Introduction:

At present, the understanding about chronic spontaneous urticarial (CSU) is relatively scarce, particularly with regard to its etiopathogenesis. Due to the lack of data on etiology, the available treatment is only aimed at symptomatic control, with the majority of patients being resistant both to the first and second lines of therapy. Taking into account the impact that CSU may have on the patient and the current difficulties in its control, investigation of biomarkers that predict response to treatment if highly needed.

Methods:

A review was conducted on biomarkers that allow guiding the therapeutic escalation of these patients in clinical practice, allowing a more effective and early control of urticaria.

Results:

Many biomarkers are being studied to predict response to therapy, but definitive results are still missing. Nevertheless, most studies point out that a high C-reactive protein or D-dimer, as well as autoimmune-based urticaria, are usually linked to a poor response to anti-H1. In which concerns the two subtypes of auto-immunity involved in CSU, if IgG anti-FcεRI or anti-IgE predominates (autoimmunity type IIb), patients usually have a positive autologous serum skin test (ASST), a positive basophil activation test (BAT), basopenia, eosinopenia and low or very-low total serum IgE, and response to omalizumab will be slow and/or poor, but there is tendency to a favourable outcome on cyclosporine. If IgE anti-self predominates (autoimmunity type I or autoallergy), response to cyclosporine will be poor, but positive and rapid to omalizumb, and these patients usually have a normal or high IgE that will increase after omalizumab therapy, whereas the other parameters typical of type IIb are absent. High D-dimer predicts an unfavourable response to the three therapies.

Conclusion:

In CSU resistant to second-generation antihistamines, patients who respond favourably to cyclosporine and slowly to omalizumab have mostly underlying type IIb autoimmunity, whereas patients refractory to cyclosporine therapy, but who respond rapidly to omalizumab, have underlying type I or auto-allergic autoimmunity. These subtypes can be indirectly evaluated by total serum IgE, blood cell count, ASST and BAT, but more studies with large cohorts are needed to have more correct predictive data on patients’ response to therapy in CSU.

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