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Celiac disease (CD) is a well-known, permanent, genetically determined intolerance to gluten that results in entheropathy, characterized by the typical malabsorption syndrome. After the ingestion of prolamines found in wheat, rye and barley, an altered immune response, dominated by T cells of Th1 type, starts at the gut level and plays an important role in tissue damage. This abnormal response not only results in the entheropathy, but also involves a number of extraintestinal manifestations [1]. In fact, a wide spectrum of symptoms characterizes CD in children and adults, and the classical symptoms are now reported infrequently.
Many studies demonstrate the strict association between CD and endocrine autoimmune diseases. Patients with CD are, in fact, at a greater risk of developing endocrine disorders, such as Type 1 diabetes mellitus (T1DM), autoimmune thyroid disease and pubertal disorders.
The presence of a common genetic predisposition, such as HLA-DQ2 or DQ8 haplotypes, partially seems to explain the association between CD and autoimmune diseases. It has been suggested that the development of multiple autoimmunity may be owing to shared epitopes between an environmental agent and common antigens present in several endocrine tissues. Body proteins can undergo modifications creating epitopes recognized as non-self, in this manner, leading to breakage of immune tolerance and precipitation of autoimmune disease. In CD, the ingestion of gliadin causes an immune response against a unique autoantigen, the enzyme tissue transglutaminase, that could share similar epitopes with other cryptic antigens that are unmasked, especially in endocrine glands [2,3]. This could be the case for T1DM. Indeed, the prevalence of T1DM in patients with CD is approximately 4.5%, 20-times higher than that in the general population. On the other side, in patients with T1DM, CD is currently estimated to affect up to 16.4% in selected populations [4,5]. Usually, even if at the onset of T1DM a temporary rise in antigliadin antibodies (AGAs) is described (in 3-4% of patients) along with the expression of the immunological chaos present at the onset of an endocrine autoimmune disease, in the majority of patients (up to 88.5%), CD is diagnosed months or years after the clinical onset of T1DM [6]. This could depend on the difficulty of suspecting and then diagnosing a silent, atypical or latent CD, thus resulting in the...