Gliadin AB - IgG

General information:

Gluten enteropathy (celiac disease) is a chronic disease affecting both children and adults, predominantly in women, with the target organ being the small intestine, atrophy of the villous apparatus and leading to maldigestion and malabsorption. GE is characterized by immune-mediated damage to the jejunal mucosa that develops in genetically susceptible individuals from gluten ingestion. GE sufferers cannot tolerate gliadin, the alcohol-soluble fraction of gluten. Gluten, on the other hand, is a protein found in wheat, rye, barley and oats. Some patients tolerate oats without any consequences, but strict control and individual assessment is necessary. When GE patients take gliadin, their small intestinal mucosa is damaged by an immunologically mediated inflammatory reaction, ultimately leading to malabsorption. In its classic form, celiac disease presents with growth retardation, weight loss and diarrhea, but in atypical forms there may be mild or absent symptoms. Various risk factors have been described that increase the possibility of developing GE:

• Family burden.
• Caucasian race.
• European origin.
• Female.
• Type 1 diabetes, early osteoporosis
• Dermatitis herpetiformis, Down syndrome, iron deficiency anemias, delayed puberty
• The quantity and quality of gluten in food may play a role as a risk factor. Early feeding of gluten-containing foods may be a risk factor for later onset of GE.
• Certain infections can facilitate an immune response to gluten leading to GE. Antibodies directed against the VP7 capsid of rotaviruses cross-react with tissue transglutaminase, the major autoantigen in GE.

Tissue transglutaminase antibody testing, anti-gliadin antibodies in combination with anti-gliadin antibodies and anti-deamidated gliadin antibodies aid in diagnosis in patients with suspected gluten enteropathy The enzyme tissue transglutaminase is the most important autoantigen in GE. Therefore, the determination of antibodies against it is of primary importance for the detection of GE in children and adults. Gliadin peptides in complex with the tissue transglutaminase of the organism itself bind to molecules DQ2, DQ7, DQ8 of HLA and activate gliadin-specific T-cells. The result is chronic inflammation of the intestinal mucosa. False-negative GE samples in IgA testing can be found in cases with selective IgA deficiency. Therefore, it is good to test the level of IgA. In case of deficiency, the corresponding IgG is determined.

Antibody: IgA tissue anti-transglutaminase antibodies Sensitive (%): 95 Spec.(%): 90 Course: Corresponds to IgA anti-endomysium antibodies

Sample required:

Venous blood

Key words:

Gliadin ab IgG