What has the relief of allergic conjunctivitis by intranasal steroids taught us about the pathophysiology of allergic rhinoconjunctivitis?

Authors


  • Conflicts of interest: FB has received research funding from Glaxo SmithKline. RN has no conflicts to declare.

Correspondence:
Robert M. Naclerio, Section of Otolaryngology-Head and Neck Surgery, University of Chicago, 5841 S. Maryland Avenue, MC 1035, Chicago, IL 60637, USA.
E-mail: rnacleri@surgery.bsd.uchicago.edu

Summary

Patients with allergic rhinitis (AR) report ocular symptoms 40–70% of the time. These symptoms can be burdensome and have a major impact on patients' quality of life. Most clinicians believe that ocular symptoms result from direct contact of allergen with the conjunctiva, although other explanations such as a nasal-ocular reflex, blockage of the nasal lacrimal duct, and systemic effects of cytokines released from the nasal mucosa can explain the association. However, if direct contact by an allergen is the sole explanation, how do we explain the efficacy of intranasal steroids on the eye symptoms of AR, especially because most intranasal steroids have <0.5% systemic bioavailability? This paper highlights a potential mechanism for the development of ocular symptoms after nasal exposure to antigen, the nasal-ocular reflex, and speculates how intranasal steroids can affect this reflex and eye symptoms. Two nasal-challenge studies assessing the nasal-ocular reflex are presented. The first shows the presence of a nasal-ocular reflex in response to localized nasal-antigen challenge, which is initiated by the release of histamine and blocked by a topical, intranasal antihistamine. The second study shows that the nasal-ocular reflex is augmented with repeated nasal antigen challenge, a response that is inhibited by pretreatment with an intranasal steroid. These studies provide an explanation for the way in which treatment with intranasal steroids can work locally in the nose to reduce ocular symptoms in patients with AR. This explanation, however, would only be valid if the majority of eye symptoms in patients with AR were caused by the nasal-ocular reflex and not by direct contact of antigen with the conjunctiva – an assumption supported by clinical studies.

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