor than
Microbial Infections (trigger)
males
WHAT IS GLUTEN? 4,8
Name for proteins found in wheat and
other grains such as barley, rye, and to
some extent oats
Gluten helps food maintain their shape
Gliadin and glutenin: comprise ~80% of
protein contained in wheat seed
Binds to the serotypes formed from the
DQ2 and DQ8 genes
Gluten is the “glue”
http://www.elisilvernd.com/health-news/what-exactly-is-gluten
IMMUNOLOGICAL MECHANISM 1,5,6
http://www.nature.com/scientificamerican/journal/v301/n2/box/scientificamerican0809-54_BX3.html
THE ROLE OF TISSUE TRANSGLUTAMINASE (TTG) 1,4
Calcium dependent enzyme
Extracellular and Intracellular
Irreversible crosslinking of glutamine
and lysine residues
Gliadin is the preferred substrate
https://en.wikipedia.org/wiki/Tissue_transglutaminase
STEP 1: Entrance of
gluten
STEP 2: Accumulation of
gluten
STEP 3: Release of IL-15
STEP 4: TTG Release
STEP 5: APCs present
antigens to TH cells
STEP 6: Attraction of
immune cells
STEP 7: Tc cells attack
STEP 8: Secretion of ABs
STEP 9: Damaged
epithelial cells
3,4,5,8
Seizures
Erosion of tooth
enamel
Migraines
Abdominal Pain
Bloating
Dermatitis
Herpetiformis
Symptoms
Diarrhea
Weight Loss
Short Stature
Malabsorption
Vomiting
Iron Deficiency
Anemia
DERMATITIS HERPETIFORMIS HAS BEEN LINKED
TO PATIENTS WITH CD 2
https://en.wikipedia.org/wiki/Dermatitis_herpetiformis
CD IS MOST COMMONLY DIAGNOSED BY SEROLOGIC TESTS 5,6
Routine Lab Test
Blood count, electrolytes, calcium, vitamin B12, folic acid
levels
Serologic Tests
Detect antibodies, IgA and IgG
Show variability in sensitivity and specificity
Biopsy of Small Intestine
http://www.napavalley.edu/people/briddell/Documents/BIO%20218/Ana
tomical%20Pathology%20Celiac%20Disease%20Example.pdf
THERE ARE FEW TREATMENTS FOR PATIENTS WITH CD 4,5,6
Gluten-Free Diet
Includes all food, bath products, cosmetics, medications etc.
Small amount of gluten in food will effect a person with CD
Ex. Eating gluten- free food served on a plate with food containing gluten
Anti-inflammatory medications
Vaccine Trial
Experimental Possibility: blocking binding sites of the DQ2 and DQ8 HLA
molecules???
TREATMENT CONT’D 8
Consultation
Education
Lifelong diet
Identification of deficiencies
Advocacy group
Continuous follow-up
https://gfjules.com/celiac-awareness-month/
REFERENCES & ACKNOWLEDGMENTS
1. Sabatino AD,Vanoli A, Giuffrida P, Luinetti O, Solcia E, Corazza GR. 2012. The function of tissue
transglutaminase in celiac disease. Autoimmunity Reviews. 11(10): 746-753.
2. Fergunson A, Arranz E, O’Mahony S. 1993. Clinical and pathological spectrum of coeliac disease-active,
silent, latent, potential. Journal of The American Dietetic Association. 34(7): 150-151.
3. King AL, Ciclitira PJ. 2000. Celiac disease: strongly heritable, oligogenic, but genetically complex. Molecular
Genetics and Metabolism. 71(1-2): 70-75.
4. Kuper SS, Jabri B. 2012. Celiac Disease Pathophysiology. Gastrointestinal Endoscopy Clinics of North
America. 22(4): 1-28.
REFERENCES & ACKNOWLEDGMENTS
5.Murray A. 1999. The widening spectrum of celiac disease1,2. American Journal of Clinical Nutrition. 69(3):
354-365.
6. Sollid LM, Benedicte AL. 2005. Celiac Disease Genetics: Current Concepts and Practical Applications.
Clinical Gastroenterology and Hepatology. 3(9): 843-851.
7. Sollid LM, Markussen G, Ek J, Gjerde H, Vartdal F, Thorsby E. 1989. Evidence for a primary association of
celiac disease to a particular HLA-DQ alpha/beta heterodimer. The Journal of Experimental Medicine.
169(1): 345-350.
8. Thalheimer J. 2016. Getting to the bottom of food sensitivities. Environmental Nutrition. p.7.
THANK YOU DR. SPILATRO!!
Questions????
STUDY QUESTIONS: MULTIPLE CHOICE
1. Celiac disease is the result of the intolerance to the proteins most commonly found in which three grains?
A. rice, wheat, rye
B. oats, wheat, rice
C. wheat, barley, rye
D. oats, wheat, rye
2. Which of the following statements concerning celiac disease is TRUE? (select all correct answers)
A. Symptoms of celiac disease often mimic those of other intestinal disturbances.
B. It occurs more frequently amongst the elderly
C. Celiac disease occurs in 5 percent of Americans.
D. There is no cure for celiac disease.
STUDY QUESTIONS: MULTIPLE CHOICE
3. Why does the immune system respond to gluten in patients with celiac disease?
A. It is a foreign protein
B. It is modified by the transglutaminase enzyme
C. It is very large and disrupts the villi
D. It is modified by the alanine transaminase enzyme
4. Which of the following statements concerning celiac disease is NOT true?
A. Celiac disease is more often in females than in males.
B. Celiac sprue is another name for the disease
C. Celiac disease patients have excessive growth of villi
D. Individuals with celiac disease often have malabsorption issues