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CELIAC DISEASE1.pptx
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- 2. DEFINITION • An immune-mediatedsystemic disorder • Elicited by gluten and related prolamines • In genetically (mainly HLA) susceptible individuals • Characterized by a combination of: gluten dependent clinical manifestations, anti-tissue transglutaminase (TG2) antibodies and enteropathy
- 3. CLINICAL SPECTRUM • SymptomaticCD Frank clinical features(chronic diarrhea, failure to thrive ,weight loss) • Silent CD No symptoms but +ve serology and HPE. In most cases identified by serologic screening in at-risk groups
- 4. • latent CD -Normal HPE but before or after have shown Gluten dependent enteropathy Potential CD Normal HPE but Positive serology . It might or might not be symptomatic
- 5. Increased prevalence ofCD in children with • Type 1 diabetes • Autoimmune liver disease • Autoimmune thyroid disease • lgA deficiency • Down's syndrome • Turner syndrome • Williams' syndrome • First degree relatives with CD 2-12 % 12-13 % up to 7 % 2-8% 5-12 % 2-5 % up to 9 % 10-20 % Garampazzi A, Rapa A, Mura S et al. Clinical pattern of celiac disease is still changing. J Pediatr Gastroenterol Nutr. 2007;45:611-4.
- 6. Prevalent, But UnderDiagnosed - Those not diagnosed have a higher death rate - Raise awareness IMPROVE SCREENING
- 9. Who Should BeTested for CD? Group 1: Group 2: unexplained symptomsand signs chronic or intermittent diarrhoea, failure to thrive, weight loss, stunted growth, delayed puberty, amenorrhoea, iron-deficiency anaemia, nausea or vomiting, chronic abdominal pain, cramping or distension, chronic constipation, chronic fatigue, recurrent aphthous stomatitis (mouth ulcers), dermatitis herpetiformis-like rash, fracture With inadequate traumas/osteopenia/osteoporosi , and abnormal liver biochemistry. Asymptomatic increased risk forCD Type 1 diabetes mellitus (TlDM) Autoimmune thyroid disease Autoimmune liver disease lgA deficiency Down syndrome Turner syndrome Williams syndrome First-degree relatives
- 10. DIAGNOSTIC TOOLS • CD-specificAntibody Tests • Histological Analysis of Duodenal Biopsies • HLA Testing for HLA-DQ2 and HLA-DQ8
- 11. ANTIBODIES • Anti-tTG /TG2(tissue transglutaminase) • Anti-EMA {Endomysial antibody} • Anti- DGP ( deamidated Gliadin Peptides) - lgA level should be done with EMA/tTG • Anti- Gliadin/Anti- Reticulin
- 12. False Positive tTG/Serology - Other autoimmune conditions - Infections -Tumors - Tissue damage
- 13. FALSE NEGATIVE SEROLOGY(tTG) • Children younger than 2 yr • Restricted gluten consumption • Severe symptoms • On immunosuppressive medications • Technical problems
- 14. HISTOPATHOLOGY • Crypt Hyperplasia •Crypt to villous ratio is increased • Intra-Epithelial Lymphocytosis • Abnormal surface epithelium • Subtotal to total villous atrophy
- 15. ENDOSCOPY & BIOPSY Biopsiesshould be taken preferably upper endoscopy during bulb {at least 1 biopsy) second or third portion of duodenum {at least 4 biopsies)
- 17. Normal small bowelCeliac disease Gluten Gluten-free diet 19
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- 19. Causes of FlatMucosa (Villous Atrophy) • Celiac Disease • Giardiasis • HIV Enteropathy • PEM • CMPI • Bacterial Overgrowth • Primary immunodeficiency • Tropical sprue • Chemotherapy & irradiation • Eosinophilic Gastroenteritis
- 20. Genetics • Multiple genesinvolved • The most consistent genetic component depends on the presence of HLA-DQ (DQ2 and/or DQ8) genes • One or both of these genes are found in 95% of celiac patients • Having one or more of these genes doesn't mean you will develop celiac, but if you have the disease you likely have the gene. -•
- 21. HLA TYPING • HLADQ2 and DQ8 - Strong negative predictive value - Present in > 95 % patients of CD - Present in > 30% normal population - Weak positive predictive value
- 22. • Diagnosis withoutbiopsy is still not recommended in India & Developing countries • Reliable HLA testing and EMA estimation is not widely available • Secondly tTG is being done by various labs with different kits and their standardization is doubtful, so >10 times criteria is also difficult to implement.
- 25. Symptoms Present? Yes FOLLOW UP CELIACDISEASE Gluten FreeDiet Nutritional Education Dietician Periodic assessment af Symptoms, Diet & Serology Reinforce adherence Yes No Evaluate for other causes of symptoms Consider Re- Biopsy
- 26. Management of CeliacDisease Six key elements • Consultation with a skilled dietitian • Education about the disease • Lifelong adherence to a gluten-free diet • Identification and treatment of nutritional deficiencies • Access to an advocacy group • Continuous long-term follow-up by a multidisciplinary team
- 27. Treatment Only treatment forceliac disease is a gluten-free diet (GFD) < 20 ppm - Strict, lifelong diet - Avoid: Wheat Rye Barley
- 28. 10 MG GLIADIN~250MG WHEAT FLOUR (LESS THAN AN 1/8 TEASPOON FLOUR)
- 29. Sources of gluten Potentialsources - Candy - Cured Pork Products - Drink mixes - Gravy - Imitation meat / seafood - Sauce - Soy sauce - Beer
- 30. GFD limitations • Impairsquality of life • Psychological impact • Increase risk of obesity- overfeeding/low fibre • Altered eating pattern • Chronic inadequacy of micronutrients (low iron, Zn, Ca, Mg, vit D)
- 31. Treatment challenges • Dietarycompliance • To get gluten free diet • No reliable test- detect gluten in food products • No identification mark for GFD products • GFD-more costly • Lack of varieties
- 32. Barriers to compliance Timepressure Competing priorities - family, job, etc. Feelings of deprivation Social events Assessing gluten content in foods - Label reading
- 33. Follow-up for dietaryadherance • Pretreatment values taken • IgA levels fall earlier than IgG • Either IgA TTG or AGA can be used • Serological normalization precedes histological recovery • Measurement of TTG after 6 months of GFD- decrease in antibody titer indicates recovery • Persistent or recurrent symptoms with GFD - Rise in antibody levels indicates dietary nonadherence • Asymptomatic patient- measurement of TTG at intervals of 1 year or longer may serve as a monitor of adherence to the GFD
- 34. Follow-up • Growth andmaturation assessment • Assessment for nutritional deficiency • Counselling and psychological support
- 35. RESPONSE TO AGLUTEN-FREE DIET 90% IMPROVE (within 2 weeks) 10% FAIL TO IMPROVE Dietary indiscretion Lactose or fructose Intolerance Microscopic colitis Wrong Diagnosis Pancreatic Insufficiency Bacterial overgrowth Refractory sprue
- 36. CONCLUSION • CD iscommon • lgA tTG -good screening test for CD. ( exceptions < 2 years) • A gluten-free diet (GFD) should be introduced only after the completion of the diagnostic process, when a conclusive diagnosis has been made{ expensive and lifelong diet).
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