Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2006 Oct;6(5):383-9.
doi: 10.1097/01.all.0000244801.79475.66.

Pharmacology of ocular allergy

Affiliations
Review

Pharmacology of ocular allergy

Beth Lillian Schultz. Curr Opin Allergy Clin Immunol. 2006 Oct.

Abstract

Purpose of review: To evaluate the pharmacology of current drug development directed towards ocular allergy. Increased worldwide prevalence of ocular allergy has stimulated expansion of management strategies towards physiologic and immunologic drug targets.

Recent findings: Present drug targets are located in the conjunctival mucosal surface at the initial site of allergen exposure. Pharmacologic intervention attends to early and late phase reactions. Targets generating a response include mast cells, IgE, released preformed mediator histamine, and newly formed mediators, such as prostaglandins, leukotrienes and cytokines. Methods to simulate allergy and measure efficacy of drugs are the conjunctival allergen challenge and the conjunctival provocation test. Pharmacologic outcome is measured via cytologic biomarkers and clinical signs/symptoms of redness, itching, lid swelling and chemosis. Endpoint instruments such as the Ocular Allergy Index and Eye Allergy Patient Impact Questionnaire have emerged from the field of pharmacoeconomics.

Summary: Important pharmacologic properties of targets have been revealed. First, histamine is more specifically antagonized by second generation antihistamines. Second, newly formed mediators and downstream responders (prostaglandins, leukotrienes, interleukins, intercellular adhesion molecule 1, tumor necrosis factor, vascular cell adhesion molecule, eosinophils and neutrophils) are more selectively antagonized by dual/multiple-action agents.

PubMed Disclaimer

MeSH terms

Substances