title: Anti-ulcer drugs promote IgE formation toward dietary antigens in adult patients.
abstract: Recently, we have demonstrated that anti-ulcer drugs, such as H2-receptor blockers and proton pump inhibitors, promote the development of immediate type food allergy toward digestion-labile proteins in mice. The aim of this study was to examine the allergological relevance of these findings in humans. In an observational cohort study, we screened 152 adult patients from a gastroenterological outpatient clinic with negative case histories for atopy or allergy, who were medicated with H2-receptor blockers or proton pump inhibitors for 3 months. IgE reactivities to food allergens before and after 3 months of anti-acid treatment were compared serologically. Ten percent of the patients showed a boost of preexisting IgE antibodies and 15% de novo IgE formation toward numerous digestion-labile dietary compounds, like milk, potato, celery, carrots, apple, orange, wheat, and rye flour. Thus, the relative risk to develop food-specific IgE after anti-acid therapy was 10.5 (95% confidence interval: 1.44-76.48). The long-term effect was evaluated 5 months after therapy. Food-specific IgE could still be measured in 6% of the patients, as well as significantly elevated serum concentrations of ST2, a Th2-specific marker. An unspecific boost during the pollen season could be excluded, as 50 untreated control patients revealed no changes in their IgE pattern. In line with our previous animal experiments, our data strongly suggest that anti-ulcer treatment primes the development of IgE toward dietary compounds in long-term acid-suppressed patients.
authors.affiliation: Center of Physiology and Pathophysiology, Medical University Vienna, Vienna, Austria.
authors.forename: Eva
authors.initials: E
authors.lastname: Untersmayr
authors.forename: Noémi
authors.initials: N
authors.lastname: Bakos
authors.forename: Isabella
authors.initials: I
authors.lastname: Schöll
authors.forename: Michael
authors.initials: M
authors.lastname: Kundi
authors.forename: Franziska
authors.initials: F
authors.lastname: Roth-Walter
authors.forename: Krisztina
authors.initials: K
authors.lastname: Szalai
authors.forename: Angelika B
authors.initials: AB
authors.lastname: Riemer
authors.forename: Hendrik J
authors.initials: HJ
authors.lastname: Ankersmit
authors.forename: Otto
authors.initials: O
authors.lastname: Scheiner
authors.forename: George
authors.initials: G
authors.lastname: Boltz-Nitulescu
authors.forename: Erika
authors.initials: E
authors.lastname: Jensen-Jarolim
mesh_terms: D000328:Adult; D000485:Allergens / Q000276:immunology; D000897:Anti-Ulcer Agents / Q000008:administration & dosage / Q000009:adverse effects*; D015331:Cohort Studies; D004032:Diet; D004063:Digestion; D004415:Dyspepsia / Q000188:drug therapy; D005502:Food; D005512:Food Hypersensitivity / Q000209:etiology*; D006635:Histamine H2 Antagonists / Q000009:adverse effects; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood* / Q000276:immunology; D007371:Interferon-gamma / Q000097:blood; D000072179:Interleukin-1 Receptor-Like 1 Protein; D018793:Interleukin-13 / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D008565:Membrane Proteins / Q000097:blood; D054328:Proton Pump Inhibitors; D011956:Receptors, Cell Surface; D012307:Risk Factors; D012882:Skin Tests; D013997:Time Factors
chemical_list: D000485:Allergens; D000897:Anti-Ulcer Agents; D006635:Histamine H2 Antagonists; C079241:IL1RL1 protein, human; D000072179:Interleukin-1 Receptor-Like 1 Protein; D018793:Interleukin-13; D008565:Membrane Proteins; D054328:Proton Pump Inhibitors; D011956:Receptors, Cell Surface; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma