3 learning resources available for this topic
Celiac disease is an autoimmune disorder triggered by gluten consumption in genetically susceptible individuals, leading to small intestinal villous atrophy and malabsorption. The condition affects approximately 1% of the population and can present with gastrointestinal symptoms, extraintestinal manifestations, or remain asymptomatic.
Gluten proteins (gliadin and glutenin) are deamidated by tissue transglutaminase, creating immunogenic peptides that trigger T-cell mediated immune responses in HLA-DQ2 or HLA-DQ8 positive individuals. This inflammatory cascade leads to villous atrophy, crypt hyperplasia, and increased intestinal permeability, resulting in malabsorption of nutrients including iron, folate, vitamin B12, and fat-soluble vitamins.
Diagnosis requires a combination of positive serology (anti-tissue transglutaminase, anti-endomysial antibodies), characteristic histological changes on duodenal biopsy, and clinical response to a gluten-free diet. Malabsorption may present as iron-deficiency anemia, osteoporosis, growth retardation in children, or unexplained weight loss, requiring systematic evaluation of nutritional deficiencies and monitoring of treatment response.