The Immunology of Gluten Sensitivity beyond the Intestinal Tract

Celiac disease and gluten-sensitive enteropathy are terms that have been used to refer to a disease process affecting the small bowel. However, evidence has been accumulated in literature demonstrating that gluten sensitivity or celiac disease can exist even in the absence of enteropathy, but affecting many organs. Based on overwhelming evidence, immunological pathogenesis has been demonstrated in the joint, the heart, thyroid, bone, and, in particular, the brain cerebellum and neuronal synapsin I. When blood samples of patients with celiac disease are tested against gliadin and different tissue antigens, in addition to gliadin antibody, a significant percentage of them exhibit elevation in antibodies against transglutaminase, heat shock protein, collagen, thyroid, myosin, endothelial cell, bone antigen (transglutaminase), myelin basic protein, cerebellar and synapsin. This elevation of autoantibodies in patients with celiac disease may result in neuroimmune disorders. In fact, in comparison to the general population, the incidence of various autoimmune disorders, including gluten ataxia, is increased up to 30-fold in patients with celiac disease. Therefore, immune evaluation of patients with gluten sensitivity or celiac disease, in addition to gliadin and transglutaminase, should include antibody measurement against thyroglobulin, thyroid peroxidase, heat shock protein, bone transglutaminase, myelin basic protein, cerebellar peptide and synapsin. This novel laboratory approach to gluten sensitivity and autoimmunity may enable clinicians to detect markers of autoimmune diseases. Early identification of gluten sensitive and celiac disease patients and implementation of a gluten-free diet may result in significant improvement and control of associated diseases.