Volume 121, Issue 1 , Pages 122-128, January 2008
Anti-CD20 (rituximab) treatment improves atopic eczema
Background
Atopic eczema (AE) is a chronic inflammatory skin disorder characterized by eczematous skin lesions, pruritus, and typical histopathologic features.
Objective
We asked whether depletion of B cells by monoclonal anti-CD20 antibody therapy (rituximab) would improve severe AE.
Methods
Six patients (4 women and 2 men) with severe AE received 2 intravenous applications of rituximab, each 1000 mg, 2 weeks apart. To evaluate the efficacy of rituximab, we monitored clinical parameters (eczema area and severity index, pruritus), total and allergen-specific IgE levels, skin histology, and inflammatory cells and cytokine expression in the skin and peripheral blood before and after therapy (ClinicalTrials.gov Identifier: NCT00267826).
Results
All patients showed an improvement of their skin symptoms within 4 to 8 weeks. The eczema area and severity index significantly decreased (before therapy, 29.4 ± 4.3; week 8, 8.4 ± 3.6; P < .001). Histologic alterations such as spongiosis, acanthosis, and dermal infiltrate, including T and B cell numbers, also dramatically improved. However, whereas blood B cells were below detectable levels as a consequence of rituximab administration, skin B cells were reduced by approximately 50% only. Expression of IL-5 and IL-13 was reduced after therapy. Moreover, whereas allergen-specific IgE levels were not altered, we observed a slight reduction in total IgE concentrations in blood.
Conclusions
B cells play a major role in AE pathogenesis. Treatment with an anti-CD20 antibody leads to an impressive improvement of AE in patients with severe disease.
Key words: Atopic dermatitis, B cells, biologics, cytokines, inflammation, rituximab, T cells
Abbreviations used: AE, Atopic eczema, EASI, Eczema area and severity index, ECP, Eosinophil cationic protein
Supported by grants from the Swiss National Science Foundation (310000-107526) and Roche Pharma AG, Reinach.
Disclosure of potential conflict of interest: The authors have declared that they have received research support from Roche Pharma AG.
PII: S0091-6749(07)02253-1
doi:10.1016/j.jaci.2007.11.016
© 2008 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Volume 121, Issue 1 , Pages 122-128, January 2008
