Celiac disease (CD) is an immune-mediated chronic inflammatory disorder characterized by permanent gluten intolerance in genetically susceptible individuals. Exposure to gluten perpetuates an enteropathy leading to malabsorption with chronic diarrhea, weight loss, and abdominal distension. The small intestine mucosa is abnormal, and jejunal biopsy demonstrates various degrees of villous atrophy, absence of surface mucosa, and crypt hyperplasia. The diagnosis is based on the demonstration of a more or less pronounced villus atrophy in a jejunal biopsy. The villous atrophy improves after withdrawal of gluten from the diet. If undetected or neglected, CD may cause considerable late complications from malabsorption or secondary autoimmune diseases (Feigbery 1999; Maki and Collins 1997; Holmes 1996). The therapy consists of permanently excluding gluten from the diet and allows the healing of the mucosal lesion. Abnormalities of humeral and cell-mediated immunity suggest that celiac disease is an immunologic disorder (Walker-Smith 1996). It is caused by inappropriate immune response to the gliadin component in the dietary gluten (Dieterich 1997). Genetic susceptibility is present, and 90% of the patients have HLA DRG 3 DQ-2 haplotype, and some have the HLA DR4 DQ8 gene (Hadjivassiliou 1998). A close relationship exists between the biochemical properties of tissue transglutaminase and the basic molecular mechanisms responsible for CD, and possibly with the neuropsychiatric manifestations of CD (Gentile 2002). Anti–tissue transglutaminase antibody assay has been used as a serologic screening test for CD. In addition, antiendomysial, antigliadin, and antireticulin antibodies are associated with the disease. Nevertheless, the clinical symptomatology affecting the gastrointestinal (GI) system, histological abnormalities on gut biopsy, and presence of antiendomysial antibodies do not always coexist. Also, presentation with minor symptoms, such as irritable bowel syndrome, anaemia, slight weight loss, and fatigue, has become increasingly common, and in many cases the disease may be clinically silent, despite manifest small-bowel mucosal lesions. Therefore, CD is underdiagnosed (Catassi et al. 1996; Feigbery 1999; Holmes 1996; Kolho et al. 1998; Maki and Collins 1997).
Serum antigliadin antibody levels as a screening criterion before jejunal biopsy indication for celiac disease in a developing country