Introduction: Omalizumab is approved for severe chronic spontaneous urticaria (CSU), non-responsive to non-sedating H1‑antihistamines. However, there is little data to predict patients’ response to omalizumab. We aim to identify possible predictors of response to omalizumab in CSU patients. Methods: Retrospective chart-review study (2006‑2015), of CSU adults treated with omalizumab for 6 or more months. Statistical analyses: descriptive statistics, chi-square, odds ratio analysis and generalized linear models. Results: Twenty-three patients (3 men) were included. Prior to omalizumab, all were medicated with montelukast, quadruple daily dose of non-sedating H1-antihistamine and systemic oral corticosteroids; additionally, 15 were on H2-antihistamines. IVIg, cyclosporine and azatioprine had previously been tried in 8 patients with no efficacy. Using generalized linear models, patients showed a reduction, per omalizumab administration, of 16% (p<0.001) of the UAS (urticaria activity score) score and 20% (p<0.001) of the UAS7 (urticaria activity score 7). Women had a reduction, per omalizumab administration, of the UAS (15%, p<0.001) and UAS7 (17%, p<0.001); compared to men’s UAS (2%, p=0.067) and UAS7 (8%, p=0.067) score’s. Patients with baseline total serum IgE>500kU/L had a reduction, per omalizumab administration, of the UAS (28%, p<0.001) and UAS7 (41%, p<0.001) scores; compared to IgE<100kU/L patients who had a reduction of the UAS (12%, p<0.001) and UAS7 (20%, p<0.001) scores. Conclusions: Response to omalizumab seems to be faster in patients with higher baseline total serum IgE and in women. A lack of response to immune-modulating therapies prior to omalizumab does not predict a lack of response to omalizumab.
|Translated title of the contribution||Identification of different response patterns to omalizumab in patients with chronic spontaneous urticaria|
|Number of pages||11|
|Journal||Revista Portuguesa de Imunoalergologia|
|Publication status||Published - 1 Jun 2018|
- Chronic spontaneous urticaria
- Total IgE