Fexofenadine: A review of its use in the treatment of urticaria in pediatric and adult populations

Urticaria is classified according to its duration as acute or chronic and according to the triggers as spontaneous or inducible (see Tab. 1 and 2).

Tab. 1. Classification of urticaria by duration [2]

Tab. 2. Classification of urticaria by causes [2]

The pathogenesis of urticaria is not fully understood. It is a disease primarily driven by mast cells. Effectors react with the membrane of mast cells, activating them and thus leading to the release of inflammatory mediators and stimulation of signaling pathways that cause the formation of wheals and angioedema (see Fig. 1 and 2) [2].

In urticaria, dysregulation of mast cells and basophiles releases inflammatory mediators. These inflammatory mediators, such as histamine, TNF-α, and interleukins, stimulate signalling pathways that lead to the symptoms of urticaria. In most patients urticaria cannot be avoided. The guidelines strongly recommend treatment with oral second-generation H₁ antihistamines as first line [1]. This group of agents is effective and well tolerated. Second-generation antihistamines do not cross or only minimally cross the blood-brain barrier and therefore only slightly or non-sedating as well as free of anticholinergic adverse side effects. In addition to histamine, other inflammatory mediators are released. In patients who do not respond to histamine, short-term treatment of up to ten days with glucocorticoids can be considered. Other therapeutic options, such as treatment with omalizumab, should be evaluated by specialized centers [2].

Fexofenadine HCl is a well-tolerated and long-established treatment of urticaria in both adults and children [2]. The approved dose for urticaria treatment in adults and children 12 years of age and older is 180 mg tablets once daily or 60 mg two times daily. Fexofenadine suspension is available for children 6 months of age and older [2, 3]. Second-generation antihistamines pass the blood-brain barrier to a lesser extent than first-generation antihistamines. Central side effects such as a sedative effect therefore occur to a lesser extent. Within the group of second-generation antihistamines, there are significant differences with regard to sedative effects. While fexofenadine does not occupy any of the H₁ receptors of the cerebral cortex, 20 to 50 % of these receptors are occupied after ingestion of cetirizine [4].

_{Conflict of interest: M. Murrieta-Aguttes and M. Amessou are employees of Sanofi.}

_{Disclosures: Medical Writing and Publication funded by Sanofi.}