Background and Goals: The widely used serum endomysial (EmA) and transglutaminase 2 (TG2-ab) antibodies predict forthcoming villous damage and celiac disease when the small-bowel mucosa structure is still normal. However, these autoantibodies may remain negative in this early stage of the disease. We hypothesized that the antibodies against deamidated gliadin peptides (DGP-AGA) might appear before the other antibodies and would thus be useful in the diagnosis and follow-up of patients with early-stage celiac disease.
Study: Serum DGP-AGA, TG2-ab, and EmA were measured at baseline and after 1 year on a gluten-free diet in 42 adults proven to have early-stage celiac disease despite normal small-bowel mucosal morphology (Marsh I-II), and in 20 celiac subjects evincing villous atrophy (Marsh III). Thirty-nine subjects with no signs of celiac disease served as nonceliac controls.
Results: Sensitivity to detect early-stage celiac disease was 79% for DGP-AGA, 64% for TG2-ab, and 81% for EmA. Specificities were 95%, 100%, and 100%, respectively. The corresponding efficiencies of the tests were 89% for DGP-AGA, 81% for TG2-ab, and 91% for EmA. All 3 antibodies were significantly decreased on a gluten-free diet.
Conclusions: This study showed that the sensitivity of DGP-AGA was superior to TG2-ab and comparable to EmA in celiac patients having early-stage celiac disease with normal villous morphology. On the basis of these results, DGP-AGA would seem to offer a promising new method for case-finding and follow-up in this entity.
*Pediatric Research Centre, University of Tampere and Tampere University Hospital
†Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital and Medical School
∥Tampere School of Public Health, University of Tampere, Tampere
‡Department of Medical Genetics, Haartman Institute, and Research Program for Molecular Medicine, University of Helsinki
§Research and Development, Finnish Red Cross Blood Service, Helsinki, Finland
This study and the Celiac Disease Study Group are supported by the Academy of Finland Research Council for Health, the Competitive Research Funding of the Pirkanmaa Hospital District, the Sigrid Juselius Foundation, the Foundation for Paediatric Research, the EU Commission Marie Curie Excellence Grant (FP6 contract MEXT-CT-2005-025270), Marie Curie mobility grant (MRTNCT-2006-036032; TRACKS), the National Graduate School of Clinical Investigation, the Ehrnrooth Foundation, and the Finnish Celiac Society.
Reprints: Katri Kaukinen, MD, PhD, University of Tampere and Medical School, FIN-33014 Tampere, Finland (e-mail: firstname.lastname@example.org).
Received June 1, 2010
Accepted September 8, 2010