Celiac disease (CD) is a T-cell-immune mediated enteropathy triggered by gluten ingestion in genetically susceptible individuals. The estimated global prevalence is 1% (range 0.7-1.4%), and the clinical manifestation results from a complex interplay of genetic, immunologic, and environmental factors. Although it occurs predominantly in predisposed individuals with the genetic haplotypes HLA-DQ2, HLA-DQ8, or DQA1*05 haplotypes, several other predisposing genes have been described. Clinical presentations are variable and include both gastrointestinal and extraintestinal manifestations, contributing to underdiagnosis. Diagnosis is based on a combination of positive serologic tests-such as IgA tissue transglutaminase and IgG deaminated gliadin peptide in IgA-deficient patients, which are used for screening- characteristic histological findings on duodenal biopsy, and symptom resolution following initiation of a gluten-free diet (GFD). Poorly controlled disease may lead to complications, including osteoporosis, malnutrition, vitamin deficiencies, and small bowel lymphoma. A strict gluten-free diet is the only effective treatment, with symptom improvement typically observed within weeks of initiation of therapy. However, adherence is often challenging, socially isolating, and a multidisciplinary approach is essential for optimal management. Several non-dietary therapeutic strategies are currently under investigation. This review summarizes current evidence on epidemiology, pathophysiology, diagnosis, and management of CD, while highlighting emerging therapeutic strategies and approaches to patient care.
Amakye et al. (2026) studied this question.