Pavel Kolkhir1, Martin K Church2, Sabine Altrichter2, Per Stahl Skov3, Tomasz Hawro2, Stefan Frischbutter2, Martin Metz2, Marcus Maurer4. 1. Dermatological Allergology, Allergie-Centrum-Charité, Department of Dermatology and Allergy, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany; Division of Immune-Mediated Skin Diseases, I.M. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia. 2. Dermatological Allergology, Allergie-Centrum-Charité, Department of Dermatology and Allergy, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. 3. Dermatological Department, University Hospital of Southern Denmark, Odense, Denmark; RefLab ApS, Copenhagen, Denmark. 4. Dermatological Allergology, Allergie-Centrum-Charité, Department of Dermatology and Allergy, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. Electronic address: marcus.maurer@charite.de.
Abstract
BACKGROUND: Chronic spontaneous urticaria (CSU) is characterized by the degranulation of skin mast cells and the influx of basophils and eosinophils to affected skin sites. Blood basopenia has been linked to severe antihistamine-resistant CSU and type IIb autoimmunity, whereas the role of eosinophils in CSU is largely unknown. OBJECTIVE: To analyze data from 1613 patients with CSU from 2 centers to study the prevalence, role, and relevance of eosinopenia in CSU. METHODS: Peripheral blood eosinophil and basophil counts were measured by automated hematology analyzers. Patient files were screened for clinical characteristics, results of laboratory tests, the autologous serum skin test, the serum-induced basophil histamine release assay, and response to second-generation H1-antihistamines and omalizumab. RESULTS: Ten percent of patients with CSU had eosinopenia. Eosinopenia was associated with the female sex, high disease activity, autologous serum skin test and basophil histamine release assay positivity, low total IgE, and high levels of C-reactive protein and IgG-antithyroperoxidase (P ≤ .007). Nonresponders to second-generation H1-antihistamines or omalizumab had significantly lower eosinophils as compared with responders (P < .05 and P < .01, respectively). Blood eosinophil counts correlated with basophil counts (r = 0.396; P < .001), and 81% of patients with CSU with undetectable eosinophils had basopenia. The combination of eosinopenia and basopenia is a better predictor of nonresponse to second-generation H1-antihistamines than eosinopenia alone (odds ratio of 9.5 vs 4.8). CONCLUSIONS: Eosinopenia in patients with CSU is associated with type IIb autoimmunity, high disease activity, and poor response to treatment. Eosinophils should be explored as biomarkers and investigated for their contribution to the pathogenesis of CSU.
BACKGROUND: Chronic spontaneous urticaria (CSU) is characterized by the degranulation of skin mast cells and the influx of basophils and eosinophils to affected skin sites. Blood basopenia has been linked to severe antihistamine-resistant CSU and type IIb autoimmunity, whereas the role of eosinophils in CSU is largely unknown. OBJECTIVE: To analyze data from 1613 patients with CSU from 2 centers to study the prevalence, role, and relevance of eosinopenia in CSU. METHODS: Peripheral blood eosinophil and basophil counts were measured by automated hematology analyzers. Patient files were screened for clinical characteristics, results of laboratory tests, the autologous serum skin test, the serum-induced basophil histamine release assay, and response to second-generation H1-antihistamines and omalizumab. RESULTS: Ten percent of patients with CSU had eosinopenia. Eosinopenia was associated with the female sex, high disease activity, autologous serum skin test and basophil histamine release assay positivity, low total IgE, and high levels of C-reactive protein and IgG-antithyroperoxidase (P ≤ .007). Nonresponders to second-generation H1-antihistamines or omalizumab had significantly lower eosinophils as compared with responders (P < .05 and P < .01, respectively). Blood eosinophil counts correlated with basophil counts (r = 0.396; P < .001), and 81% of patients with CSU with undetectable eosinophils had basopenia. The combination of eosinopenia and basopenia is a better predictor of nonresponse to second-generation H1-antihistamines than eosinopenia alone (odds ratio of 9.5 vs 4.8). CONCLUSIONS: Eosinopenia in patients with CSU is associated with type IIb autoimmunity, high disease activity, and poor response to treatment. Eosinophils should be explored as biomarkers and investigated for their contribution to the pathogenesis of CSU.
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