To the Editor Chronic spontaneous urticaria (CSU) is a rather frequent disease of variable severity characterized by recurrent wheals with or without angioedema for more than 6 weeks. Some patients show a continuous and very severe disease refractory to antihistamine treatment which worsens dramatically their quality of life. The anti-IgE mAb omalizumab is indicated as second line treatment in these cases. The clinical response largely depends on the endotype (either IgG-mediated autoimmune [type IIb] or IgE-mediated "autoallergic" [type I]) of the disease. Positive in-vitro tests of basophil activation (either BAT or BHRA), antinuclear antibodies, autologous serum skin test (ASST) and low total IgE levels have been associatedwith a slow or absent response to the drug (1-5). Conversely, elevated total IgE are generally associated with a prompt response to omalizumab (5-12). Atopic diseases are a well-known cause of elevated IgE, but whether atopic status may be used as a marker of Type I CSU, thus predicting a rapid response to omalizumab, is still unclear (11). The association between CSU and thyroid autoimmunity has been known for almost 30 years (12) but, although typical type IIb CSU patients frequently show low IgE and autoimmune thyroiditis (14), whether thyroid autoimmunity may alone predict a poor or absent response to omalizumab is still undefined. In one study, the prevalence of thyroid autoimmunity was similar in CSU patients with different levels of total IgE (15). The present study investigated whether atopic status and thyroid autoimmunity may be practically useful to discriminate type I and type IIb CSU.