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Gluten is the general name given to a protein that is present in various types of cereals, from the most common such as wheat, barley, oats and rye to einkorn, triticale, spelled, farro and kamut. Among its functions is that of acting as a binding element in pastry and bakery doughs, contributing to the union of the rest of the ingredients and the water molecules they contain, and achieving a firm consistency.
What is celiac disease?
Celiac disease, also known as celiac disease or gluten-sensitive enteropathy, is an autoimmune disease developed in genetically predisposed people and in which one of the main triggers is the consumption of gluten. It is characterized by an inflammation of the mucosa of the small intestine.
This digestive and genetic disease causes lesions in the small intestine and causes the absorption of nutrients contained in food to be altered, in addition to conditioning an alteration in the permeability of the intestinal mucosa. All this can be the origin of the appearance of symptoms, both digestive and extra-digestive.
According to current estimates, celiac disease affects between 1 and 2 percent of the population throughout their lives. It affects both children and adults of all ages. The female/male ratio is 2/1.
There is an alteration that occurs with a pathological response to the consumption of gluten in which the analytical patterns of celiac disease are not manifested. In other words, the results of the intestinal biopsy are not compatible with those of celiac disease and both the tests to assess the genetic and serological markers provide negative results. This alteration is called non-celiac gluten sensitivity and it is very likely that it is the consequence of a hypersensitivity process, either type I, III or IV, against gluten.
Genetic implication in celiac disease.
More than 90% of celiac patients present the HLA DQ2 protein heterodimer, either encoded by the HLA DQA1*05 and DQB1*02 alleles in the cis position (haplotype DQ2.5), more common in central and northern Europe, or in trans position (combination of haplotypes DQ7.5 [alleles DQA1*05 and DQB1*03:01] and DQ2.2 [alleles DQA1*02 and DQB1*02]), more frequent in the Mediterranean basin. The remainder show the second risk heterodimer, HLA DQ8 (encoded by the DQA1*03 and DQB1*0302 alleles), or carry one of the separate HLA DQ2 alleles, DQB1*02 (as part of the DQ2 molecule. 2) or DQA1*05 (in the DQ7.5 molecule). On the other hand, there are some publications that attribute risk of celiac disease (CD) to the HLA DQ9 heterodimer, specifically DQ9.3 (DQA1*03 and DQB1*0303 alleles), but its relationship with the disease has not yet been well established. . HLA genetic testing can be performed using different approaches as described below. In addition to knowing the risk haplotypes that the patient may have, it is interesting to know the genetic load (1 or 2 copies) of DQB1*02 (DQ2) and DQB1*0302 (DQ8). The interpretation of the results of the genetic study in an individual allows establishing several risk groups based on the alleles that it possesses. The greatest risk is attributed to carriers of the DQ2 heterodimer with two copies of the DQB1*02 allele, such as DQ2.5/DQ2.5 homozygotes and DQ2.5/DQ2.2 heterozygotes; reducing the risk in carriers of a single copy of the DQB1*02 allele and in HLA DQ8 homozygotes (DQ8/DQ8). The isolated presence of the DQA1*05 allele does not rule out CD, although it can be excluded in those genotypes without any risk allele. The 30% of the healthy population presents some of these haplotypes, therefore HLA-DQ genetic typing should be used to support the diagnosis of CD, and has a high negative predictive value, allowing the exclusion of the disease with a certainty 99% .
What does this test consist of (Complete typing HLA-DQA1/DQB1.)?
Detection of all types of DQ, those related to EC (DQ2.5, DQ2.2, DQ7.5, DQ8) and those not currently related (for example DQ5, DQ6, etc). By studying all the possible haplotypes encoded by the DQA1 and DQB1 genes, this test is able to identify the genetic load of all the DQs involved in CD.
For which people is this study indicated?
Traditionally, the diagnosis of CD was based on an intestinal biopsy when positive IgA anti-transglutaminase antibodies were detected. At the ESPGHAN (European Society for Pediatric Gastroenterology, Hepatology and Nutrition) meeting convened in 2012, a new diagnostic scheme was proposed that includes HLA typing as the first option in asymptomatic patients but at risk of developing the disease. In children/adolescents with symptoms and positive anti-transglutaminase IgA antibodies with a high value, HLA typing is proposed and if it is positive, CD is confirmed without the need for biopsy.
It would be justified or interesting to carry out a genetic test on people who meet any of the following requirements:
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30 N Gould Ste N, Sheridan, WY 82801, USA
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