In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease, and since then it has become an invaluable resource to people worldwide who seek information about celiac disease and the gluten-free diet.
In 1998 I created The Gluten-Free Mall, Your Special Diet Superstore! which was also another Internet first—it was the first gluten-free food site to offer a shopping cart-style interface, and the ability for people to order gluten-free products manufactured by many different companies at a single Web site.
I am also co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.
*IMMCO Diagnostics, Inc., Buffalo, New York 14228; Departments of Microbiology and Dermatology, State University of New York at Buffalo, Buffalo, New York 14214; and Department of Dermatology, Warsaw School of Medicine, Warsaw, Poland; ** Department of Gastroenterology and Pediatrics, Selesian School of Medicine, Warsaw, Poland
Clinical Diagnostic Immunology 9:1295-1300, 2002.
Celiac.com 12/31/2002 - Background: Immunoglobulin A (IgA) deficiency is 10-15 times more common in patients with Celiac Disease (CD) than in normal subjects. Serological tests have become the preferred methods of detecting both symptomatic and asymptomatic patients with CD. However, commercially available serological methods are limited in that they detect only the IgA isotype of antibodies (with the exception of IgG gliadin assays); hence, IgA deficient celiac disease patients may yield false negative serology.
Methods: Fifteen celiac disease and ten non-CD IgA deficient pediatric cases were
examined for IgA and IgG antibodies to endomysium, gliadin and tissue
Results: Twenty five specimens with IgA deficiency were examined. Fifteen were celiac disease cases and ten were non-CD cases. All fifteen IgA deficient celiac disease cases were positive for endomysium antibodies of the IgG isotype and for IgG gliadin antibodies. All but one of the IgA deficient celiac disease cases were also positive for IgG tissue transglutaminase antibodies. None of the non-CD IgA deficient cases were positive for any of the antibody markers. All the specimens examined were also negative for IgA specific antibodies to endomysium, gliadin, and tissue transglutaminase.
Conclusions: IgG specific antibody tests for endomysium, gliadin and tissue transglutaminase are useful for the identification of IgA deficient celiac disease patients. IgG antibody tests along with tests routinely being used in clinical laboratories can reliably detect all active celiac disease patients. In addition, the levels of these CD-specific IgG antibodies could be used to monitor patient dietary compliance.