Hematologic parameters as biomarkers for antihistamine and omalizumab resistance in chronic spontaneous urticaria.

Biomarkers of resistance to H-antihistamines (AH) and omalizumab in chronic spontaneous urticaria (CSU) are still a matter of debate. To identify clinical and laboratory attributes of the patient that may be predictive of AH and omalizumab resistance in CSU. We conducted a retrospective observational study by using the electronic patient record data base of patients with CSU and of sex- and age-matched controls. Patients with CSU were divided into three study groups: the CSU group, patients who responded to AHs; the antihistamine-resistant CSU (AH-CSU) group, patients refractory to a fourfold AH dose; and the control group, composed of a random sample of age- and sex-matched subjects, with a case-control ratio of 1:2. The patients in the AH-CSU group treated with omalizumab were compared according to the response or resistance to omalizumab. 106 subjects in the AH-CSU group, 483 in the CSU group, and 1198 in the control group were compared. Both AH-CSU (112.7 ± 43.1 kU/mL) and CSU (129.5 ± 52.4 kU/mL) groups were associated with higher plasma total IgE levels than control group (103.2 ± 49.5 kU/mL; < 0.001). The AH-CSU group was characterized by a higher plasma high-sensitivity C-reactive protein level (6.4 ± 3.7 mg/L) than the CSU group (4.3 ± 1.4 mg/L; < 0.001) and the control group (3.1 ± 1.8 mg/L; < 0.001). The AH-CSU and CSU groups were characterized by a lower mean ± standard deviation basophil counts (0.18 ± 0.16 cells ×10/L and 0.19 ± 0.11 cells ×10/L, respectively) than the control group (0.22 ± 0.09 cells ×10/L; < 0.001). The mean platelet volume as higher in the AH-CSU group (11.2 ± 0.3 fL) than in the CSU group (11.1 ± 0.4 fL; = 0.002) and in the control group (10.3 ± 0.4 fL; < 0.001). There were no significant differences in the mean levels of lymphocytes, monocytes, eosinophils, basophils, and platelets, and the rates of eosinopenia and basopenia between the patients in the AH-CSU group who responded to and those who were resistant to omalizumab. This study provided additional data of interest to examine the pathophysiologic role of low-grade inflammation and basopenia in patients with CSU and resistant to AHs and omalizumab.