Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.
Celiac.com 12/08/2008 - Celiac disease is a life-long autoimmune enteropathy that results in damage to the small intestinal mucosa. When people with celiac disease eat the gluten proteins found in wheat, rye and barley, they damage the cells that line the small intestine, which interferes with normal digestion and absorption of nutrients. Recent studies have shown that most people present with a silent, non-diarrheal form of the disease, and show no obvious symptoms. People with celiac disease face rates of autoimmune disease that are10 times higher than the general population.
People with untreated celiac disease have higher rates of thyroid problems, which generally improve with the adoption of a gluten-free diet. A connection between the span of gluten consumption and autoimmune diseases has been observed in people with celiac disease. Tissue transglutaminase (TGase) is a ubiquitous enzyme and manifests in all tissues, with both intra- and extracellular localization.
A team of researchers recently set out determine if tissue transglutaminase-2 IgA antibodies (anti-TGase II) present in blood samples from celiac disease patients react with thyroid tissue and possibly contribute to thyroid disease.
The research team made up of doctors Afzal J. Naiyer, Jayesh Shah, Lincoln Hernandez, Soo-Youl Kim, Edward J. Ciaccio, Jianfeng Cheng, Sanil Manavalan, Govind Bhagat, and Peter H.R.Green. The team took blood samples from 40 people with active celiac disease, but not following a gluten free diet, samples from 46 celiac patients on a gluten-free diet (CD), 40 normal controls (NC), and 25 with Crohn’s disease.
They screened all samples for anti-thyroperoxidase antibodies (TPO-AB) and thyroglobulin antibodies (TG-AB), and conducted indirect immunofluorescence on primate thyroid tissue sections using TPO-AB– and TG-AB–negative blood samples.
The team performed indirect immunofluorescence on thyroid seronegative, anti-TGase II–positive CD+ blood samples (n1/423) and observed staining patterns on thyroid follicular cells and extracellular matrices that was identical with monoclonal anti-human TGase II antibody.
Signs of TGase II as the antigen in thyroid tissue were reinforced by elimination of the IIF pattern when sera were depleted of anti-TGase II by pretreatment with human recombinant TGase II. The team saw no such staining of thyroid tissue in blood samples from celiac disease patients who were negative for TGase II antibodies, or samples from the non-celiac control group.
Thyroid antibodies were found in 43% of CD+ patients, substantially higher than NC and CROHN patients ( p < 0.0001). Moreover, a positive correlation was observed between anti-TGase II and TPO-AB titers (p1/40.0001; r1/40.63).
The results show that anti-TGase II antibodies bind to TGase II in thyroid follicles and extracellular matrix, and that titers correlate with TPO antibody titers. This indicates that anti-TGase II antibodies might contribute to the development of thyroid disease in people with celiac disease.
Thyroid Volume 18, Number 11, 2008