Thanks!
I believe this is the report referenced:
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 then a 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). If deposits are found then a 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 the disease is on a progressive course. 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).
|