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With some early onset and a large percentage of late onset disease, other disorders appear prior to the coeliac diagnosis [1] or allergic-like responses (IgE or IgA, IgG) markedly increased in GSE. Many of these disorders persist on a strict gluten-free diet (GF diet or GFD), and are thus independent of coeliac disease after triggering.
The IgG antibody is similar to AGA IgA, but is found at higher levels in patients with the IgA-less phenotype. It is also associated with coeliac disease and non-celiac gluten sensitivity. [5] [6] [7] Anti-gliadin antibodies are frequently found with anti-transglutaminase antibodies.
The IRP response differs from typical responses that stimulate IL15 release, such as viral infection. In addition, other cytokines such as IL12 and IL2, which are typically associated with T-helper cell stimulation, are not involved. In these two ways the innate peptide activation of T-cells in coeliac disease is strange.
[27] [28] Additional testing has been conducted using IgA trans-glutaminase autoantibodies which has been identified as a specific and sensitive for the detection of celiac disease. [ 29 ] [ 30 ] Henoch–Schönlein purpura (HSP) is a systemic vasculitis caused by deposits of IgA and complement component 3 (C3) in small blood vessels.
Of note, selective IgA deficiency can complicate the diagnosis of one such condition, celiac disease, as the deficiency masks the high levels of certain IgA antibodies usually seen in celiac disease. [18] As opposed to the related condition CVID, selective IgA deficiency is not associated with an increased risk of cancer. [19]
Most attention to anti-transglutaminase antibodies is given with respect to celiac disease. A recent study of children published in 2007 demonstrated that the level of ATA in correlates with the scalar Marsh score for the disease in the same patient. [9] High levels of ATA are found in almost all instances of celiac disease. [10]
A four-of-five rule was proposed 2010 for confirming celiac disease, with the disease confirmed if at least four of the following five criteria are satisfied: [2] [68] typical symptoms of celiac disease; positivity of serum celiac disease immunoglobulin, A class autoantibodies at high titer; human leukocyte antigen (HLA)-DQ2 or DQ8 genotypes;
There are indications that patients with non-coeliac gluten sensitivity show a reappearance of symptoms in far shorter time than is the case for coeliac disease: in non-coeliac gluten sensitivity, symptoms usually relapse in a few hours or days of gluten challenge. [13] [14]