Background: A distinct feature of COVID-19 mediated olfactory dysfunction (OD) is the lack of nasal obstruction and rhinorrhea, indicating a sensorineural mechanism for smell loss. Recent data suggests that local inflammation of the olfactory neuroepithelium may play a key role in COVID-19 OD.
Objective: We aimed to determine the differences in inflammation within the nasal cavity between those with and without OD during acute COVID-19 infection.
Methods: Patients with COVID-19 infection were stratified into those with self-reported OD and those without self-reported OD. Mucous samples were obtained using a nasosorption device and multiplex assay was then used to quantify cytokine levels. Smell loss was measured using the University of Pennsylvania Smell Identification Test (UPSIT).
Results: A total of 21 patients were included: 11 without self-reported OD, 10 with self-reported OD. Median UPSIT scores were 14.5 and 28 for patients with and without self-identified OD respectively with a median difference of 14 [95% CI: 8-20]. Only 1 patient in the group without self-identified OD was normosmic on UPSIT testing. IFN-gamma levels were significantly higher in patients with UPSIT ≤ 25 compared to those with UPSIT > 25 (difference 15.9; 95% CI 1.03 to 187.2; p=0.023). There was a nonsignificant trend towards elevated IL-1β and IL-6 in those with OD.
Conclusion: Increased IFN-gamma levels were significantly associated with anosmia and severe hyposmia, suggesting that local intranasal inflammation plays a role in acute COVID-19 OD. Further studies are needed to investigate the role of local inflammation in COVID-19 OD.