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11/5/2018 FINDING SLIDES FOR TODAYS WEBINAR COPE WEBINAR SERIES FOR HEALTH PROFESSIONALS November 5, 2018 www.villanova.edu/COPE Gluten-Related Disorders: Click on Alessio Fasano MD How to Distinguish Facts from Fantasies webinar


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COPE WEBINAR SERIES FOR HEALTH PROFESSIONALS November 5, 2018 Gluten-Related Disorders: How to Distinguish Facts from Fantasies Moderator: Lisa Diewald MS, RD, LDN Program Manager MacDonald Center for Obesity Prevention and Education

Nursing Education Continuing Education Programming Research

FINDING SLIDES FOR TODAY’S WEBINAR

www.villanova.edu/COPE Click on Alessio Fasano MD webinar description page

DID YOU USE YOUR PHONE TO ACCESS THE WEBINAR?

If you are calling in today rather than using your computer to log on, and need CE credit, please email cope@villanova.edu and provide your name so we can send your certificate. OBJECTIVES 1.Recognize the differences between celiac disease, non-celiac gluten sensitivity and wheat allergy. 2.Discuss the epidemiology of celiac disease and why prevalence is increasing 3.Identify the role of the gut microbiome and intestinal permeability in autoimmune disease

CE DETAILS

  • Villanova University College of Nursing is accredited as a

provider of continuing nursing education by the American Nurses Credentialing Center Commission on Accreditation

  • Villanova University College of Nursing Continuing

Education/COPE is a Continuing Professional Education (CPE) Accredited Provider with the Commission on Dietetic Registration

  • The American College of Sports Medicine’s Professional

Education Committee certifies that Villanova University College of Nursing Continuing Education, Center for Obesity Prevention and Education (COPE) meets the criteria for

  • fficial ACSM Approved Provider status (10/2018-9/2021).

Providership #698849

CE CREDITS

  • This webinar awards 1 contact hour for nurses and 1

CPEU for dietitians

  • Suggested CDR Learning Need Codes: 2000, 5110, 5220

and 6000

  • Level 2
  • CDR Performance Indicators: 8.1.2, 8.1.5, 8.3.1, 8.3.6
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GLUTEN AND GLUTEN-RELATED DISORDERS: HOW TO DISTINGUISH FACTS FROM FANTASIES

Alessio Fasano, MD Chief of Pediatric Gastroenterology and Nutrition Mass General Hospital for Children Professor of Pediatrics Harvard Medical School DISCLOSURE

The planners of this program have no conflicts of interest to disclose. Any presenter conflict of interest was resolved prior to the planning of this

  • program. Any additional disclosure information will be provided to participants

during the live activity. The Nurse Planner has reviewed the presentation and determined that it is evidence-based, balanced and unbiased Accredited status does not imply endorsement by Villanova University, COPE

  • r the American Nurses Credentialing Center of any commercial products or

medical/nutrition advice displayed in conjunction with an activity.

Alessio Fasano, M.D.

  • W. Allan Walker Chair in Pediatric Gastroenterology and Nutrition

Professor of Pediatrics Harvard Medical School Mucosal Biology and Immunology Research Center And Center for Celiac Research And Treatment Massachusetts General Hospital for Children

Celiac Disease And Other Gluten Related Disorders: How To Distinguish Facts From Fantasies

Conflict of Interest Disclosure Company Relationship Content Area

Alba Therapeutics Stock Holder Alternative treatments to gluten free diet for celiac patients Inova Diagnostics Consultant Innovate Biopharmaceuticals, Inc. Consultant Mead Johnson Nutrition Speaking Agreement

Alessio Fasano, MD

I disclose the following financial relationships with commercial entities that produce health care related products or services relevant to the content I am planning, developing, or presenting:

The Controversy On Who Should Be On A GFD

Only People With Celiac Disease Everybody

The Source Supporting GFD For Everybody

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The Epidemics Of Gluten Related Disorders

  • Quality of gluten: GE grains
  • Quantity of gluten
  • Gluten cannot be digested

The Epidemics Of Gluten Related Disorders

  • Quality of gluten: GE grains
  • Quantity of gluten
  • Gluten cannot be digested

Kasarda D. J Agric Food Chem. 2013;61: 1155–1159 Kasarda D. J Agric Food Chem. 2013;61: 1155–1159.

+ GMO Grains

Aegilops tauschii DD 14 chromosomes 50,000 genes

  • T. aestivum AABBDD

42 chromosomes 150,000 genes

  • T. turgidum AABB

28 chromosomes 100,000 genes

The Epidemics Of Gluten Related Disorders

  • Quality of gluten: GE grains
  • Quantity of gluten
  • Gluten cannot be digested
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Kasarda D. J Agric Food Chem. 2013;61: 1155–1159

The Epidemics Of Gluten Related Disorders

  • Quality of gluten: GE grains
  • Quantity of gluten
  • Gluten cannot be digested

What is so Special About Gluten?

Gliadin Glutenin Gluten (gliadin+glutenin) Maiuri et al. Scand J

  • Gastroenterol. 1996; 31:247-53.

Shan L et al, Science. 2002; 297:2275-9. Lammer K et al, Gastroenterology 2008;135:194-204. Lammer K et al, Immunology. 2011;132:432-40

Structural Characteristics of Alpha-Gliadin

Celiac Disease

The Banana Babies

WK Dicke, 1905 - 1962 1st case of CD at UMB: 1938

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Celiac Disease as a Unique Model of Autoimmunity

  • The only autoimmune disease in which specific

MHC class II HLA (DQ2 and/or DQ8) are present in >95% of patients;

  • The auto-antigen (tissue Transglutaminase) is

known;

  • The environmental trigger (gluten) is known;
  • Elimination of the environmental trigger leads to

a complete resolution of the autoimmune process that can be re-ignited following re-exposure to gluten

Gastrointestinal Manifestations (“Classic”)

Most common age of presentation: 6-24 months

  • Chronic or recurrent diarrhea
  • Abdominal distension
  • Anorexia
  • Failure to thrive or weight loss
  • Abdominal pain
  • Vomiting
  • Constipation
  • Irritability

Rarely: Celiac crisis

Non Gastrointestinal Manifestations

  • Dermatitis Herpetiformis
  • Dental enamel hypoplasia
  • f permanent teeth
  • Osteopenia/Osteoporosis
  • Short Stature
  • Delayed Puberty
  • Iron-deficient anemia

resistant to oral Fe

  • Hepatitis
  • Arthritis
  • Epilepsy with occipital

calcifications

Most common age of presentation: older child to adult

Listed in descending order of strength of evidence

The Clinical Manifestations of Celiac Disease are More Heterogeneous Than Previously Appreciated

  • A. Fasano, N Engl J Med 2003;348:2568-70.

0.21% 0.45% 0.93%

The Epidemics of Celiac Disease

The Epidemics Of Celiac Disease:

Which Additional Factors are Driving this Epidemics?

  • Quality of gluten;
  • Quantity of gluten;
  • Breast Feeding;
  • Timing of gluten introduction
  • Maturity of gut functions influencing Ag trafficking and

handling:

  • GALT
  • PRRs
  • Mucous production
  • Barrier function
  • Changes in microbiome composition.
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Published on October 2, 2014

Take Home Messages

  • Window of tolerance concept not supported anymore;
  • Breast feeding in general or introduction of gluten while breast feeding

showed no protective effect on CD onset in at-risk infants;

  • Early introduction (16 weeks) of gluten traces to potentially induce

tolerance did not protect against CD in at-risk infants;

  • Delaying the introduction of gluten in at-risk infants does not prevent

CD but merely postpones its onset by approximately 8 months (significant difference at 2 years FU that disappeared by 5 years FU);

  • GI infections during the first year of life seems influential in increased

the risk of CD onset;

  • High-risk HLA profiles seems to be the most influential factor predictor
  • f increased risk of CD onset;
  • The high prevalence of CD among the study cohort suggests that the

CD epidemics continues.

The Epidemics Of Celiac Disease:

Which Additional Factors are Driving this Epidemics?

  • Quality of gluten;
  • Quantity of gluten;
  • Breast Feeding;
  • Timing of gluten introduction
  • Maturity of gut functions influencing Ag trafficking and

handling:

  • GALT
  • PRRs
  • Mucous production
  • Barrier function
  • Changes in microbiome composition.

Key Open Questions Concerning Celiac Disease:

  • Best diagnostic strategies?
  • Endoscopy yes/no for diagnosis?
  • How to properly follow up CD patients?
  • Should CD patients be actively screened for other

autoimmune diseases?

  • How to manage CD patients with discrepancies between

serology and histology?

  • Are POC tests useful/appropriate for diagnosis and/or

management of CD?

  • Is the GFD highly effective in controlling CD?
  • How to properly check for gluten cross-contamination?
  • Are there any alternative/complementary treatments to

the GFD at the horizon?

Not Only Celiac Disease

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Gluten Free Market

For the American general population adopting a gluten-free diet is becoming an increasingly popular solution. The market for gluten-free food and beverage products grew at a compound annual growth rate of 28 percent from 2004 to 2011, to finish with almost $6.7 billion in retail sales last year. By the end of 2016 the market is expected to reach about $14.6 billion in sales.

How Many People in the US Are Embracing a GFD?:

Percentage of U.S. Adults Trying to Cut Down or Avoid Gluten in Their Diets Reaches New High in 2016, Reports NPD

The Fad Factor of the GFD

Based on internet interview users age 18y+ who eats GF food Approx 50M Approx 24M Approx 7M Approx 9M

Why People in the US Embrace a GFD?:

Approx 400,000

The Gluten Free Diet: Not Only Celiac Disease The Gluten Free Diet: Not Only Celiac Disease

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Cases of reaction to ingestion of gluten-containing grains in which both allergic and autoimmune mechanisms have been ruled out (diagnosis by exclusion criteria)

  • Triggered by the ingestion of gluten-containing grains;
  • Negative immuno-allergy tests to wheat;
  • Negative CD serology (EMA and/or tTG) and in which IgA deficiency

has been ruled out;

  • Negative duodenal histopathology;
  • Possible presence of biomarkers of gluten immune-reaction

(AGA+);

  • Presence of clinical symptoms that can overlap with CD or wheat

allergy symptomatology;

  • Resolution of the symptoms following implementation of a GFD and

relapse after re-exposure to gluten-containing grains (double blind)

Sapone A. et al BMC Med 2012, Ludvigsson JF et al Gut 2013, Catassi C. Et al, Nutrients 2013

Gluten Sensitivity (NCGS): Facts

Definition

  • A. Epithelial Events

Timeline: Hours

Immune-Mechanisms Involved in the Pathogenesis

  • f Gluten Related Disorders

Clemente MG et al Gut 2003; Drago et al Scand J Gastroenterol 2006; Sapone A. et al. JADD 2012

  • B. Innate Immunity Events

Timeline: Days

  • C. Adaptive Immunity Events

Timeline: Weeks-Years

Gluten Sensitivity (NCGS):

Consensus Conferences to Define NCGS

Sapone A, Bai JC, Ciacci C, Dolinsek J, Green PH, Hadjivassiliou M, Kaukinen K, Rostami K, Sanders DS, Schumann M, Ullrich R, Villalta D, Volta U, Catassi C, Fasano A. Spectrum of gluten- related disorders: consensus on new nomenclature and classification. BMC Med. 2012 Feb 7;10:13 Ludvigsson JF, Leffler DA, Bai JC, Biagi F, Fasano A, Green PH, Hadjivassiliou M, Kaukinen K, Kelly CP, Leonard JN, Lundin KE, Murray JA, Sanders DS, Walker MM, Zingone F, Ciacci C. The Oslo definitions for coeliac disease and related terms. Gut. 2013 Jan;62(1):43-52 Catassi C, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A. Non- Celiac Gluten sensitivity: the new frontier of gluten related disorders. Nutrients. 2013 Sep 26;5(10):3839-53. Catassi C, Elli L, Bonaz B, Bouma G, Carroccio A, Castillejo G, Cellier C, Cristofori F, de Magistris L, Dolinsek J, Dieterich W, Francavilla R, Hadjivassiliou M, Holtmeier W, Körner U, Leffler DA, Lundin KE, Mazzarella G, Mulder CJ, Pellegrini N, Rostami K, Sanders D, Skodje GI, Schuppan D, Ullrich R, Volta U, Williams M, Zevallos VF, Zopf Y, Fasano A. Diagnosis of Non-Celiac Gluten Sensitivity (NCGS): The Salerno Experts' Criteria. Nutrients. 2015 Jun 18;7(6):4966-77. doi: 10.3390/nu7064966.

Immune-mediated (likely innate immune)

Sapone A, Lammers KM, Mazzarella G, Mikhailenko I, Cartenì M, Casolaro V, Fasano A. Differential mucosal IL-17 expression in two gliadin-induced disorders: gluten sensitivity and the autoimmune enteropathy celiac disease. Int Arch Allergy Immunol. 2010;152(1):75-80. Sapone A, Lammers KM, Casolaro V, Cammarota M, Giuliano MT, De Rosa M, Stefanile R, Mazzarella G, Tolone C, Russo MI, Esposito P, Ferraraccio F, Cartenì M, Riegler G, de Magistris L, Fasano A. Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity. BMC Med. 2011 Mar 9;9:23 Junker Y, Zeissig S, Kim SJ, Barisani D, Wieser H, Leffler DA, Zevallos V, Libermann TA, Dillon S, Freitag TL, Kelly CP, Schuppan D. Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4. J Exp Med. 2012 Dec 17;209(13):2395-408.

Gluten Sensitivity (NCGS): Facts

Pathogenesis

Clinical manifestations of NCGS

Frequency Intestinal Extra‐intestinal

Very Common Bloating Lack of wellbeing Abdominal pain Tiredness Common Diarrhea Headache Epigastric pain Anxiety Nausea Foggy mind Aerophagia Numbness GER Joint/muscle pain Aphtous stomatitis Skin rash/dermatitis Alternating bowel habits Constipation Undetermined Hematochezia Weight loss Anal fissures Anemia Loss of balance Depression Rhinitis/asthma Weight increase Interstitial cystitis Ingrown hairs Oligo or polimenorrhea Sensory symptoms Disturbed sleep pattern Hallucinations Mood swings Autism Schizophrenia

The Salerno NCGS diagnostic criteria (Nutrients, 2015)

Gluten and The Brain

Chronic Headache Short Memory Loss Anxiety Depression ADHD? Autism? Ataxia Seizures Schizophrenia? Irritability

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The Controversial Questions About Gluten Sensitivity

Are The Epidemics Of Autism, ADHD and Schizophrenia Also Related to The Rise of Non-Celiac Gluten Sensitivity?

Case Presentation: Diagnosis of Gluten Sensitivity

Description of the Case

AJ 39 y old F

  • 6 months history of:
  • Recurrent abdominal pain (mainly epigastric)
  • Heartburn

One month after the onset of GERD symptoms pt developed headaches, dizziness, numbness of fingers, paresthesia, gradual reduction of legs’ muscle strength that forced her on a wheelchair. Suspecting GERD, pt was placed on PPI, but no resolution of symptoms. 0 1 2 3 4 5 6

Description of the Case

Suspecting neurological causes, patient underwent to:

  • MRI
  • Evoked potentials

Other diagnoses that were considered include:

  • Lyme disease;
  • Epstein Barr Virus
  • Pernicious Anemia
  • Lupus

Both resulted negative All were ruled out 0 1 2 3 4 5 6

Description of the Case

Because of the persistence of GERD symptoms pt underwent to an EGD reported as normal (including duodenal biopsy that showed only increased IEL). She was also screened for CD and tested negative Despite negative results, pt decided to embrace a GFD

  • Within 3 weeks her GI symptoms resolved
  • Within 2 months her neurological symptoms also
  • improved. Six month after implementation of the GFD

she was able to walk with the assistance of a cane. Twelve months later she regained completely her walking function.

0 1 2 3 4 5 6

Biomarkers

YES YES NO

Gluten Related Disorders Pathogenesis Autoimmune Allergic Not Autoimmune Not allergic (Innate immunity?) Celiac Disease Gluten Ataxia Dermatitis herpetiformis Wheat allergy Gluten sensitivity Respiratory Allergy Food Allegy WDEIA Contact Urticaria Symptomitic Silent Potential

Proposed New Classification of Gluten Related Disorders

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Differential Diagnosis Between CD, GS, and WA

Celiac Disease Gluten Sensitivity Wheat Allergy

Time interval between gluten exposure and

  • nset of symptoms

Weeks-Years Hours-Days Minutes-Hours Pathogenesis Autoimmunity (Innate+ Adaptive Immunity) Immunity? (Iinnate Immunity?) Allergic Immune Response HLA HLA DQ2/8 restricted (~97% positive cases) Not-HLA DQ2/8 restricted (50% DQ2/8 positive cases) Not-HLA DQ2/8 restricted (35-40% positive cases as in the general population) Auto-antibodies Almost always present Always absent Always absent Enteropathy Almost always present Always absent (slight increase in IEL) Always absent (eosinophils in the lamina propria) Symptoms Both intestinal and extra-intestinal (not distinguishable from GS and WA with GI symptoms) Both intestinal and extra- intestinal (not distinguishable from CD and WA with GI symptoms) Both intestinal and extra- intestinal (not distinguishable from CD and GS when presenting with GI symptoms) Complications Co-morbidities Long term complications Absence of co-morbidities and long term complications (long follow up studies needed to confirm it) Absence of co-morbidities. Short-term complications (incliuding anaphylaxis)

Gluten Sensitivity and IBS

No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR.

Source Department of Gastroenterology, Eastern Health Clinical School, Monash University, Box Hill, Victoria, Australia; Department

  • f Gastroenterology, Central Clinical School, Monash University, The Alfred Hospital, Melbourne, Victoria, Australia.

Abstract

BACKGROUND & AIMS: Patients with non-celiac gluten sensitivity (NCGS) do not have celiac disease but their symptoms improve when they are placed on gluten-free diets. We investigated the specific effects of gluten after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates (fermentable, oligo-, di-, monosaccharides, and polyols [FODMAPs]) in subjects believed to have NCGS. METHODS: We performed a double-blind cross-over trial of 37 subjects (aged 24-61 y, 6 men) with NCGS and irritable bowel syndrome (based on Rome III criteria), but not celiac disease. Participants were randomly assigned to groups given a 2-week diet of reduced FODMAPs, and were then placed on high-gluten (16 g gluten/d), low-gluten (2 g gluten/d and 14 g whey protein/d), or control (16 g whey protein/d) diets for 1 week, followed by a washout period of at least 2 weeks. We assessed serum and fecal markers of intestinal inflammation/injury and immune activation, and indices of fatigue. Twenty-two participants then crossed

  • ver to groups given gluten (16 g/d), whey (16 g/d), or control (no additional protein) diets for 3 days. Symptoms were

evaluated by visual analogue scales. RESULTS: In all participants, gastrointestinal symptoms consistently and significantly improved during reduced FODMAP intake, but significantly worsened to a similar degree when their diets included gluten or whey protein. Gluten-specific effects were

  • bserved in only 8% of participants. There were no diet-specific changes in any biomarker. During the 3-day rechallenge,

participants' symptoms increased by similar levels among groups. Gluten-specific gastrointestinal effects were not reproduced. An order effect was observed. CONCLUSIONS: In a placebo-controlled, cross-over rechallenge study, we found no evidence of specific or dose-dependent effects of gluten in patients with NCGS placed diets low in FODMAPs. www.anzctr.org.au. ACTRN12610000524099.

Food intolerance occurs when the body lacks a particular enzyme to digest nutrients, nutrients are too abundant to be completely digested, or a particular nutrient cannot be properly digested, Common examples are lactose intolerance, FODPAM intolerance, or lactulose intolerance (side effect of laxatives). Food sensitivity, an understudied area, are immune-mediated reaction to some nutrients and these reactions do not always

  • ccur in the same way when eating that particular nutrient.

Food allergy is a very specific immune system response involving either the immunoglobulin E (IgE) antibody or T-cells. Both are immune system cells that react to a particular food protein, such as milk protein.

Non Celiac Gluten Sensitivity: Facts

Definition of Food Reactions

(Consensus NIAID 2011)

FODMAP Excess fructose Lactose Oligosaccharides (fructans and/or galactans) Polyols Problem high FODMAP food source Fruits: apples, pears, nashi pears, clingstone peaches, mango, sugar snap peas, watermelon, tinned fruit in natural juice Honey Sweeteners: fructose, high fructose corn syrup Large total fructose dose: concentrated fruit sources; large serves of fruit, dried fruit, fruit juice Milk: cow, goat and sheep (regular & low-fat), Ice cream Yoghurt (regular & low-fat) Cheeses: soft & fresh (e.g. ricotta, cottage) Vegetables: artichokes, asparagus, beetroot, Brussels sprout, broccoli, cabbage, fennel, garlic, leeks, okra,

  • nions, peas, shallots.

Cereals: wheat & rye when eaten in large amounts (e.g. bread, pasta, couscous, crackers, biscuits) Legumes: chickpeas, lentils, red kidney beans, baked beans Fruits: watermelon, custard apple, white peaches, rambutan, persimmon Fruits: apples, apricots, cherries, longon, lychee, nashi pears, nectarine, pears, peaches, plums, prunes, watermelon Vegetables: avocado, cauliflower, mushrooms, snow peas Sweeteners: sorbitol(420), mannitol(421), xylitol(967), maltitol (965), isomalt (953) &

  • thers ending in '-ol'

Suitable alternative low- FODMAP food source Fruit: banana, blueberry, carambola, durian, grapefruit, grape, honeydew melon, kiwifruit, lemon, lime, mandarin, orange, passionfruit, paw paw, raspberry, rockmelon, strawberry, tangelo. Honey substitutes: maple syrup, golden syrup Sweeteners: any except polyols Milk: lactose-free, rice milk Cheese:'hard' cheeses including brie, camembert Yoghurt: lactose-free Ice cream substitutes: gelati, sorbet Butter Vegetables: bamboo shoots, bok choy, carrot, celery, capsicum, choko, choy sum, corn, eggplant, green beans, lettuce, chives, parsnip, pumpkin, silverbeet, spring

  • nion (green only), tomato

Onion/garlic substitutes: garlic- infused oil Cereals: gluten-free & spelt bread/cereal products Fruits: banana, blueberry, carambola, durian, grapefruit, grape, honeydew melon, kiwifruit, lemon, lime, mandarin, orange, passionfruit, paw paw, raspberry, rockmelon Sweeteners: sugar (sucrose), glucose, other artificial sweeteners not ending in 'ol'

Food sources of FODMAPs (where FODMAPs are problematic based on standard serving size) and suitable alternatives

Gibson PR, Sheperd SJ. J Gastroenterol Hepatol. 2010;25:252-258

Pathogenesis Of IBS‐Like Syndromes

Czaja-Bulsa G et al, Clin Nutr 2014

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The diagnosis of NCGS

Self- diagnosis Elimination diagnosis Positive diagnosis (clinical and DBPC test)

Proposed Algorithm for Differential Diagnosis Of Gluten Related Disorders

Catassi C. et al. Nutrients 2015; 7:4966-77

Key Questions About Non-Celiac Gluten Sensitivity:

  • Are current diagnostic tools (dietary re-

challenge – Salerno criteria) feasible in clinical practice?

  • Are there any validated biomarkers for the

diagnosis of NCGS?

  • How gluten and possibly other wheat

components cause symptoms on NCGS?

  • Look for an email containing a link to an evaluation. The

email will be sent to the email address that you used to register for the webinar.

  • Complete the evaluation soon after receiving it. It will expire

after 3 weeks.

  • You will be emailed a certificate within 2-3 business days.
  • Remember: If you used your phone to call in, and want CE

credit for attending, please send an email with your name to cope@villanova.edu so you receive your certificate.

TO RECEIVE YOUR CE CERTIFICATE

https://nationalceliac.org/2018‐celiac‐disease‐ symposium/

Facing Today’s Facts on Celiac Disease and Gluten Sensitivity November 10-11, 2018 Registration:

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QUESTIONS & ANSWERS

Moderator: Lisa K. Diewald MS, RD, LDN Email: cope@villanova.edu Website: www.willanova.edu/COPE