Abstract
Celiac disease (CD) is a chronic, small-intestinal, immune-mediated enteropathy due to gluten exposition in genetically predisposed individuals. It occurs in about 1% of the population and often remains an underdiagnosed condition. This could be due to the fact that the adult population often lacks the classical signs and symptoms of CD, manifesting only atypical symptoms. In this review we analyzed the main extra-intestinal manifestations of CD which include cutaneous and endocrinological disorders, abnormal liver function tests, and neuropsychiatric features. When CD is not diagnosed and therefore is not treated with a gluten-free diet (GFD), it can predispose to severe complications, not only gastrointestinal. Thus, it is important for clinicians to quickly recognize the atypical manifestations of CD, considering that an early diagnosis can significantly impact on a patient’s prognosis.
Highlights
Celiac disease (CD) is defined as a chronic, small intestinal, immune-mediated enteropathy precipitated by exposure to dietary gluten in genetically predisposed subjects [1,2]
The pathogenesis of CD recognizes the role of genetic factors—almost all patients possess class II human leukocyte antigen (HLA) DQ2 and DQ8, or their variants, even though they are carried by up to 40% of people with European and Asian origins
The aim of this review is to provide a clinical overview of the spectrum of atypical CD
Summary
There is growing evidence about the predisposition of CD patients to develop several skin disorders, including psoriasis, atopic dermatitis (AD), urticaria, alopecia areata (AA), chronic ulcerative stomatitis, and dermatitis herpetiformis (DH), the only one with a demonstrated gluten-related immune mechanism [1,9]. In patients suffering from CD, the direct gliadin toxicity within the intestinal surface leads to an impaired permeability of the hemato-intestinal barrier, which results in the passage of gluten peptides into the bloodstream. This mechanism is at the root of the. The inflammatory cascade is activated by the action of tTG2 which catalyzes the structural subversion of gluten, creating new epitopes. These have an increased affinity for HLA-DQ2 e DQ8, which accounts for the susceptibility of these individuals to CD development. The activation of Th1 response can in turn stimulate the proliferation of B lymphocytes which release autoantibodies including those against gluten and tTG2 [4,10]
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