Auteur Topic: Tissue Transglutaminase Antibodies in Indiv. with Celiac Disease Bind to Thyroid  (gelezen 3596 keer)


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Een artikel in MaryAnnLiebert, het officiele journaal van de Amerikaanse Thyroid Assoiatie.

De 1e paar kolommen - zie de link - is vrij te lezen.

Thyroid. November 2008
Tissue Transglutaminase Antibodies in Individuals with Celiac Disease Bind to Thyroid Follicles and Extracellular Matrix and May Contribute to Thyroid Dysfunction

1Department of Medicine, Celiac Disease Center at Columbia University, College of Physicians and Surgeons, New York, New York.
2Department of Medicine, Tulane University Medical Center, New Orleans, Louisiana.
3National Cancer Center, Kyonggi-do, Republic of Korea.
4Department of Medicine, Sound Shore Medical Center, New Rochelle, New York.
5Department of Pathology, College of Physicians and Surgeons, Columbia University.

Department of Medicine
Celiac Disease Center at Columbia University

College of Physicians and Surgeons

Individuals with active celiac disease (CD+) have an increased incidence of thyroid dysfunction, which improves on a gluten-free diet (CD−).
We investigated whether tissue transglutaminase-2 IgA antibodies (anti-TGase II) present in sera of patients with celiac disease react with thyroid tissue and possibly contribute to thyroid disease.

Serum from 40 active celiac patients taken before a gluten-free diet (CD+), 46 patients on a gluten-free diet (CD−), 40 normal controls (NC), and 25 with Crohn's disease (CROHN) was used.
All sera were screened for antithyroperoxidase antibodies (TPO-AB) and thyroglobulin antibodies (TG-AB), and indirect immunofluorescence (IIF) was performed on primate thyroid tissue sections using TPO-AB– and TG-AB–negative sera.

IIF with thyroid seronegative, anti-TGase II–positive CD+ sera (n=23) demonstrated staining of thyroid follicular cells and extracellular matrix, in an identical pattern with monoclonal anti-human TGase II antibody.
Evidence of TGase II as the antigen in thyroid tissue was supported by elimination of the IIF pattern when sera were depleted of anti-TGase II by pretreatment with human recombinant TGase II.
No staining of thyroid tissue was observed when sera from CD+ patients that were negative for TGase II antibodies, or sera from NC subjects were used.
Thyroid antibodies were found in 43% of CD+ patients, significantly higher than NC and CROHN patients (p<0.0001).
In addition, a positive correlation was observed between anti-TGase II and TPO-AB titers (p=0.0001; r=0.63).

Anti-TGase II antibodies bind to TGase II in thyroid tissue, and titers correlate with TPO antibody titers.
These findings suggest that anti-TGase II antibodies could contribute to the development of thyroid disease in celiac disease.

Groeten, Ine