Abstract
Celiac disease is a small intestinal inflammatory disease with autoimmune features that is triggered and maintained by the ingestion of the storage proteins (gluten) of wheat, barley, and rye. Prevalence of celiac disease is increased in patients with mono- and/or polyglandular autoimmunity and their relatives. We have reviewed the current and pertinent literature that addresses the close association between celiac disease and endocrine autoimmunity. The close relationship between celiac disease and glandular autoimmunity can be largely explained by sharing of a common genetic background. Further, between 10 and 30% of patients with celiac disease are thyroid and/or type 1 diabetes antibody positive, while around 5–7% of patients with autoimmune thyroid disease, type 1 diabetes, and/or polyglandular autoimmunity are IgA anti-tissue transglutaminase antibody positive. While a gluten free diet does not reverse glandular autoimmunity, its early institution may delay or even prevent its first manifestation. In conclusion, this brief review highlighting the close association between celiac disease and both monoglandular and polyglandular autoimmunity, aims to underline the need for prospective studies to establish whether an early diagnosis of celiac disease and a prompt gluten-free diet may positively impact the evolution and manifestation of glandular autoimmunity.
Highlights
Celiac disease (CeD) is defined as a life-long intolerance to dietary gluten that results in small intestinal inflammation, villous atrophy, crypt hyperplasia, and often malabsorption
CeD is considered sufficiently prevalent and the benefits of diagnosis and treatment by gluten withdrawal are such that it is advocated to screen all patients with type 1 diabetes mellitus (T1D) for this disorder
Some common pathogenic mechanisms have been further implicated, such as increased intestinal permeability resulting from zonulin upregulation and dysfunction of tight junctions in both CeD
Summary
Celiac disease (CeD) is defined as a life-long intolerance to dietary gluten that results in small intestinal inflammation, villous atrophy, crypt hyperplasia, and often malabsorption. CeD is considered sufficiently prevalent and the benefits of diagnosis and treatment by gluten withdrawal are such that it is advocated to screen all patients with T1D (and autoimmune thyroid disease) for this disorder Both endoscopic-histological diagnosis and the presence of circulating IgA antibodies (Ab) to tissue transglutaminase (TG2) confirm the diagnosis. The ubiquitous enzyme TG2, the CeD autoantigen, is central to the pathogenesis of CeD, since it can deamidate specific glutamine residues in certain gluten peptides that remain undigested and reach the subepithelial small intestinal lamina propria This deamidation of the gluten peptides and their haptenization by binding to TG2 itself (autocatalysis) thereby increases their affinity to DQ2 or DQ8 on professional antigen presenting cells like macrophages, dendritic, and B cells, favoring the subsequent gluten specific destructive T cell response [1,10,11,12]
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