Celiac disease is a chronic autoimmune enteropathy that affects about 1% of the global population, and can occur at any age. It develops in genetically predisposed individuals after exposure to dietery gluten. Gluten, a mixure of wheat proteins, is a ubiquitous component of today’s diet and can be found in bread and other baked goods, pasta, cookies and cakes. Similar proteins to gluten can also be found in rye and barley, while oats are considered safe and do not cause symptoms of celiac disease in most people. Gluten peptides, which result from incomplete digestion, enter the lamina propria of the small intestine and thus activate both innate and adaptive immune response in genetically predisposed individuals. Genetic predisposition includes the presence of HLA-DQ2 and DQ8 haplotypes present on antigenpresenting cells. HLA-DQ2 and DQ8 bind deaminated gluten residues and thus activate CD4+ T cells. In addition to CD4+ T cells, CD8+ T cells, interferons, interleukins IL-7, IL-15, IL-21 and B cells which produce antibodies to tissue transglutaminase and deaminated gliadin peptide, are involved in the pathogenesis of celiac disease. The symptoms of celiac disease are a consequence of inflammation, micronutrient defficiency and an autoimmune response to tissue transglutaminase and can present with both intestinal and extraintestinal symptoms. Due to the possibility of affecting almost every organ system, diagnosis of celiac disease is often difficult and delayed. The diagnosis includes serology and confirmation of anti-tTG antibodies, as well as biopsy of the small intestine mucosa. Celiac disease can successfully be managed with a strict, lifelong gluten-free diet. Late diagnosis or untreated celiac disease can lead to the development of numerous complications, both non-malignant and malignant, while proper adherence to a gluten-free diet prevents their development. The aim of this paper is to present the possible complications of celiac disease and highlight the importance of early diagnosis and treatment.