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Factors driving olfactory loss in patients with chronic rhinosinusitis: a case control study
Author(s) -
Schlosser Rodney J.,
Smith Timothy L.,
Mace Jess C.,
Alt Jeremiah,
Beswick Daniel M.,
Mattos Jose L.,
Payne Spencer,
Ramakrishnan Vijay R.,
Soler Zachary M
Publication year - 2020
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.22445
Subject(s) - medicine , nasal polyps , confounding , chronic rhinosinusitis , asthma , sinusitis , olfaction , diabetes mellitus , prospective cohort study , olfactory system , case control study , multivariate analysis , gastroenterology , surgery , endocrinology , neuroscience , psychiatry , biology
Background Olfactory dysfunction (OD) in chronic rhinosinusitis (CRS) is common. It is likely that numerous factors such as sex, race, age, allergies, asthma, smoking, and other comorbidities play a role in CRS‐related OD. In order to determine which aspects of OD are due solely to CRS and which are associated with other confounders, control populations are needed to allow appropriate risk assessments. Methods Prospective, multi‐institutional enrollment of patients with CRS and control subjects without CRS was performed. Demographic information, comorbidities, and olfactory testing (Sniffin’ Sticks) of threshold (T), discrimination (D), and identification (I) scores (TDI) was collected. Results A total of 224 patients with CRS and 164 control subjects were enrolled. Olfaction was worse in CRS patients compared to controls (mean ± standard deviation (SD) TDI = 22.4 ± 9.5 vs 28.8 ± 7.0, respectively, p < 0.001). Only 27% of CRS patients were normosmic compared to 49% of controls ( p < 0.001). When stratifying by nasal polyp (NP) status, CRSwNP patients had significant impairments in TDI, T, D, and I compared to controls with mean differences of 11.2, 3.3, 3.5, and 4.4 points, respectively (all p < 0.001). In contrast, CRSsNP patients only had impaired T when compared to controls with a mean difference of 2.2 points ( p < 0.001). Multivariate modeling of TDI scoring showed that OD was driven by polyps, asthma, diabetes, and age. CRSsNP was not independently associated with worse TDI scores. Conclusion OD in CRS patients is multifactorial. Independent drivers appear to be polyp status, asthma, diabetes, and age. OD in patients with CRSsNP is similar to controls with the exception of impaired thresholds.