Chronic Rhinosinusitis and COVID-19

Abstract

The COVID-19 pandemic has raised awareness about olfactory dysfunction, although a loss of smell was present in the general population before COVID-19. Chronic rhinosinusitis (CRS) is a common upper airway chronic inflammatory disease that is also one of the most common causes of olfactory dysfunction. It can be classified into different phenotypes (ie, with and without nasal polyps) and endotypes (ie, type 2 and non-type 2 inflammation). However, scientific information regarding CRS within the context of COVID-19 is still scarce. This review focuses on (1) the potential effects of severe acute respiratory syndrome coronavirus 2 infection on CRS symptoms, including a loss of smell, and comorbidities; (2) the pathophysiologic mechanisms involved in the olfactory dysfunction; (3) CRS diagnosis in the context of COVID-19, including telemedicine; (4) the protective hypothesis of CRS in COVID-19; and (5) the efficacy and safety of therapeutic options for CRS within the context of COVID-19.

Keywords: Angiotensin converting enzyme 2; Biologics; COVID-19; Chronic rhinosinusitis; Corticosteroids; Inflammation endotypes; Olfactory dysfunction; Olfactory training; SARS-CoV-2; Telemedicine.

Figure 1

Patients with chronic rhinosinusitis with nasal polyps (CRSwNP) who have COVID-19 share type 1 and 2 inflammatory endotypes. This has clear implications for the diagnosis (symptom presentation and evolution) and treatment options.

Figure 2

Impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (left) in patients without chronic rhinosinusitis with nasal polyps (type 1 predominant) and (right) in those with chronic rhinosinusitis with nasal polyps (type 2 predominant). Type 2 eosinophilic inflammation may decrease angiotensin converting enzyme 2 (ACE2) expression in sinonasal epithelial cells, which potentially represents a protective effect for SARS-CoV-2 infection. ILC, innate lymphoid cell.