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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]
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 release of IL15 is a major factor in coeliac disease as IL15 has been found to attract intraepithelial lymphocytes (IEL) that characterize Marsh grade 1 and 2 coeliac disease. [6] Lymphocytes attracted by IL-15 are composed of markers enriched on natural killer cells versus normal helper T-cells .
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]
[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.
Coeliac disease is associated with immune complex glomerulonephritis. [102] Anti-gliadin IgA antibodies are found also more commonly in patients with IgA Nephropathy. The paper finds a link between GSE and IgA Nephropathy, but not between CD and nephropathy. [103] Calcium oxalate correlates with severity of fat malabsorption in coeliac disease.
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;
As antibody-negative coeliac disease is recognised, HLA status, persistence or progression of the duodenal IEL numbers following a gluten challenge, followed by symptomatic improvement on a gluten-free diet, has been used to be more certain about the diagnosis, which was made in 22% of one series of over 200 adult cases.