Current opinion in otolaryngology & head and neck surgery · 2009
The role of allergy in rhinosinusitis.
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Pant Harshita, Ferguson Berrylin J, Macardle Peter J
Аннотация
PURPOSE OF REVIEW: To examine the current evidence for IgE and non-IgE-mediated hypersensitivity mechanisms in acute and chronic rhinosinusitis.
RECENT FINDINGS: Epidemiological studies show that classical IgE-mediated allergy is present in a proportion of acute rhinosinusitis patients. There is conflicting evidence whether the prevalence of IgE-mediated allergy is greater in chronic rhinosinusitis than in individuals without chronic rhinosinusitis. Despite presence of classical IgE-mediated allergy, based on elevated allergen-specific serum IgE levels and positive skin prick tests, currently there is no direct evidence for allergy as a major cause of sinonasal inflammation in chronic rhinosinusitis. There is increasing evidence that non-IgE-mediated fungal hypersensitivity and nonallergic IgE-associated inflammation may contribute to the pathogenesis in some forms of chronic rhinosinusitis, including allergic fungal sinusitis. Specific IgE to bacterial superantigens may also be elevated in nasal polyps and modulate eosinophilic inflammation. Recent insights into mucosal immune mechanisms yield intriguing prospects for the roles of mucosal IgE, mast cells and non-IgE-mediated hypersensitivity mechanisms that require further examination in rhinosinusitis.
SUMMARY: There is a need for further immunological studies of the systemic and mucosal cellular and humoral mechanisms in well defined patient groups and controls to better understand the role of IgE and non-IgE-mediated hypersensitivity mechanisms and nonhypersensitivity functions of IgE in rhinosinusitis.
RECENT FINDINGS: Epidemiological studies show that classical IgE-mediated allergy is present in a proportion of acute rhinosinusitis patients. There is conflicting evidence whether the prevalence of IgE-mediated allergy is greater in chronic rhinosinusitis than in individuals without chronic rhinosinusitis. Despite presence of classical IgE-mediated allergy, based on elevated allergen-specific serum IgE levels and positive skin prick tests, currently there is no direct evidence for allergy as a major cause of sinonasal inflammation in chronic rhinosinusitis. There is increasing evidence that non-IgE-mediated fungal hypersensitivity and nonallergic IgE-associated inflammation may contribute to the pathogenesis in some forms of chronic rhinosinusitis, including allergic fungal sinusitis. Specific IgE to bacterial superantigens may also be elevated in nasal polyps and modulate eosinophilic inflammation. Recent insights into mucosal immune mechanisms yield intriguing prospects for the roles of mucosal IgE, mast cells and non-IgE-mediated hypersensitivity mechanisms that require further examination in rhinosinusitis.
SUMMARY: There is a need for further immunological studies of the systemic and mucosal cellular and humoral mechanisms in well defined patient groups and controls to better understand the role of IgE and non-IgE-mediated hypersensitivity mechanisms and nonhypersensitivity functions of IgE in rhinosinusitis.