The cutoff time of 8 days between fast and slow responders was chosen because it corresponds with the peak plasma level of omalizumab after its initial injection.3 We hypothesized that a slow response to omalizumab occurs in patients with CSU in whom IgG antibodies to unoccupied IgE receptors (FcepsilonRI) activate mast cell mediator release to cause wheal and angioedema formation.4 This hypothesis is based on the knowledge that omalizumab first complexes soluble IgE then sequesters IgE released from mast cells, thus uncovering membrane FcepsilonRI, which subsequently decays slowly over several weeks.5 To test this, the basophil histamine release assay (BHRA) was used. Quantification of free serum IgE, IgE neutralization, and omalizumab concentrations A commercially available recoveryELISA kit was used for the quantification of free IgE, IgE neutralization rates, and omalizumab levels in patient serum (BioTeZ Berlin Buch GmbH, Berlin, Germany) as described previously.E4 Characteristic All complete responders (n = 56) Complete response within 8 d Complete response after 8 d P value Age (y) 48 (33-60) 49 (37-58) 42 (31-63) .544 Sex Female 40 (71.4%) 28 (71.8%) 12 (70.6%) .583 Male 16 (28.6%) 11 (28.2%) 5 (29.4%) BMI 27.3 ± 4.8 27.9 ± 4.9 26.1 ± 4.6 .192 UAS7low * 24.0 ± 9.7 23.0 ± 9.3 26.5 ± 4.6 .215 Disease durationlow * 36 (16-102) 40 (18-103) 24 (14-85) .240 ASST+low * 23 of 46 (50.0%) 12 of 33 (36.4%) 11 of 13 (84.6%) <.01 BHRA+low * 9 of 55 (16.4%) 1 of 38 (2.6%) 8 of 17 (47.1%) <.001 Anti-FcepsilonRI+low * 5 of 44 (11.4%) 4 of 30 (13.3%) 1 of 14 (7.1%) .485 Anti-IgE+low * 1 of 44 (2.3%) 1 of 30 (3.3%) 0 of 14 (0.0%) .682 Total IgElow * 205.4 ± 229.6 239.2 ± 250.6 130.0 ± 155.0 .104 Free IgE after omalizumabdagger 31.8 ± 47.7 31.2 ± 39.6 33.2 ± 64.7 .893 % IgE neutralizationdagger 94.7 ± 13.4 96.7 ± 2.2 90.0 ± 24.5 .106 Omalizumab (μg/mL)dagger 16.2 ± 7.8 16.6 ± 7.2 15.2 ± 9.2 .557 Table I CSU responders to omalizumab: