Neuronal Transglutaminase Antibodies

Determination of anti-neuronal transglutaminase IgA and IgG antibodies for persons with gluten intolerance

Transglutaminase (TGs) – what they are, what they do, and when you should test for auto-antibodies against TGs
The transglutaminases form an enzyme family belonging to the transferases. Transglutaminases catalyse the acyl transfer of protein-bound glutamine residues to primary amines. In humans there are 8 different TGs known. Tissue transglutaminase (TG2) is known from celiac disease diagnosis, TG3 from the diagnosis of autoimmune diseases of the skin (e. g. Dermatitis herpetiformis Duhring). TG6 is the transglutaminase of the central nervous system. Dysfunctions of transglutaminases are of clinical relevance.

What is an ataxia and what does it have to do with TGs?
Ataxia is a disorder of movement coordination. Movements are not performed in the right scope or in a coordinated manner. There is evidence that ataxia may also have immunological causes. In ataxia in combination with already diagnosed celiac disease, one should look for the differential diagnosis of ataxia for antibodies against TG6. Although the clinical spectrum of celiac disease usually refers to the gastrointestinal tract, sometimes to the skin, it can also affect the nervous system. Extra-intestinal manifestations of celiac disease may include: epilepsy and headache (especially in children) and cerebellar ataxia and extra-cerebellar concomitant symptoms such as peripheral neuropathy. These neurological manifestations and dysfunctions of celiac disease also occur in similar form in non-celiac gluten sensitivity (NCGS). Anti-gliadin antibodies (typical of celiac disease) and anti-TG2 / 3 antibodies are not found in NCGS. That is why you do not immediately correlate these neurological disorders to the diet.
In the neurological context, NCGS may continue to cause behavioral problems, depression or hyperactivity. If these symptoms are present, an indication to test for TG6 antibodies is based in the therapeutic consequence, because patients with gluten ataxia can benefit from a gluten-free diet.
In addition to celiac disease, anti-hnTG6 antibodies were also diagnosed in a number of other neurological disorders:
Polio, schizophrenia and amyotrophic lateral sclerosis. Therefore, testing is in this context useful as well.


Conclusion
•    Autoantibodies against transglutaminase 6 (neuronal transglutaminase) have been demonstrated in patients with gluten ataxia but may also be present in other gluten-sensitive neurological symptoms (anti-hnTG6 IgA or IgG).
•    Apparently, patients with gluten-sensitive diseases have an anti-TG immune response that can trigger a systemic autoimmune disease.
•    Gluten-free diets significantly reduce the level of anti-hnTG6 antibodies in gluten-sensitive patients. This means that this group of patients benefits from TG6 diagnostics and a standard therapy being complemented with a gluten-free diet.

New products:
•    anti-human-neuronal Transglutaminase IgA (anti-hnTG6 IgA) (K 9388)     (sample matrix is plasma and serum)
•    anti-human-neuronal Transglutaminase IgG (anti-hnTG6 IgG) (K 9389)     (sample matrix is plasma and serum)


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