Abstract
BackgroundRecent consensus statements demonstrate the breadth of the chronic rhinosinusitis (CRS) differential diagnosis. However, the classification and mechanisms of different CRS phenotypes remains problematic.MethodStatistical patterns of subjective and objective findings were assessed by retrospective chart review.ResultsCRS patients were readily divided into those with (50/99) and without (49/99) polyposis. Aspirin sensitivity was limited to 17/50 polyp subjects. They had peripheral blood eosinophilia and small airways obstruction. Allergy skin tests were positive in 71% of the remaining polyp subjects. IgE was<10 IU/ml in 8/38 polyp and 20/45 nonpolyp subjects (p = 0.015, Fisher's Exact test). CT scans of the CRS without polyp group showed sinus mucosal thickening (probable glandular hypertrophy) in 28/49, and nasal osteomeatal disease in 21/49. Immunoglobulin isotype deficiencies were more prevalent in nonpolyp than polyp subjects (p < 0.05).ConclusionCRS subjects were retrospectively classified in to 4 categories using the algorithm of (1) polyp vs. nonpolyp disease, (2) aspirin sensitivity in polyposis, and (3) sinus mucosal thickening vs. nasal osteomeatal disease (CT scan extent of disease) for nonpolypoid subjects. We propose that the pathogenic mechanisms responsible for polyposis, aspirin sensitivity, humoral immunodeficiency, glandular hypertrophy, eosinophilia and atopy are primary mechanisms underlying these CRS phenotypes. The influence of microbial disease and other factors remain to be examined in this framework. We predict that future clinical studies and treatment decisions will be more logical when these interactive disease mechanisms are used to stratify CRS patients.
Highlights
The syndrome of chronic rhinosinusitis (CRS) has been defined by mucopurulent anterior or posterior nasal discharge, regional facial or dental pain, sinus region tenderness, fetid odor, and other symptoms that do not respond to 12 weeks of adequate therapy [1,2]
In the absence of nasal polyposis, we proposed that the sinus thickening in the CRSsNP group was due to glandular hypertrophy [7,8]
Our results suggest that 17% of CRS and one third of all nasal polyp subjects have aspirin sensitivity
Summary
The syndrome of chronic rhinosinusitis (CRS) has been defined by mucopurulent anterior or posterior nasal discharge, regional facial or dental pain, sinus region tenderness, fetid odor, and other symptoms that do not respond to 12 weeks of adequate therapy [1,2]. This clinical definition has been updated to divide CRS into those with ("CRSwNP") and without nasal polyposis Additional differences in presentation, natural history, background of atopy or other phenotypes, eosinophilia, pathophysiological mechanisms, and responses to therapy may occur within each subset. The classification and mechanisms of different CRS phenotypes remains problematic
Sign-in/Register to view highlights & summary 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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
