Minimal persistent inflammation in allergic rhinitis: implications for current treatment strategies

REVIEW ARTICLE

Clinical & Experimental Immunology

Volume 158 Issue 3, Pages 260 - 271

Published Online: 25 Aug 2009
Journal Compilation © 2008 British Society for Immunology

G. W. Canonica and E. Compalati

Allergy and Respiratory Diseases, Clinic Dipartmento di Medicina Interna e Specialita Mediche (DIMI), University of Genova, Genova, Italy

Correspondence to G. W. Canonica, Allergy and Respiratory Diseases, Clinic Dipartmento di Medicina Interna e Specialita Mediche (DIMI), University of Genova, Viale Benedetto XV, no. 6, 16132 Genova, Italy.
E-mail: canonica@unige.it

ABSTRACT

Patients with allergic rhinitis have traditionally been placed into 'seasonal' and 'perennial' categories, which do not account for the subclinical inflammatory state that exists in many patients. In subjects with seasonal and perennial allergic rhinitis, even subthreshold doses of allergen have been found to cause inflammatory cell infiltration in the nasal mucosa, including increases in expression of cellular adhesion molecules, nasal and conjunctival eosinophilia, and other markers of inflammation, which do not result in overt allergy symptoms. This state – which has been termed 'minimal persistent inflammation'– may contribute to hyperreactivity and increased susceptibility to development of clinical symptoms as well as common co-morbidities of allergic rhinitis, such as asthma. Treating overt allergy symptoms as well as this underlying inflammatory state requires agents that have well-established clinical efficacy, convenient administration, potent anti-inflammatory effects and proven long-term safety, so that long-term continuous administration is feasible.

Of the three major classes of commonly used allergic rhinitis medications – intranasal corticosteroids, anti-histamines, and anti-leukotrienes – intranasal corticosteroids appear to represent the most reasonable therapeutic option in patients who would benefit from continuous inhibition of persistent inflammation.

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Accepted for publication 14 August 2009