celiac disease

presented By:Evana AL YoussefSupervisor: Dr.Sana Janakat 14-12-2011

presented By:Evana AL YoussefSupervisor: Dr.Sana Janakat 14-12-2011

Celiac DiseaseCeliac Disease

Jordan University of Science and TechnologyFaculty of AgricultureDepartment of Nutrition and Food science

© 2004, 2002 Elsevier Inc. All rights reserved.

Outline:Outline:

What is Celiac Disease?

What is gluten

Signs and Symptoms

Mechanism Of Action

Risk Factors for Celiac Disease

Diagnosis

Pathology

What is Celiac Disease?

What is gluten

Signs and Symptoms

Mechanism Of Action

Risk Factors for Celiac Disease

Diagnosis

Pathology


Outline…..cont:Outline…..cont:

Treatment

Follow-up

Summary

References

Treatment

Follow-up

Summary

References


Celiac Disease:Celiac Disease:

Malabsorption damaged small intestine

Inherited Autoimmune Disorder

Intolerance to Gluten Wheat, Ray and Barley

Malabsorption damaged small intestine

Inherited Autoimmune Disorder

Intolerance to Gluten Wheat, Ray and Barley


Celiac Disease−CauseCeliac Disease−Cause

Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000. Updated by Peter L. Beyer, 2002.


What is gluten?What is gluten?

THE Protein flour that form the structure of dough

Specific peptide fraction of Protein Found in: Wheat Rye Barely

Glutenins, Secalinus Hordenis

Gliadins.

THE Protein flour that form the structure of dough

Specific peptide fraction of Protein Found in: Wheat Rye Barely

Glutenins, Secalinus Hordenis

Gliadins.


What are symptoms of CD:What are symptoms of CD:


Small Intestine villi:Small Intestine villi:

Absorption

Normal villiFlattened villi

Malabsorption


Celiac Disease−PathophysiologyCeliac Disease−Pathophysiology

(Adapted from Bray GA. Gray DS, Obesity, part 1: Pathogenisis. West J Med 149:429, 1988; and Lew EA, Garfinkle L; Variations in mortality by weight among 750,000 men and women. J Clin Epidemiol 32:563, 1979.)



Mechanism:Mechanism:

Body attacks normal tissue resulting in damage to lining of small intestinal villi

Villi contain blood vessels which absorb nutrients

Villi increase area for absorption of nutrients

Body attacks normal tissue resulting in damage to lining of small intestinal villi

Villi contain blood vessels which absorb nutrients

Villi increase area for absorption of nutrients


Mechanism…..cont.:Mechanism…..cont.:

Digested nutrients are carried away by circulating blood

If villi are damaged, vitamins, minerals, calcium, carbohydrates, protein, and fats are not absorbed well

Digested nutrients are carried away by circulating blood



Mechanisms:Mechanisms:


Mechanism:Mechanism:


Risk Factor of CDRisk Factor of CD

Malignant disease: lymphomas

Deficiencies in folic acid, vitamin B12, fat-soluble & vitamins

Increased mortality due to increased risk of malignancy

Type 1 diabetes mellitus

Arthritis, Osteoporosis

Malignant disease: lymphomas

Deficiencies in folic acid, vitamin B12, fat-soluble & vitamins

Increased mortality due to increased risk of malignancy

Type 1 diabetes mellitus

Arthritis, Osteoporosis


Risk Factor….cont:Risk Factor….cont:

endomysial antibody negative

few respond to steroids

Down syndrome

Unexplained iron-deficiency anemia

Dermatitis herpetiformis

endomysial antibody negative

few respond to steroids

Down syndrome

Unexplained iron-deficiency anemia

Dermatitis herpetiformis


Dermatitis Herpetiformis:Dermatitis Herpetiformis:


Differential Diagnosis of Celiac Disease Differential Diagnosis of Celiac Disease

Anorexia nervosa

Autoimmune enteropathy

Bacterial overgrowth

Collagenous sprue

Crohn's disease

Human immunodeficiencyvirus enteropathy

Infective gastroenteritis

Anorexia nervosa

Autoimmune enteropathy

Bacterial overgrowth

Collagenous sprue

Crohn's disease

Human immunodeficiencyvirus enteropathy

Infective gastroenteritis

Irritable bowel syndrome

Ischemic enteritis

Lactose intolerance

Pancreatic insufficiency

Soy protein intolerance

Intestinal lymphoma

Irritable bowel syndrome

Ischemic enteritis

Lactose intolerance

Pancreatic insufficiency

Soy protein intolerance

Intestinal lymphoma


Haw is celiac disease diagnosed:Haw is celiac disease diagnosed:

Initial Blood Tests

Historical evaluated

Serology tests

Biopsy of small intestine

Initial Blood Tests

Historical evaluated

Serology tests

Biopsy of small intestine


Other Ways CD can Present:Other Ways CD can Present:

Dermatitis Herpetiformis Silent Celiac Latent Celiac

Dermatitis Herpetiformis Silent Celiac Latent Celiac

.Blood test +

.Biopsy -

.Clinical - symptoms

.Biopsy +

.Clinical -symptoms.Blood test +

.skinManifestation . 90% have no GI symptoms


Serology TestsSerology Tests

Kind subscription

Anti-tissue transglutaminase antibody (tTG – IgA and IgG)

most sensitive

Anti-endomysial antibody (EMA-IgA

highly specific marker

Anti-deaminated gliadin peptide (DGP – IgA and IgG)

(-) tTG or EMA OR IgA deficient

Anti-gliadin antibody (AgA – IgG and IgA)

used for children < 2 yr


Endoscopic and biopsy findings in patients with and without celiac diseaseEndoscopic and biopsy findings in patients with and without celiac disease

Normal small intestine

Celiac Disease

Normal villi

Villous atrophy


Normal Human Duodenal Mucosa (A) and Peroral Small Bowel Biopsy Specimen (B) from a Patient with Gluten Enteropathy

Normal Human Duodenal Mucosa (A) and Peroral Small Bowel Biopsy Specimen (B) from a Patient with Gluten Enteropathy

(From Floch MH. Nutrition and Diet Therapy in Gastrointestinal Disease. New York: Menum Medical Book Co., 1981)


Diagnostic:Diagnostic:


COROLLARY: ALWAYS TEST FOR TOTAL SERUM IGA WHEN LOOKING FOR CELIAC DISEASECOROLLARY: ALWAYS TEST FOR TOTAL SERUM IGA WHEN LOOKING FOR CELIAC DISEASE

In this subset of patients, research shows that IgG-EMA and IgG-TTG can be detected and are as sensitive and as specific for the diagnosis of celiac disease.

In this subset of patients, research shows that IgG-EMA and IgG-TTG can be detected and are as sensitive and as specific for the diagnosis of celiac disease.


Pathology:Pathology:

many mucosal enzymes are altered due to the damage to the absorptive cells

decrease in disaccharides, peptidases, alkaline phosphatase, ATPase, and esterase Length of small intestine varies from patient to patient

correlates with severity of clinical symptoms

usually proximal small intestine more severely involved

many mucosal enzymes are altered due to the damage to the absorptive cells

decrease in disaccharides, peptidases, alkaline phosphatase, ATPase, and esterase Length of small intestine varies from patient to patient

correlates with severity of clinical symptoms

usually proximal small intestine more severely involved


Pathology:Pathology:

Loss of normal villous structure

increase in the number of intraepithelial lymphocytes and gamma/delta T cells

These changes decrease the amount of epithelial surface available for digestion and absorption in the involved bowel

Loss of normal villous structure

increase in the number of intraepithelial lymphocytes and gamma/delta T cells

These changes decrease the amount of epithelial surface available for digestion and absorption in the involved bowel


Treatment: Treatment:

THE GLUTEN FREE DIET CAN BE LOW IN:

High protein

High calorie

High Iron , folic acid, vit B12 , A, K, and D as water soluble B vitamins (thiamine, riboflavin, niacin, folate)

Calcium

Zinc

Magnesium

Fiber

THE GLUTEN FREE DIET CAN BE LOW IN:

High protein

High calorie

High Iron , folic acid, vit B12 , A, K, and D as water soluble B vitamins (thiamine, riboflavin, niacin, folate)

Calcium

Zinc

Magnesium

Fiber


Treatment:Treatment:

The only treatment is the lifelong adherence to the gluten-free diet.

Gluten small intestine start to heal

overall health improves

The only treatment is the lifelong adherence to the gluten-free diet.

Gluten small intestine start to heal

overall health improves


Fallow Up:Fallow Up:

Serologic markers (serum IgA tTG) used to monitor compliance with a gluten-free diet

Antibody levels return to normal within three to 12 months of starting a gluten-free diet.

A repeat small bowel biopsy three to four months after initiation of a gluten-free diet is not necessary if the patient responds appropriately to therapy.

If the patient does not respond as expected despite adherence to a gluten-free diet, the physician should consider diseases that may mimic celiac disease.

Serologic markers (serum IgA tTG) used to monitor compliance with a gluten-free diet

Antibody levels return to normal within three to 12 months of starting a gluten-free diet.

A repeat small bowel biopsy three to four months after initiation of a gluten-free diet is not necessary if the patient responds appropriately to therapy.

If the patient does not respond as expected despite adherence to a gluten-free diet, the physician should consider diseases that may mimic celiac disease.


Celiac Disease−Medical and Nutritional ManagementCeliac Disease−Medical and Nutritional Management



Summary:Summary:

People with celiac disease cannot tolerate gluten, a protein in wheat, rye, and barley.

Untreated celiac disease damages the small intestine and interferes with nutrient absorption.

Without treatment, people with celiac disease can develop complications such as osteoporosis, anemia, and cancer.

A person with celiac disease may or may not have symptoms.

People with celiac disease cannot tolerate gluten, a protein in wheat, rye, and barley.

Untreated celiac disease damages the small intestine and interferes with nutrient absorption.

Without treatment, people with celiac disease can develop complications such as osteoporosis, anemia, and cancer.

A person with celiac disease may or may not have symptoms.


Summary:Summary:

Celiac disease is treated by eliminating all gluten from the diet. The gluten-free diet is a lifetime requirement.

A dietitian can teach a person with celiac disease about food selection, label reading, and other strategies to help manage the disease.


Diagnosis involves blood tests and, in most cases, a biopsy of the small intestine.

Celiac disease is treated by eliminating all gluten from the diet. The gluten-free diet is a lifetime requirement.

A dietitian can teach a person with celiac disease about food selection, label reading, and other strategies to help manage the disease.


Diagnosis involves blood tests and, in most cases, a biopsy of the small intestine.


References:References:

Celiac Disease: Diagnostic clues to Unmaskan Imposter Malnick, Stephen, MD. Postgraduate Medicine 1997; 101: 239-244

Presutti J,Cangemi J, Cassidy H, Hill D, Celiac Disease. American Family Physician. December 15, 2007: 1795-1802

Lancet. 2003 Aug 2;362(9381):383-91.Celiac disease. Green PH, Jabri B.

Department of Medicine, Columbia University College of Physicians and Surgeons, New York 10032, USA [email protected]

Celiac Disease: Diagnostic clues to Unmaskan Imposter

Malnick, Stephen, MD. Postgraduate Medicine 1997; 101: 239-244

Krause's book 2008. 681-684 (1352)-Disease of the small intestine-celiac disease

Celiac Disease: Diagnostic clues to Unmaskan Imposter Malnick, Stephen, MD. Postgraduate Medicine 1997; 101: 239-244

Presutti J,Cangemi J, Cassidy H, Hill D, Celiac Disease. American Family Physician. December 15, 2007: 1795-1802

Lancet. 2003 Aug 2;362(9381):383-91.Celiac disease. Green PH, Jabri B.

Department of Medicine, Columbia University College of Physicians and Surgeons, New York 10032, USA [email protected]

Celiac Disease: Diagnostic clues to Unmaskan Imposter

Malnick, Stephen, MD. Postgraduate Medicine 1997; 101: 239-244

Krause's book 2008. 681-684 (1352)-Disease of the small intestine-celiac disease


Reference: Reference:

Presutti J,Cangemi J, Cassidy H, Hill D, Celiac Disease. American Family Physician. December 15, 2007: 1795-1802. 5. 1981.)

Celiac disease: http://www.nature.com/mi/journal/v2/n1/fig_tab/mi200875f1.html#figure-title.

INSERM U793, University Paris Descartes, Paris, France Correspondence: N Cerf-Bensussan, ([email protected]) Received 8 October 2008; Accepted 8 October 2008; Published online 29 October 2008.

From Floch MH. Nutrition and Diet Therapy in Gastrointestinal Disease. New York: Menum Medical Book Co.,

Presutti J,Cangemi J, Cassidy H, Hill D, Celiac Disease. American Family Physician. December 15, 2007: 1795-1802. 5. 1981.)

Celiac disease: http://www.nature.com/mi/journal/v2/n1/fig_tab/mi200875f1.html#figure-title.

INSERM U793, University Paris Descartes, Paris, France Correspondence: N Cerf-Bensussan, ([email protected]) Received 8 October 2008; Accepted 8 October 2008; Published online 29 October 2008.

From Floch MH. Nutrition and Diet Therapy in Gastrointestinal Disease. New York: Menum Medical Book Co.,


Reference:Reference:

www.CeliacHealth.org

www.Celiac.org

www.glutenfree.com

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health NIH Publication No. 08–4269 September 2008

1Fasano A, Berti I, Gerarduzzi T, et al. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States. Archives of Internal Medicine. 2003;163(3):268–292. 2Ibid.

www.CeliacHealth.org

www.Celiac.org

www.glutenfree.com

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health NIH Publication No. 08–4269 September 2008

1Fasano A, Berti I, Gerarduzzi T, et al. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States. Archives of Internal Medicine. 2003;163(3):268–292. 2Ibid.


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celiac disease

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