In Reference to Anosmia and Ageusia: Common Findings in COVID-19 Patients.

Dear Editor:

We thank Vaira et al. for their important communication. The authors observed that 19.4% of paucisymptomatic COVID‐19 patients have fever, anosmia, and ageusia, which was previously reported in only 1 Asian study.

We agree about the importance to consider these symptoms in the COVID‐19 infection but, regarding our European multicenter study investigating the prevalence of olfactory and gustatory dysfunctions in COVID‐19 patients, we believe that the prevalence is significantly higher than reported by Vaira et al. Based on the evaluation of 417 hospitalized or confined mild‐to‐moderate COVID‐19 patients (RT‐PCR+), we found that 85.6% and 88.0% of patients reported olfactory and gustatory dysfunctions, respectively. Naturally, we cannot provide specific rates of anosmic and hyposmic patients because the use of these terms (anosmia/hyposmia) requires the realization of psychophysical or electrophysiological tests.

Vaira et al. did not specify the diagnosis method for their patients (clinical vs. RT‐PCR+ diagnosis). The study of the otolaryngological manifestations in COVID‐19 requires rigorous diagnosis criteria because, even now, some patients have seasonal influenza, which may be a confounding clinical factor.

Our study corroborates the observation of Vaira et al. that a significant number of COVID‐19 patients have olfactory dysfunction without nasal obstruction or rhinorrhea. One‐fifth of COVID‐19 patients had this unusual clinical presentation. Based on an old publication investigating the olfactory disorder in upper respiratory viral infection, authors suggested that the olfactory dysfunction may be related to direct damage by the virus on the olfactory receptors. In fact, the coronavirus has already been identified as an agent responsible of anosmia. The pathophysiological mechanisms would be more complex than presumed and do not just involve mucosa receptors. Basic science research suggested that there would have an entry of the virus into the brain and the olfactory bulb through the human angiotensin‐converting enzyme 2 receptor (ACE2). Interestingly, another study suggested that there would be a lot of ACE2 polymorphisms and ACE2 expression levels between Asian and European populations. Hence, the difference of prevalence of olfactory dysfunction between Asia and Europe could result of different genetic patterns. Moreover, a preprint study recently supported that the SARS‐CoV‐2 would affect more specifically the glial cells of the olfactory bulb, which have a higher ACE2 expression than the neurons. This hypothesis would explain the fact that 44% of patients recover olfaction within the 14 days following the infection, which seems to be a rapid recovery rate in case of neuron injury.