This may be more than you are interested in knowing...
As for antigliadin vs. deamidated antigliadin antibodies... here is some additonal info gathered from a recent article by Marios Hadivassiliou, a leader in gluten related neurological disease research. I'm copy/pasting this from a post I made elsewhere. Mostly, it explains that the new deamidated antigliadin antibodies are not so great for diagnosing gluten sensitivity that manifests in non-gut ways (neurological disease like ataxia, pn, migraines, or dermatitis herpetiformis which is a skin rash, or other non-gut symptoms).
Quote:
Lancet Neurol. 2010 Mar;9(3):318-330.
Gluten sensitivity: from gut to brain.
Hadjivassiliou M, Sanders DS, Grünewald RA, Woodroofe N, Boscolo S, Aeschlimann D.
Department of Neurology, Royal Hallamshire Hospital, Sheffield, UK.
Gluten sensitivity is a systemic autoimmune disease with diverse manifestations. This disorder is characterised by abnormal immunological responsiveness to ingested gluten in genetically susceptible individuals. Coeliac disease, or gluten-sensitive enteropathy, is only one aspect of a range of possible manifestations of gluten sensitivity. Although neurological manifestations in patients with established coeliac disease have been reported since 1966, it was not until 30 years later that, in some individuals, gluten sensitivity was shown to manifest solely with neurological dysfunction. Furthermore, the concept of extraintestinal presentations without enteropathy has only recently become accepted. In this Personal View, we review the range of neurological manifestations of gluten sensitivity and discuss recent advances in the diagnosis and understanding of the pathophysiological mechanisms underlying neurological dysfunction related to gluten sensitivity. Copyright © 2010 Elsevier Ltd. All rights reserved.
PMID: 20170845
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The article gives a nice review of the various neurological manifestations of gluten sensitivity and some of his more recent findings.
Of particular note is a diagnostic flowchart for a patient with possible neurological manifestion of gluten sensitivity (ataxia, peripheral neuropathy, seizures).
The blood tests to be included are:
antigliadin (AGA IgA and IgG antibodies)
anti-deamidated gliadin (DGP IgA and IgG antibodies)
anti-TG2 (TG2 IgA and IgG antibodies)
If the above are all negative, then additionally test for:
anti-TG6 (TG6 IgA and IgG antibodies... not widely available yet)
HLA DQ2 or DQ8 varients.
Quote:"In practice, it is best to do serological tests for both IgA and IgG autoantibodies to TG2 (and, if available, anti-TG6 and anti-TG3) as well as antibodies to gliadin and DGPs."
If any of the tests for gliadin, deamidated gliadin, TG2, or TG6 are positive (IgA or IgG antibodies), or HLA DQ2 or HLA DQ8 are present, then the recommendation is to proceed to biopsy.
If there is enteropathy > strict gluten free diet is warranted. If there is no enteropathy, testing for IgA deposits against TG on the biopsy should be performed (limited availability, done mostly in research so far). If deposits are found > strict gluten free diet is warranted.
Quote:Anti-TG2 antibodies are deposited in the small bowel mucosa of patients with gluten sensitivity, even in the absence of enteropathy. Furthermore, such deposits have been found in extraintestinal sites, such as muscle and liver. Widespread deposition of transglutaminase antibodies has also been found around blood vessels of the brain in patients with gluten ataxia.
In the case of an uncertain diagnosis, consideration should be given to offering strict gluten free diet particularly if there is no other aetiology and it is a progressive disease. Of note, improvement or stabilization does not occur until after a year of strict gluten free diet with serological elimination of antibodies.
SO... Hadjviassiliou's team recommends BOTH the original antigliadin antibody AND the newer anti-deamidated antibody (both IgG and IgA classes). I am happy to have this clarification and direction!
More specifically, they say this:
Quote:
"Detection of antibodies to deamidated gliadin peptides (DGP) is more specific for detection of coeliac disease than are classic AGA assays. However, unlike autoantibodies to TG2, anti-DGP antibodies can be either IgA or IgG class and not all patients have both. IgG anti-DGP has been reported to have 100% positive predictive value in adults and should therefore be included in the analysis.
At present, whether these assays are similarly sensitive for detection of neurological manifestations of gluten sensitivity is not known. Recent evidence suggests that anti-DGP antibodies might be present in only 26% of patients with gluten sensitivity who are negative for TG2 IgA. This finding is consistent with our observation of detectable anti-DGP IgA/IgG in only 25% of patients with ataxia without enteropathy who test positive for autoantibdoies to one or more transglutaminase isozymes.
They also note that IgG class antibodies to TG2 or TG6 are more common than IgA class antibodies in patients with gluten related neurological disease, in contrast to celiac disease where IgA class antbodies are more common.
Quote:IgG class antibodies are present in only 60% of patients with coeliac disease, whereas the occurrence was 90% in patients with gluten ataxia who were positive for anti-transglutaminase. This shift from IgA to IgG might reflect the target organ involved (cerebellum rather than small bowel).