title: An intranasal glucocorticoid inhibits the increase of specific IgE initiated during birch pollen season.
abstract: BACKGROUND
  Recent in vitro findings show that glucocorticoids in combination with IL-4 can induce the synthesis of IgE, indicating that glucocorticoids may promote allergy.
  
  
  OBJECTIVE
  A double-blind, placebo-controlled study was performed to evaluate the effect of an intranasal glucocorticoid on the levels of birch pollen-specific IgE antibodies in serum from patients with allergic rhinitis.
  
  
  METHODS
  Eighteen patients with allergic rhinitis received treatment with an intranasal glucocorticoid (beclomethasone dipropionate, 400 microg/day) or placebo for 5 weeks, starting from the beginning of the birch pollen season. Blood samples for anti-birch IgE evaluation were taken before treatment was initiated and at 2 and 5 weeks after the beginning of the study.
  
  
  RESULTS
  The beclomethasone group (n = 9) had significantly lower symptom scores when compared with the placebo group (n = 9) (0.86 +/- 0.26 vs 2.79 +/- 0.76, p value = 0.01). Both the treatment group and the placebo group showed a trend of an increase in anti-birch IgE levels 2 weeks after the beginning of the treatment (from 33.1 +/- 13.1 kU/L to 44.9 +/- 20.9 kU/L in the beclomethasone group and from 53.2 +/- 18.9 kU/L to 64.1 +/- 22.1 kU/L in the placebo group). Treatment with beclomethasone returned anti-birch IgE levels to baseline by the end of the study, whereas in the placebo group the anti-birch IgE levels continued to increase (final values, 33.1 +/- 11.9 kU/L vs 72.6 +/- 23.2 kU/L, respectively). The change in IgE antibody levels in the placebo group was significantly higher than that in the beclomethasone group. No statistically significant changes in total IgE or soluble CD23 levels were detected.
  
  
  CONCLUSIONS
  We conclude that treatment with an intranasal glucocorticoid initiated at the beginning of the pollen season inhibits the induced increase in specific IgE.
authors.affiliation: Department of Clinical Pharmacology, Göteborg University, Gothenburg, Sweden.
authors.forename: T
authors.initials: T
authors.lastname: Pullerits
authors.forename: L
authors.initials: L
authors.lastname: Praks
authors.forename: M
authors.initials: M
authors.lastname: Sjöstrand
authors.forename: S
authors.initials: S
authors.lastname: Rak
authors.forename: B E
authors.initials: BE
authors.lastname: Skoogh
authors.forename: J
authors.initials: J
authors.lastname: Lötvall
mesh_terms: D000281:Administration, Intranasal; D000293:Adolescent; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000888:Antibodies, Anti-Idiotypic / Q000097:blood; D000918:Antibody Specificity; D001507:Beclomethasone / Q000627:therapeutic use; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage* / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D017455:Receptors, IgE / Q000378:metabolism; D006255:Rhinitis, Allergic, Seasonal / Q000188:drug therapy*
chemical_list: D000893:Anti-Inflammatory Agents; D000888:Antibodies, Anti-Idiotypic; D005938:Glucocorticoids; D017455:Receptors, IgE; C026408:anti-IgE antibodies; D007073:Immunoglobulin E; D001507:Beclomethasone