Effect of Anti-IgE in Chronic Urticaria
Information source: Johns Hopkins University
Information obtained from ClinicalTrials.gov on June 20, 2008
Link to the current ClinicalTrials.gov record.
Condition(s) targeted: Urticaria
Intervention: XolairÂ® (Omalizumab) (Drug)
Phase: Phase 2
Sponsored by: Johns Hopkins University
Official(s) and/or principal investigator(s):
Sarbjit Saini, M.D., Principal Investigator, Affiliation: Johns Hopkins Asthma and Allergy Center, Division of Allergy and Clinical Immunology
This study is being done to find out if a drug called Xolair (omalizumab), an anti-IgE
antibody, is safe and effective for people with chronic urticaria (hives) with persistent
symptoms in spite of taking antihistamines.
Official title: Effect of Anti-IgE in Chronic Urticaria
Study design: Treatment, Randomized, Double-Blind, Placebo Control, Parallel Assignment, Safety/Efficacy Study
Omalizumab (Xolair®) is a recombinant humanized monoclonal antibody that binds specifically
to the FcEpsilonR1 binding site on human IgE. The binding of omalizumab inhibits the ability
of IgE to bind to basophils or mast cells. Free IgE levels fall by 89% and 98% over 16 and
24 weeks of therapy respectively (Busse, 2001). Total IgE levels rise in patients treated
with omalizumab though almost all IgE is bound and thus inactive. Omalizumab has also been
shown to decrease expression of the FcEpsilonR1 receptor on both basophils and mast cells
(Beck et al, 2004). Omalizumab recently received FDA approval for the treatment of moderate
to severe persistent allergic asthma in pediatric (12 years of age and above) and adult
patients. Studies have also shown efficacy in the treatment of allergic rhinitis and similar
anti-IgE compounds have been efficacious as food allergy therapeutics (Casale, 2001, and
Given the efficacy of omalizumab in the treatment of moderate to severe allergic asthma, the
researchers will conduct a double-blind study to evaluate the safety and efficacy of
omalizumab in a small number of patients with chronic urticaria with persistent symptoms in
spite of background antihistamine therapy. Omalizumab is currently not indicated for
patients with chronic urticaria. The primary hypothesis is that omalizumab will lead to a
reduction in serum IgE levels and blood basophil high affinity IgE receptor expression in
subjects with chronic idiopathic urticaria. Additionally, clinical outcomes such as quality
of life, symptoms scores, and medication use will be explored. This study should allow for
further understanding of the role IgE plays in chronic urticaria.
Minimum age: 18 Years.
Maximum age: 80 Years.
- Males and non-pregnant, non-breastfeeding females
- Chronic urticaria defined as symptoms >50% of the days or 3 days per week for more
than 12 weeks
- History of angioedema
- Chronic daily therapy with anti-histamines and stable doses of antihistamines for at
least 4 weeks.
- High baseline score for pruritis (at least 2 on a 3 point scale)
- No other etiology identified for chronic urticaria such as drug-related or physical
urticaria as determined by history, physical examination and laboratory studies
- Concomitant use of systemic corticosteroids for 1 month prior to enrollment. Topical
steroid use will not be permitted, but inhaled topical steroids are allowed.
- Current use of immunosuppressive medication (cyclosporine, IVIg, methotrexate,
cyclophosphamide). Any such medication will be discontinued for at least 6 weeks
- Treatment with any investigational agent within 30 days of screening
- Previous treatment with omalizumab
- Recent history of drug or alcohol abuse (within 3 years prior to study)
- Active atopic dermatitis requiring the use of topical steroid agents
- Clinically relevant cardiovascular, hepatic, neurologic, psychiatric, endocrine, or
other major systemic disease making the protocol or interpretation of the study
Locations and Contacts
Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224-6821, United States
Beck LA, Marcotte GV, MacGlashan D, Togias A, Saini S. Omalizumab-induced reductions in mast cell Fce psilon RI expression and function. J Allergy Clin Immunol. 2004 Sep;114(3):527-30.
Sabroe RA, Francis DM, Barr RM, Black AK, Greaves MW. Anti-Fc(episilon)RI auto antibodies and basophil histamine releasability in chronic idiopathic urticaria. J Allergy Clin Immunol. 1998 Oct;102(4 Pt 1):651-8.
Sabroe RA, Fiebiger E, Francis DM, Maurer D, Seed PT, Grattan CE, Black AK, Stingl G, Greaves MW, Barr RM. Classification of anti-FcepsilonRI and anti-IgE autoantibodies in chronic idiopathic urticaria and correlation with disease severity. J Allergy Clin Immunol. 2002 Sep;110(3):492-9.
Saini SS, MacGlashan DW Jr, Sterbinsky SA, Togias A, Adelman DC, Lichtenstein LM, Bochner BS. Down-regulation of human basophil IgE and FC epsilon RI alpha surface densities and mediator release by anti-IgE-infusions is reversible in vitro and in vivo. J Immunol. 1999 May 1;162(9):5624-30.
Zweiman B, Valenzano M, Atkins PC, Tanus T, Getsy JA. Characteristics of histamine-releasing activity in the sera of patients with chronic idiopathic urticaria. J Allergy Clin Immunol. 1996 Jul;98(1):89-98.
Baiardini I, Giardini A, Pasquali M, Dignetti P, Guerra L, Specchia C, Braido F, Majani G, Canonica GW. Quality of life and patients' satisfaction in chronic urticaria and respiratory allergy. Allergy. 2003 Jul;58(7):621-3.
Soter NA. Acute and chronic urticaria and angioedema. J Am Acad Dermatol. 1991 Jul;25(1 Pt 2):146-54. Review.
Kaplan AP. Clinical practice. Chronic urticaria and angioedema. N Engl J Med. 2002 Jan 17;346(3):175-9. Review. No abstract available.
Grattan CE. Basophils in chronic urticaria. J Investig Dermatol Symp Proc. 2001 Nov;6(2):139-40. Review.
Kern F, Lichtenstein LM. Defective histamine release in chronic urticaria. J Clin Invest. 1976 May;57(5):1369-77.
Starting date: November 2004
Ending date: September 2007
Last updated: May 6, 2008