Celiac disease (CD) is an autoimmune inflammatory disease of the small intestine that is triggered in genetically susceptible persons by the ingestion of the gluten-containing grains wheat, rye, barley, and possibly oats. The condition is thought to result from the activation of both a T-cell and B-cell immune response, leading to mucosal inflammation, villous atrophy, and crypt hyperplasia, and is self-perpetuating with continued exposure to gluten.
The classical presentation of CD, with gluten-induced abnormal intestinal mucosa and intestinal malabsorption, has now been shown to be less common than silent or atypical presentation, in which patients do not have intestinal symptoms, although they have abnormal intestinal mucosa. Atypical clinical manifestations of CD include dermatitis herpetiformis, insulin-dependent diabetes mellitus, autoimmune thyroid disease, and chronic fatigue. Untreated CD is associated with multiple important short- and long-term complications including nutritional derangements, anemia, reduced bone density, as well as intestinal lymphoma. It has been reported that gastrointestinal carcinomas or T-cell lymphomas develop in up to 15 percent of patients with untreated or refractory CD, but it is widely believed that strict adherence to a gluten free diet reduces the risk of these complications.
CD is often under-diagnosed, even in countries such as Finland where the level of awareness of the disease is high, and in the United States, a survey conducted in 2001 found that US celiac patients experience symptoms for an average of 11 years before diagnosis. Although the true prevalence of CD is difficult to estimate because of its variable presentation, recent epidemiologic studies using sensitive and specific serologic tests have revealed that it is one of the most common lifelong disorders among European and American Caucasians, with a prevalence i n the general population that is likely close to 1%.
The new serologic tests have altered the classic diagnostic pathway of CD in adults, which was based on clinical suspicion and duodenal biopsy. In 2004, the Agency for Healthcare Research and Quality issued a systematic review of the evidence regarding screening patients for CD. The results of that review indicate that tests for endomysial (EMA) and tissue transglutaminase (tTG) IgA autoantibodies have over 95 percent sensitivity, and close to 100 percent specificity, whereas biopsy with a strict cut-off requiring villous atrophy has high specificity, but poor sensitivity.
The question of who should be screened for CD remains controversial. Although it is well established that complications may develop in the absence of treatment, the natural history of undiagnosed celiac disease remains unclear. In addition, the need for a new gold standard for diagnosing CD in an era of advanced serologic testing has been recognized. For the present, the best epidemiologic approach to the diagnosis of CD may be a systematic process of case-finding in which patients with symptoms or typical or atypical conditions known to be associated with the disease are targeted.
Tests for tTG autoantibodies are easier to perform and less subjective and time-consuming than tests for autoantibodies to EMA. FDA-approved ELISA kits for detection of antibody are available from Bio-Rad Laboratories, Scimedx Corporation and IMMCO Diagnostics, Inc. The FDA has also approved a fluorescent-based microparticles immunoassay developed by Biomedical Diagnostics.
Even though the predictive value of anti-gliadin antibody (AGA) testing is not as strong as the tTG autoantibody tests, they still populate reference laboratory menus and are definitely worth mentioning. AGA testing is useful for testing pediatric populations and for individuals with IgA deficiency. Anti-gliadin antibody testing can also be used to monitor patients
for dietary compliance, and to determine when patients have become gluten free. Several companies make AGA test kits including ALPCO, and Inverness Medical Innovations.
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