Abstract
Chronic spontaneous urticaria (CSU) is defined as itchy weals, angio-oedema, or both, arising spontaneously without external physical stimuli. Symptoms of the disease continue to develop for more than 6 weeks. It carries a high socioeconomic burden with considerable health care costs. Second generation H1-antihistamines are the mainstay of urticaria treatment and are the only licensed option. However, many patients are resistant to H1-antihistamine therapy. Omalizumab has proven to be an effective therapeutic option in patients with recalcitrant chronic urticaria. Ciclosporin appears to be more beneficial in patients with functional histamine releasing autoantibodies as a cause of their disease. This review article will highlight the major therapeutic options available today for the management of CSU knowing that good quality evidence for efficacy of many agents is scarce except for H1-antihistamines and omalizumab.
Financial & competing interests disclosure
C Grattan is on the advisory bodies for Novartis, GSK and CSL Behring. The authors have no other 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 apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Chronic spontaneous urticaria is defined as itchy weals, angioedema or both, arising spontaneously without external physical stimuli and lasting for more than 6 weeks.
It is a common disease that can be debilitating and carries a high socioeconomic burden.
Most of the current treatment options are targeted at symptoms and are not disease-modifying.
Second-generation H1-antihistamines are the mainstay of urticaria treatment and are the only licensed option but are not effective for all patients.
Omalizumab has proven to be an effective therapeutic option in patients with recalcitrant chronic urticaria.
Ciclosporin appears to be more beneficial in patients with functional histamine-releasing autoantibodies as a cause of their disease.
Future research should focus on better understanding of the cellular and biochemical events involved in the pathophysiology of the disease and development of drugs targeting disease suppression.