Anosmia: an evolution of our understanding of its importance in COVID-19 and what questions remain to be answered.
Identifieur interne : 001701 ( Main/Exploration ); précédent : 001700; suivant : 001702Anosmia: an evolution of our understanding of its importance in COVID-19 and what questions remain to be answered.
Auteurs : Sven Saussez [France, Belgique] ; Jerome R. Lechien [France, Belgique] ; Claire Hopkins [Royaume-Uni]Source :
- European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery [ 1434-4726 ] ; 2020.
Abstract
BACKGROUND
From the start of the pandemic, many European otolaryngologists observed an unprecendented number of anosmic patients. Early reports proposed that anosmia could be the first or even the only symptom of COVID-19 infection, prompting calls for self-isolation in affected patients.
METHODS
In the present article, we review the COVID-19 anosmia literature and try to answer the following two questions: first, why is COVID-19 infection responsible for such a high incidence of anosmia? Second, in patients with more severe forms is anosmia really less prevalent and why?
RESULTS
In terms of the etiology of olfactory dysfunction, several hypotheses were proposed at the outset of the pandemic; that olfactory cleft inflammation and obstruction caused a localized conductive loss, that there was injury to the sustentacular supporting cells in the olfactory epithelium or, given the known neurotropic potential of coronavirus, that the virus could invade and damage the olfactory bulb. Olfactory cleft obstruction may contribute to the olfactory dysfunction in some patients, perhaps most likely in those that show very early resolution, it cannot account for the loss in all patients. Moreover, disordered regrowth and a predominance of immature neurons have been shown to be associated with parosmia, which is a common finding amongst patients with Covid-related anosmia. A central mechanism therefore certainly seems to be consistent with the group of patients with more prolonged olfactory deficits. Sustentacular cells showing ACE-2 immunohistochemical expression 200 to 700 times greater than nasal or tracheal epithelia seem to be the main SARS-CoV-2 gateway. As the pathophysiology of COVID-19 anosmia seems to be better understood, the question of why patients with a moderate to severe form of COVID-19 infection have less olfactory involvement remains unresolved. Different potential explanations are discussed in this review.
CONCLUSIONS
The last 5 months have benefited from great international collaborative research, first highlighting and then proving the value of loss of smell and taste as a symptom of COVID-19. Adoption of loss of smell into the case definition by international public health bodies will facilitate control of disease transmission.
DOI: 10.1007/s00405-020-06285-0
PubMed: 32909060
Affiliations:
- Belgique, France, Royaume-Uni
- Angleterre, Grand Londres, Province de Hainaut, Région de Bruxelles-Capitale, Région wallonne, Île-de-France
- Bruxelles, Liège, Londres, Paris
- Université de Mons, Université libre de Bruxelles
Links toward previous steps (curation, corpus...)
Le document en format XML
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>From the start of the pandemic, many European otolaryngologists observed an unprecendented number of anosmic patients. Early reports proposed that anosmia could be the first or even the only symptom of COVID-19 infection, prompting calls for self-isolation in affected patients.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>In the present article, we review the COVID-19 anosmia literature and try to answer the following two questions: first, why is COVID-19 infection responsible for such a high incidence of anosmia? Second, in patients with more severe forms is anosmia really less prevalent and why?</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>In terms of the etiology of olfactory dysfunction, several hypotheses were proposed at the outset of the pandemic; that olfactory cleft inflammation and obstruction caused a localized conductive loss, that there was injury to the sustentacular supporting cells in the olfactory epithelium or, given the known neurotropic potential of coronavirus, that the virus could invade and damage the olfactory bulb. Olfactory cleft obstruction may contribute to the olfactory dysfunction in some patients, perhaps most likely in those that show very early resolution, it cannot account for the loss in all patients. Moreover, disordered regrowth and a predominance of immature neurons have been shown to be associated with parosmia, which is a common finding amongst patients with Covid-related anosmia. A central mechanism therefore certainly seems to be consistent with the group of patients with more prolonged olfactory deficits. Sustentacular cells showing ACE-2 immunohistochemical expression 200 to 700 times greater than nasal or tracheal epithelia seem to be the main SARS-CoV-2 gateway. As the pathophysiology of COVID-19 anosmia seems to be better understood, the question of why patients with a moderate to severe form of COVID-19 infection have less olfactory involvement remains unresolved. Different potential explanations are discussed in this review.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>The last 5 months have benefited from great international collaborative research, first highlighting and then proving the value of loss of smell and taste as a symptom of COVID-19. Adoption of loss of smell into the case definition by international public health bodies will facilitate control of disease transmission.</p>
</div>
</front>
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<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">From the start of the pandemic, many European otolaryngologists observed an unprecendented number of anosmic patients. Early reports proposed that anosmia could be the first or even the only symptom of COVID-19 infection, prompting calls for self-isolation in affected patients.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">In the present article, we review the COVID-19 anosmia literature and try to answer the following two questions: first, why is COVID-19 infection responsible for such a high incidence of anosmia? Second, in patients with more severe forms is anosmia really less prevalent and why?</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">In terms of the etiology of olfactory dysfunction, several hypotheses were proposed at the outset of the pandemic; that olfactory cleft inflammation and obstruction caused a localized conductive loss, that there was injury to the sustentacular supporting cells in the olfactory epithelium or, given the known neurotropic potential of coronavirus, that the virus could invade and damage the olfactory bulb. Olfactory cleft obstruction may contribute to the olfactory dysfunction in some patients, perhaps most likely in those that show very early resolution, it cannot account for the loss in all patients. Moreover, disordered regrowth and a predominance of immature neurons have been shown to be associated with parosmia, which is a common finding amongst patients with Covid-related anosmia. A central mechanism therefore certainly seems to be consistent with the group of patients with more prolonged olfactory deficits. Sustentacular cells showing ACE-2 immunohistochemical expression 200 to 700 times greater than nasal or tracheal epithelia seem to be the main SARS-CoV-2 gateway. As the pathophysiology of COVID-19 anosmia seems to be better understood, the question of why patients with a moderate to severe form of COVID-19 infection have less olfactory involvement remains unresolved. Different potential explanations are discussed in this review.</AbstractText>
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<AffiliationInfo><Affiliation>Department of Otorhinolaryngology and Head and Neck Surgery, CHU Saint-Pierre, School of Medicine, CHU de Bruxelles, Université Libre de Bruxelles, Brussels, Belgium. Sven.saussez@umons.ac.be.</Affiliation>
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</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Otolaryngology-Head and Neck Surgery, School of Medicine, UFR Simone Veil, Foch Hospital, Université Versailles Saint-Quentin-en-Yvelines (Paris Saclay University), Paris, France.</Affiliation>
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<affiliations><list><country><li>Belgique</li>
<li>France</li>
<li>Royaume-Uni</li>
</country>
<region><li>Angleterre</li>
<li>Grand Londres</li>
<li>Province de Hainaut</li>
<li>Région de Bruxelles-Capitale</li>
<li>Région wallonne</li>
<li>Île-de-France</li>
</region>
<settlement><li>Bruxelles</li>
<li>Liège</li>
<li>Londres</li>
<li>Paris</li>
</settlement>
<orgName><li>Université de Mons</li>
<li>Université libre de Bruxelles</li>
</orgName>
</list>
<tree><country name="France"><region name="Île-de-France"><name sortKey="Saussez, Sven" sort="Saussez, Sven" uniqKey="Saussez S" first="Sven" last="Saussez">Sven Saussez</name>
</region>
<name sortKey="Lechien, Jerome R" sort="Lechien, Jerome R" uniqKey="Lechien J" first="Jerome R" last="Lechien">Jerome R. Lechien</name>
<name sortKey="Lechien, Jerome R" sort="Lechien, Jerome R" uniqKey="Lechien J" first="Jerome R" last="Lechien">Jerome R. Lechien</name>
</country>
<country name="Belgique"><region name="Région wallonne"><name sortKey="Saussez, Sven" sort="Saussez, Sven" uniqKey="Saussez S" first="Sven" last="Saussez">Sven Saussez</name>
</region>
<name sortKey="Lechien, Jerome R" sort="Lechien, Jerome R" uniqKey="Lechien J" first="Jerome R" last="Lechien">Jerome R. Lechien</name>
<name sortKey="Lechien, Jerome R" sort="Lechien, Jerome R" uniqKey="Lechien J" first="Jerome R" last="Lechien">Jerome R. Lechien</name>
<name sortKey="Saussez, Sven" sort="Saussez, Sven" uniqKey="Saussez S" first="Sven" last="Saussez">Sven Saussez</name>
</country>
<country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Hopkins, Claire" sort="Hopkins, Claire" uniqKey="Hopkins C" first="Claire" last="Hopkins">Claire Hopkins</name>
</region>
<name sortKey="Hopkins, Claire" sort="Hopkins, Claire" uniqKey="Hopkins C" first="Claire" last="Hopkins">Claire Hopkins</name>
</country>
</tree>
</affiliations>
</record>
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