Biomarkers of chronic spontaneous urticaria and their clinical implications

ABSTRACT

Introduction: Chronic spontaneous urticaria (CSU) is a frequent disorder in which activation of effector cells and histamine release can be induced via several distinct pathogenetic mechanisms. Much work has been carried out to identify biomarkers useful for classifying CSU patients, and to predict their response to currently available treatments.

Areas covered: The recent literature dealing with CSU biomarkers was screened in PubMed and Google Scholar using ‘chronic spontaneous urticaria’, ‘biomarker’, ‘diagnosis’, ‘therapy’ and ‘treatment response’ as key words. The characteristics found in relevant papers were divided into clinical and serological biomarkers of (a) clinical severity/disease activity, and (b) response to treatments.

Expert opinion: A diagnostic biomarker for CSU is still missing. Most biomarkers described so far do not seem to possess sufficient specificity for this disease. Basopenia and the activation of the coagulation cascade might be biomarkers of disease activity and severity, but information available so far is insufficient to consider their routine use. Markers suggesting IgG-mediated autoimmunity (autologous serum skin test, basophil activation/histamine release assays, low total IgE) seem to identify patients less prone to respond to omalizumab but responsive to cyclosporine. In contrast, ‘autoallergy’ (i.e. the presence of IgE to autoallergens), which is often associated with elevated IgE levels seems to identify patients who will respond to omalizumab.

KEYWORDS:

• Chronic urticaria
• biomarkers
• autoimmunity
• autoallergy
• antihistamines
• omalizumab
• cyclosporine

Article highlights

• There are no diagnostic biomarker for CSU

• Basopenia has been suggested as a specific and sensitive biomarker of CSU activity, but information is currently insufficient to consider its routine clinical use.

• The activation of the coagulation cascade characterizes about 50% of severe cases and is often associated with a poor response to antihistamines and cyclosporine. However, information is still insufficient to consider its routine clinical use.

• Patients with severe CSU and a mainly IgG-mediated autoimmune pathogenesis are unlikely to respond promptly or completely to omalizumab.

• Patients with severe CSU and an IgE-mediated ‘autoallergic’ disease are the best candidates for a good response to omalizumab.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.