Celiac disease and endocrine autoimmune disorders in children: an update

Abstract

Celiac disease (CD) is a life-long inflammatory condition of the gut that occurs in genetically susceptible individuals. Several autoimmune diseases (AI) are associated with CD. To date, no conclusive evidence is available that proves if the relationship between CD and AI is mediated by gluten exposure, or if CD and AI could co-occur due to other causes, in particular the loss of the intestinal barrier function and the common genetic background. Furthermore, it is not clear yet if CD needs a regular screening program for AI. This review will cover the key studies on both the pathogenetic and clinical evidence explaining this association. We will review the reports including patients aged <18 years with CD and endocrine AI.

Keywords::

• Addison's disease
• adolescent
• autoimmune diseases
• celiac disease
• child
• thyroid autoimmunity
• Type 1 diabetes

Key issues

• • Celiac disease (CD) is a life-long inflammatory condition of the gut that occurs in genetically susceptible individuals associated with several endocrine autoimmune diseases (AI).

• • In pediatric and young patients, Type 1 diabetes (T1D) and thyroid autoimmunity (TA) are often associated with CD.

• • Epidemiological studies report that the prevalence of CD ranges from 4 to 11% in T1D patients and it is about 7% in TA patients.

• • The coexistence of CD and endocrine AI involves a complex interplay between genetic aspects, the environment, immunologic aspects and the intestinal barrier function.

• • The first reports supported the hypothesis that the AI could be ‘gluten-dependent’ because the gluten withdrawal, in the short-term follow-up, has resulted in the disappearance of T1D and TA-related autoantibodies.

• • Recent surveys show that the gluten withdrawal does not prevent the development of T1D in newborn infants with a high T1D risk nor in first-degree relatives of T1D patients with elevated levels of β-cell autoantibodies and it does not impact the trend of TA in long-term follow-up. Overall, the recent clinical advances suggest that gluten exposure cannot explain the complex relationship between CD and AI, but other pathogenetic factors, in particular the loss of the intestinal barrier function and the common genetic background, are involved.

• • The systematic screening for CD in T1D and TA is clinically useful and clearly indicated.

• • The systematic screening for the potentially associated endocrine AI in CD patients is not clearly indicated and, based on the recent clinical advances, it seems, neither clinically relevant nor cost-effective, at least until effective preventive strategies for these AI become available.

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.