Celiac disease and Sprue

What sample is needed for Gliadin Antibodies IgA and IgG?

1. Collect the venous blood to prepare the serum.
2. A fasting sample is not necessary.
3. An intestinal biopsy may be advised, and it gives characteristic changes.

What are the Indications for Gliadin Antibodies IgA and IgG?

1. These antibodies are detected in gluten-sensitive enteropathy.
2. This test is done to diagnose Celiac disease and sprue.
3. These antibodies are used to monitor the disease.
4. In successful treatment with a gluten-free diet, these antibodies will disappear from the serum.

What are the precautions for Gliadin Antibodies?

1. Other gastrointestinal diseases, such as colitis, Crohn’s disease, and lactose intolerance, can elevate Gliadin antibody levels.
2. Get the list of foods eaten in the last 24 hours.

How will you define Celiac disease/Sprue?

1. It is also called Celiac disease, Gluten-sensitivity enteropathy, nontropical sprue, or idiopathic steatorrhea.
2. Gluten-induced enteropathy includes Sprue and Celiac disease.
   1. Both diseases predominantly involved the duodenum and jejunum.
3. Celiac disease:
   1. It is sometimes called non-tropical sprue, celiac sprue, or gluten-sensitive enteropathy.
   2. Celiac disease is an autoimmune multisystem disease.
   3. Celiac disease is also called childhood non-tropical sprue.
   4. A gluten-free diet cures celiac disease.
4. The sprue:
   1. It is an infectious process that is cured by antibiotics.
   2. Sprue is a broad, nonspecific term that encompasses several conditions characterized by small-intestinal malabsorption.
   3. Sprue is a nonspecific term for celiac disease and is also known as celiac sprue.
   4. It also includes tropical sprue and non-celiac gluten sensitivity.
   5. Tropical sprue is similar to celiac disease, but it occurs in tropical regions with different underlying causes.
   6. In short, Sprue is a broad term that includes celiac disease and other conditions with similar symptoms and malabsorption.

How will you differentiate between Celeic disease and sprue?

How will you discuss the epidemiology of Celiac disease?

1. It is found predominantly in Europe and, uncommonly, in African Americans.
2. It is rare in Asia.
3. It is 10-15 times more common in IgA-deficient individuals.
4. It is 1% to 3% in patients with type 1 diabetes mellitus.
5. There is an association between T-cell lymphoma and juvenile rheumatoid arthritis.

How will you discuss the pathogenesis of Celiac disease and sprue?

1. Celiac disease is also called Gluten-sensitive enteropathy, Nontropical sprue, or idiopathic steatorrhea.
2. Celiac diseaseia an autoimmune multisystem disorder, mainly present in the GI tract.
3. Gliadin is the toxic protein of gluten.
   1. There is mucosal injury by the complex of gliadin.
   2. Gliadin is present in wheat, rye, barley, and oats.
   3. Gliadin, along with tissue transglutaminase, causes mucosal injury.
4. The findings are due to malabsorption and autoimmunity.
5. Meanwhile, sprue is a broad term that encompasses malabsorption, as in celiac disease.

What is the mechanism of Celiac disease?

1. Gliadin is the complex of gluten and tissue transglutaminase (Gluten + Transglutaminase).
2. Tissue transglutaminase is present in the thin connective tissue covering the muscles.
3. Gliadin is the toxic protein of gluten.
   1. Gluten = Gliadin + tissue transglutaminase.
4. The small bowel (mainly duodenum and jejunum) tissue Transglutaminase is the auto-antigen.
5. The disease’s pathogenesis is believed to involve an interaction between transglutaminase and the gliadin peptide in genetically susceptible individuals.
6. In both conditions (celiac disease and sprue), T-lymphocytes mediate an immune reaction against gluten.
   1. Gluten is found in wheat, rye, barley, and maybe oats.
7. There is a genetic predisposition, and it runs in families.
8. 10% of the first-degree relatives have this disease.
9. There is an association with HLA-DR3 in 90% of patients, and the same is true for dermatitis herpetiformis.
   1. Another reference states that a genetic component is present on the HLA chromosome 6.
10. The major toxic protein of wheat is gliadin.
11. There is sensitivity to Gliadin (gluten), which is the protein found in:
    1. Wheat.
    2. Wheat products.
    3. Rye.
    4. Barley.
    5. Possible oats.

What antibodies/antigens form in Celiac disease?

1. Antibodies to gliadin are toxic agents in celiac disease.
2. Patients with celiac disease cannot tolerate the proteins gliadin + gluten in wheat or wheat products.
3. Gliadin + gluten are toxic to the small intestinal mucosa and lead to characteristic pathologic changes seen on biopsy.
4. Endomycelium: It is a thin layer of connective tissue surrounding the muscle.
5. These patients develop antibodies against:
   1. Gliadin = anti-gliadin antibody (IgA and IgG)
   2. Endomysial = anti-endomysial antibody.
   3. Tissue = anti-tissue transglutaminase.

6. These patients have severe intestinal malabsorption.
7. The only treatment for these patients is to avoid wheat and wheat products.
8. These antibodies are present in the mucosa and the blood.
9. Celiac disease starts in infancy when cereals are given to the baby.
10. IgG-antigliadin antibody is more sensitive but less specific than IgA.
11. Anti-gliadin antibodies are found in 95% of those with Celiac disease and nontropical sprue.
    1. Anti-IgG gliadin antibodies are found in 96% to 97% of untreated patients. 80% may have Celiac disease.
    2. Anti-IgA gliadin antibodies are found in 75% of cases and are 95% specific for Celiac disease.
    3. Anti-gliadin IgG and IgA antibodies are positive in 45% to 85% of cases of dermatitis herpetiformis.
    4. False positive cases are seen in ulcerative colitis and Crohn’s disease.

What are the pathological changes in Celiac disease?

What are the signs and symptoms of Celiac disease?

1. Mostly, symptoms appear in children when they start eating cereals.
2. The most common presentation is:
   1. There is easy fatigability.
   2. There is abdominal bloating and pain.
   3. There may be vomiting.
   4. The patient will have chronic diarrhea.
   5. The stool is foul-smelling, pale, and fatty.
   6. Sometimes these patients become constipated.
   7. The stool is hard to flush.
   8. There are aphthous ulcers.
   9. The patient will experience weight loss.
   10. These children are irritable.
   11. Delay in the growth pattern.
   12. Sometimes, it is difficult to thrive, and the patient may have osteomalacia.
   13. There is a strong association with other autoimmune diseases like type 1 diabetes mellitus and autoimmune thyroid diseases.

What are the complications of Celiac disease?

1. There is anemia.
2. 15% to 20% of patients develop intestinal lymphoma or adenocarcinoma.
3. There is an increased incidence of gastric and esophageal carcinoma.
4. There may be neuropathy.
5. These patients may have hyposplenism.

What is the normal Gliadin-antibody?

• Values are given for the child of age >2 years:
  • Negative = <25 U/L .
  • Weak positive = 25 to 50 U/L.
  • Positive = >50 U/L.

Source 6

• Gliadin IgA/IgG = 0 to 2 years = <20 EU.
  • 0 to 3 years and older = <25 EU.
• Endomysial IgA = all ages = negative.
• Tissue transglutaminase IgA = all ages = <20 EU.

How will you diagnose celiac disease?

1. An elevated level of anti-gliadin and anti-endomysial antibodies.
   1. IgA and IgG antibody sensitivity are 90% for the active, untreated disease. When both antibodies are done, the specificity is also 90%.
2. These antibodies will detect the following diseases:
   1. Celiac disease will have 100% IgA endomysial antibodies.
   2. Celiac sprue.
3. Anti-IgA endomysial antibody:
   1. It is the antibody test of choice for diagnosing celiac disease.
   2. This antibody can be used to screen the population.
4. Anti-gliadin IgA antibody:
   1. This antibody disappears after 3 to 6 months of gluten abstinence.
   2. It may be used to monitor the diet restriction.
   3. It is the best marker for children under <3 years old.
   4. Gliadin is a component of gluten.
5. Anti-IgA transglutaminase antibody:
   1. False results may occur in IgA deficiency.
   2. More reproducible than anti-IgA endomysial antibodies.
6. Dermatitis herpetiformis 70% shows IgA endomysial antibodies.
7. Intestinal (jejunum) biopsy shows typical changes in villous atrophy.
   1. On jejunal biopsy, we will see villous atrophy.
   2.  Increased intra-epithelial lymphocytic infiltrate.
   3. There is hyperplasia of the crypts.
      1. These changes may reverse on a gluten-free diet. This will not occur in the sprue.
8. In Celiac disease, anemia may be macrocytic or hypochromic microcytic.

What are the serological tests for Celiac disease?

What are the diagnostic criteria for the Celiac disease?

1. Provisional diagnosis:
   1. Positive serological (anti-gliadin antibody) test.
   2. Typical pathological findings on biopsy of the small intestine.
2. The confirmatory test is:
   1. When a gluten-free diet is given, patients become symptom-free.
   2. Serological tests fall within the normal range or are negative.
   3. The pathological changes will improve or disappear if a biopsy is done.

How will you treat Celiac disease?

1. Start a permanently gluten-free diet.
2. Avoid wheat, barley, rye, and oats.
   1. Another reference excludes oats, which are allowed in the list of edible foods. Be sure there is no mixing of wheat, barley, or rye.
3. Or any food containing them, like bread, cake, and pies.
4. Rice, soya, potatoes, maize, jam, and sugar are allowed.
5. Gluten-free flour, bread, and pasta are available.
6. Try steroids if diet therapy is not helpful.

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