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Abstract Celiac disease (CD) is an immune-mediated condition driven by ingested gluten in genetically susceptible individuals. The disease may manifest at almost any age with heterogenous gastrointestinal and extraintestinal symptoms (Laurikka et al., 2018). Type 1 diabetes mellitus (T1DM) caused by autoimmune reaction is a major subtype of diabetes, and is mostly prevalent in adolescents and childhood (Katsarou et al., 2017). The prevalence of CD in T1DM varies from 0.8% to 16.4% and it is significantly higher comparing to the 0.5–1% prevalence in general population (Bakker et al., 2016). Celiac disease is an autoimmune disease, which, besides autoimmune thyroid disease, is one of the most frequent concomitant diseases occurring in type 1 diabetes mellitus (T1DM) (Achury et al., 2015). The etiology of CD is influenced by both environmental and genetic factors. The most characterized genetic contribution to CD is the human leukocyte antigen system (HLA), contributing to 40% of genetic variance (lundin and solid ., 2014). Individuals carrying high risk genotypes DR3-DQ2/DR3-DQ2or DR3DQ2/DR4DQ8 are more likely to develop both autoimmune diseases together than individuals carrying any other HLA genotypes (Smigoc et al., 2016). Symptoms of celiac disease are less specific in the pediatric population. Patients with T1D and CD may be asymptomatic or present with mild symptoms (Goodwin et al., 2019(. In patients with T1D, the coexistence of CD not only affects intestinal absorption of nutrients and calcium and skeletal metabolism but also may contribute to the higher risk of cardiovascular incidents and exaggerate complications such as nephropathy, retinopathy, and neuropathy (Rohre et al.,2015). The diagnosis of CD is based on the European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) criteria: by measuring antibodies to tissue transglutaminase (tTG), followed by intestinal biopsy in positive cases to confirm the diagnosis (Huspy et al., 2020). |