Celiac disease is a systemic autoimmune disorder caused by an aberrant immune response towards gluten arising in the small intestine. The prevalence of celiac disease has been gradually rising over the last decades: population screening studies captured a prevalence of roughly 2% in western countries. It can occur at all ages, but only in genetically susceptible individuals carrying the HLA-DQ2 and/or HLA-DQ8 alleles and is characterized by the production of specific autoantibodies, a spectrum of histological changes of the duodenal mucosa and a wide variety of clinical signs/symptoms.

The presence of the predisposing HLA-DQ genes is required, but not sufficient for disease development. Despite the strong impact of genetic factors on disease development, unknown environmental factors are also thought to contribute to disease onset. Among those, viral infections and changes in the small intestinal microbiota composition have been suggested to play a role in triggering the disease, in combination with the ingestion of dietary gluten. The only currently available treatment for celiac disease is a strict and life-long gluten-free diet (GFD), which leads to amelioration of clinical symptoms and restoration of the histological villous architecture in the small intestine.

According to ESPGHAN 2012 guidelines, in selected symptomatic children whose antiendomysial antibodies are positive and anti-transglutaminase levels are >10 times higher than normal values, diagnosis is straightforward and small intestinal biopsy might be avoided. However, the histological proof of small intestinal enteropathy is still required in most cases and in all adult subjects. New tools to ascertain diet compliance by testing for gluten peptides in urine or stools are now becoming available. Novel treatment alternatives to GFD are currently under investigation; some of them are already in clinical phase.

Novel insights into physiopathology and clinical features of celiac disease and gluten-related disorders have been recently published in scientific journals, thus changing both disease paradigms and clinical practice. These insights include, among others, the integrated B cell response in celiac disease, the natural history of potential celiac disease, microbiome alteration in untreated and treated celiac disease, and the differences between the events leading to celiac disease and nonceliac gluten sensitivity (NCGS). Thus, it seems that time is mature for the experts in the field to sum up current evidences on celiac disease and NCGS in a dedicated issue. We strongly believe the readers would appreciate such an effort and the journal will benefit through increased visibility among pediatric gastroenterologists.

The special issue will be open for original research articles as well as review articles focusing on several aspects of pediatric celiac disease.

Potential topics include but are not limited to the following:

• Epidemiology of celiac disease
• Celiac disease prevention
• Pathogenesis of celiac disease
• Non-celiac gluten sensitivity: a pediatric perspective
• Follow-up for celiac disease: if, when, and how
• Compliance to gluten-free diet
• Food technology of gluten-free food
• Investigational therapy for celiac disease: where are we now?