Skip Navigation LinksHome > November/December 2012 - Volume 46 - Issue 10 > Immunoglobulin A Deficiency in Celiac Disease
Journal of Clinical Gastroenterology:
doi: 10.1097/MCG.0b013e31824b2277
ALIMENTARY TRACT: Original Articles

Immunoglobulin A Deficiency in Celiac Disease

Chow, Marisa A. MD*; Lebwohl, Benjamin MD*,†; Reilly, Norelle Rizkalla MD†,‡; Green, Peter H. R. MD*,†

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Abstract

Goals: To determine the prevalence and significance of immunoglobulin A (IgA) deficiency and partial deficiency in patients with celiac disease (CD).

Background: Selective IgA deficiency is a common primary immunoglobulin deficiency and has a higher prevalence in patients with CD. The prevalence and significance of IgA deficiency and partial deficiency in patients with CD in the United States has not previously been examined.

Study: A retrospective, cohort study of 1498 adults and 317 children seen in a University Medical Center was conducted.

Results: There were 26 patients (22 adults, 4 children) with CD who were IgA deficient and 11 (9 adults, 2 children) with CD who were partially IgA deficient. The prevalence of IgA deficiency/partial deficiency was similar among adults and children (2.1% and 1.9%, respectively, P=0.99). Among adults, concomitant autoimmune disease was present in 29% of IgA-deficient/partially deficient patients versus 12% of CD patients with normal IgA levels (P=0.0081). All 4 IgA-deficient patients who had persistently positive IgG celiac serologies while adherent to a gluten-free diet and were rebiopsied had a normal repeat biopsy. Both positive tissue transglutaminase IgG and antigliadin IgG were found in these patients.

Conclusions: Selective IgA deficiency/partial deficiency is present in 2% of CD patients at this referral center and is equally prevalent among adults and children. IgA-deficient/partially deficient adults had a higher prevalence of concomitant autoimmune disease than those without IgA deficiency. In patients who are IgA deficient, IgG serologies may be persistently elevated despite histologic recovery.

© 2012 Lippincott Williams & Wilkins, Inc.

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