Gliadin Antibodies IgA

Gliadin Antibodies and Celiac disease

Sample for Gliadin Antibodies IgA

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.

Purpose of the test (Indications) for Gliadin Antibodies IgA

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

Precautions for Gliadin Antibodies IgA

1. Other gastrointestinal diseases like colitis, Crohn’s disease, and lactose intolerance can raise Gliadin antibodies’ values.
2. Get the list of foods eaten in the last 24 hours.

Definition of  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 these diseases involved duodenum and jejunum predominantly.
3. The celiac disease sometimes is called non-tropical sprue, celiac sprue, or gluten-sensitive enteropathy.
   1. Celiac disease is an autoimmune multisystem disease.
   2. Celiac disease is also called childhood non-tropical sprue.
   3. A gluten-free diet cures the celiac disease.
   4. The sprue is an infectious process that is cured by antibiotics.
4. Celiac disease is an autoimmune phenomenon.

Epidemiology of Celiac disease:

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

Pathogenesis of Celiac disease and sprue: 

1. Celiac disease is also called Gluten-sensitive enteropathy, Nontropical sprue, or idiopathic steatorrhea.

Auto-antigens are:

1. 1. Gliadin is the complex of gluten and tissue transglutaminase.
      1. Gluten protein.
      2. The small bowel (mainly duodenum and jejunum) tissue Transglutaminase is the auto-antigen.
2. Pathogenesis of the disease is believed to involve an interaction between transglutaminase and the gliadin peptide in genetically susceptible people.
3. In both conditions (celiac disease and sprue), an immune reaction is mediated by the T-lymphocytes against gluten.
   1. Gluten is found in wheat, rye, barley, and maybe oats.
4. There is a genetic predisposition, and it runs in families.
5. 10% of the first-degree relatives run this disease.
6. There is an association in HLA DR3  in 90% of the patients and the same for dermatitis herpetiformis.
   1. Another reference says that a genetic component is present in the HLA chromosome 6.
7. The major toxic protein of wheat is gliadin.
8. There is sensitivity to Gliadin and gluten are the proteins found in:
   1. Wheat.
   2. Wheat products.
   3. Rye.
   4. Barley.
   5. Possible oats.

Antibody formation in Celiac disease:

1. Antibodies to gliadin are toxic agents in celiac disease.
2. The patient with celiac disease cannot tolerate the proteins gliadin + gluten present in wheat or wheat products.
3. Gliadin + gluten is toxic to the small intestinal mucosa and leads to characteristic pathologic changes seen on biopsy.
4. These patients develop antibodies against:
   1. Gliadin = anti-gliadin antibody (IgA and IgG)
   2. Endomysial = anti-endomysial antibody.
   3. Tissue = anti-tissue transglutaminase.

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

Gliadin Antibodies IgA: Endomysial antibody and interpretations

Pathological changes in Celiac disease:

Signs and Symptoms of Celiac disease

1. Mostly the symptoms are seen in children when they start 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.
      1. The stool is foul-smelling, pale, and fatty.
      2. Sometimes these patients will be constipated.
      3. The stool is hard to flush.
   5. There are aphthous ulcers.
   6. The patient will have weight loss.
   7. These children are irritable.
   8. Delay in the growth pattern.
   9. Sometimes it is difficult to thrive, and the patient may have osteomalacia.
   10. There is a strong association with other autoimmune diseases like diabetes mellitus type 1 and autoimmune thyroid diseases.

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.

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.

Diagnosis of celiac disease

1. An elevated level of anti-gliadin and anti-endomysial antibodies.
2. IgA and IgG antibodies sensitivity are 90% for the active untreated disease. When both antibodies are done, the specificity is also 90%.
3. These antibodies will detect the following:
   1. Celiac disease 100% will have IgA endomysial antibodies.
   2. Celiac sprue.
4. Dermatitis herpetiformis 70% shows IgA endomysial antibodies.
5. Intestinal (jejunum) biopsy shows typical changes in villous atrophy.
   1. On jejunal biopsy 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.
6. In Celiac disease, anemia may be either macrocytic or hypochromic microcytic anemia.

Serological tests for Celiac disease

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, then patients become symptoms free.
   2. Serological tests become in the normal range or negative.
   3. The pathological changes will improve or disappear if a biopsy is done.

Treatment of Celiac disease

1. Start a permanently gluten-free diet.
2. Avoid wheat, barley, rye, and oats.
   1. Another reference excludes oats and is allowed in the list of eatable foods. Be sure there is no wheat, barley, or rye mixing.
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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