The Role of Antihistamines in the Treatment of Vasomotor Rhinitis

Abstract

BackgroundThe pathogenesis of vasomotor rhinitis is not understood. It is unlikely that antihistamines, based on their H1 antagonist activity alone, would be effective in this disorder.MethodsNonetheless, at least one double-blind, placebo-controlled multicenter trial has found that intranasal azelastine relieves symptoms of this disorder better than placebo. The mechanism responsible for its beneficial effect in nonallergic rhinitis is unclear but probably relates to "anti-inflammatory/antiallergic" activities.ResultsSuch mechanisms have been demonstrated for a number of different oral antihistamines, but often the concentrations required in vitro are higher than those that are normally achieved in vivo using recommended dosing. It has been postulated that intranasal administration, which can achieve high local levels, might be a factor responsible for enhancing the "anti-inflammatory/antiallergic" properties.ConclusionsInterpreting this information allows one to conclude that antihistamines may be potentially effective agents in vasomotor rhinitis, and are more likely to be so when administered intranasally, despite the fact that data documenting this beneficial effect are sparse.

Intranasal antihistamines in the treatment of idiopathic non-allergic rhinitis: a systematic review and meta-analysis

“…Azelastine HCl was given FDA approval for the treatment of patients (>12y.o.) with VMR in November 2000, based on safety studies and the results of the two trials by Banov et al (10,15) . So far, this is the first systematic review, to our knowledge, to regroup all placebo-controlled INAH trials in the treatment of IR.…”

“…Moreover, histamine release has a negligible role compared to the autonomic nervous system imbalance effect on vasodilatation. However, it has been claimed that an anti-inflammatory activity of antihistamines against the neurogenic inflammatory reflex seen in IR may be the mainstay behind the improvement of symptoms (5,15) . Mediators like substance p (SP), calcitonin gene related peptide and neurokinin A are proinflammatory peptides found in the human nasal mucosa and were thought to be implicated in the neural mechanisms of NAR (15,17) .…”

“…However, it has been claimed that an anti-inflammatory activity of antihistamines against the neurogenic inflammatory reflex seen in IR may be the mainstay behind the improvement of symptoms (5,15) . Mediators like substance p (SP), calcitonin gene related peptide and neurokinin A are proinflammatory peptides found in the human nasal mucosa and were thought to be implicated in the neural mechanisms of NAR (15,17) . Gawlik et al have induced the secretion of SP in the nasal mucosa using a non-allergenic challenge with hypertonic saline in patients with NAR and have shown the propensity of topical Azelastine HCl to reduce SP's concentration and alleviate rhinitis symptoms in the same treatment group (11) .…”

Nonallergic Rhinitis

“…15 Compared with allergic rhinitis, less rigorous safety and efficacy pharmaceutical treatment data exist for nonallergic rhinitis. However, there is a growing body of evidence for the efficacy of topical therapies, including topical antihistamine nasal sprays, [16][17][18] intranasal steroids, 19 and intranasal ipratropium bromide 20 (for rhinorrhea). Recently, a combination product containing both a topical antihistamine (azelastine) and a topical nasal steroid (fluticasone propionate), was conducted in a mixed population of patients with either perennial allergic rhinitis or vasomotor rhinitis, and was shown to be efficacious.…”

Overview of the Treatment of Allergic Rhinitis and Nonallergic Rhinopathy

“…These include prevention of mast cell and basophil degranulation, down-regulation of adhesion molecules and chemokines, reduction of inflammatory cytokine expression, suppression of neurogenic enhancement of inflammation, and augmentation of inflammatory cell apoptosis (59). These include prevention of mast cell and basophil degranulation, down-regulation of adhesion molecules and chemokines, reduction of inflammatory cytokine expression, suppression of neurogenic enhancement of inflammation, and augmentation of inflammatory cell apoptosis (59).…”