Urticaria is a common disorder that adversely affects quality of life; work-related and recreational activities are restricted, while rest, sleep, and emotions are seriously disturbed in a significant proportion of patients. The pathogenic mechanisms vary, but cutaneous mast-cell activation with release of
histamine and other vasoactive or proinflammatory mediators is thought to be the final common pathway for lesion induction in most cases. A subsequent, but incompletely understood, late-phase
allergic reaction seems to prolong the inflammatory process, particularly in certain chronic forms of the disorder. Although
histamine is considered an important mediator of
urticaria, additional substances, including the cysteinyl
leukotrienes (LTs), are putative mediators of the immediate urticarial responses and the inflammatory events that follow in some types of
urticaria. A
second-generation antihistamine,
mizolastine, which exhibits dual activity with selective H1-receptor antagonism and, as shown in animal studies, anti-5-lipoxygenase activity, represents an advance in the treatment of
urticaria. It has rapid, potent and sustained action. At the recommended 10-mg dose,
mizolastine suppresses the
histamine-induced wheal reaction as early as 1 h after
oral administration. Compared to placebo,
mizolastine significantly reduces overall patient discomfort and
pruritus in patients with
chronic idiopathic urticaria. Double-blind, placebo-controlled studies have also shown
mizolastine to be at least as effective as other
second-generation antihistamines. Furthermore, with long-term use of
mizolastine over 1 year, a reduction in
pruritus and the number of urticarial episodes was maintained with no evidence of tachyphylaxis or tolerance.
Mizolastine has also been shown to be an effective treatment for cold-induced
urticaria, causing significant delay in the whealing response to the
ice-cube test and also reducing the wheal diameter.