Abstract
Allergic rhinitis (AR) is a chronic upper respiratory disease estimated to affect between 10 and 40% of the worldwide population. The mechanisms underlying AR are highly complex and involve multiple immune cells, mediators, and cytokines. As such, the development of a single drug to treat allergic inflammation and/or symptoms is confounded by the complexity of the disease pathophysiology. Complete avoidance of allergens that trigger AR symptoms is not possible and without a cure, the available therapeutic options are typically focused on achieving symptomatic relief. Topical therapies offer many advantages over oral therapies, such as delivering greater concentrations of drugs to the receptor sites at the source of the allergic inflammation and the reduced risk of systemic side effects. This review describes the complex pathophysiology of AR and identifies the mechanism(s) of action of topical treatments including antihistamines, steroids, anticholinergics, decongestants and chromones in relation to AR pathophysiology. Following the literature review a discussion on the future therapeutic strategies for AR treatment is provided.
Highlights
Allergic rhinitis (AR) is estimated to affect between 10 and 40% of the population worldwide (Bjorksten et al, 2008; Bernstein et al, 2016) and is associated with significant medical and economic burden (Cook et al, 2007; Zuberbier et al, 2014; Marcellusi et al, 2015)
The inhibition of mast cell development and eosinophil viability by corticosteroids would likely lead to fewer numbers of mature mast cells and eosinophils in the nasal mucosa, which given the large role these cells play in the allergic reaction, would be expected to aid in symptom resolution should these results be translated to humans
The combination treatment was not significantly more effective than monotherapy at improving Th1/T-helper 2 (Th2) balance, quantified via expression of IFN-γ and T-bet (Th1) and GATA3 and IL-4 (Th2) cell-specific markers (Kim et al, 2017). Both steroids and antihistamines reportedly interfere with the ubiquitous transcription factor NF-κB (Leurs et al, 2002; Canonica and Blaiss, 2011; Uva et al, 2012) thereby preventing the expression of pro-inflammatory genes that contribute to AR symptom manifestation
Summary
The development of a single drug to treat allergic inflammation and/or symptoms is confounded by the complexity of the disease pathophysiology. Complete avoidance of allergens that trigger AR symptoms is not possible and without a cure, the available therapeutic options are typically focused on achieving symptomatic relief. Topical therapies offer many advantages over oral therapies, such as delivering greater concentrations of drugs to the receptor sites at the source of the allergic inflammation and the reduced risk of systemic side effects. This review describes the complex pathophysiology of AR and identifies the mechanism(s) of action of topical treatments including antihistamines, steroids, anticholinergics, decongestants and chromones in relation to AR pathophysiology. Following the literature review a discussion on the future therapeutic strategies for AR treatment is provided
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
