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Urinary leukotriene E 4 levels in children with allergic rhinitis treated with specific immunotherapy and anti‐IgE (Omalizumab)
Author(s) -
Kopp Matthias Volkmar,
Mayatepek Ertan,
Engels Eva,
Brauburger Jens,
Riedinger Frank,
Ihorst Gabriele,
Wahn Ulrich,
Kuehr Joachim
Publication year - 2003
Publication title -
pediatric allergy and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.269
H-Index - 89
eISSN - 1399-3038
pISSN - 0905-6157
DOI - 10.1034/j.1399-3038.2003.00068.x
Subject(s) - medicine , omalizumab , immunoglobulin e , leukotriene e4 , urinary system , placebo , immunology , leukotriene , creatinine , asthma , allergen , urine , radioallergosorbent test , allergen immunotherapy , allergy , gastroenterology , antibody , pathology , alternative medicine
Recently, we were able to demonstrate that Omalizumab, a humanized monoclonal anti‐IgE antibody, reduces in vitro leukotriene (LT) release of peripheral leukocytes stimulated with allergen in children with allergic rhinitis undergoing allergen immunotherapy. The aim of this study was to investigate the effect of anti‐IgE in combination with specific immunotherapy (SIT) on urinary leukotriene E 4 (LTE 4 ) levels. Children and adolescents with sensitization to birch and grass pollens and suffering from seasonal allergic rhinitis were included in a phase III, placebo‐controlled, multicenter clinical study. Within the four‐arm study, patients were randomized to receive SIT for either birch or grass pollen and to receive either subcutaneous anti‐IgE or placebo for 24 weeks during the pollen season. From a total population of 225 children, we collected three urine samples in a subgroup of 19 children [n = 12 boys (63%); mean age 11.8 years; range 7.2–17.5 years; Group A (n = 10): SIT (grass or birch) + anti‐IgE; Group B (n = 9): SIT (grass or birch) + placebo]. Urine samples were collected before, during and at the end of treatment. Endogenous urinary LTE 4 was separated by high‐performance liquid chromatography (HPLC) and determined by enzyme immunoassay with a specific antibody. No differences in urinary LTE 4 concentrations were observed between the anti‐IgE and the placebo groups before (A: 35.2; B: 36.5 nmol/mol creatinine), during (A: 27.0; B: 29.3) and after treatment (A: 28.9; B: 26.5 nmol/mol creatinine). We conclude that urinary LTE 4 levels are not helpful in monitoring patients treated with anti‐IgE and SIT.