Over the past months, various studies from Europe, Asia and rest of the world have been reported regarding olfactory and gustatory dysfunctions in COVID-19 patients with variable incidence.
The mean age of our population was 43.03 ± 16.10 years. Out of 152, 51.3% were males and 48.7% were females. However Lechien JR et al. [8] and Timothee Klopfenstein et al. [9] studies had reported higher incidence in female patients: 63% and 67% respectively.
Timothée Klopfenstein et al. study observed a mean duration of anosmia of 9 days.In our study, Mean duration of anosmia/hyposmia was 2.4444 ± 0.352 days [Range: 1–4 days].
Lechien et al. [8] and Kaye et al. [5] observed olfactory dysfunction as the first symptom in 11.8% and 26.6% respectively. We reported olfactory dysfunction (Anosmia/Hyposmia) as presenting symptom in 11 out of 74 symptomatic patients (14.86%), along with other symptoms in 13/74 (17.57%) patients, appeared after other symptoms in 4/74 (5.4%) patients. So the olfactory dysfunction may be the only presenting symptom in COVID-19 patients.
Lechien et al. [8] and Timothée Klopfenstein et al. [9] reported olfactory dysfunction in 86% (357/417) and 47% (54/114) of symptomatic patients respectively. Vaira et al. [10] study on 72 subjects reported olfactory dysfunction in 61.1% (44/72) of cases. Yan et al. [11] reported olfactory dysfunction in 68% in the study group (59 subjects). Luers et al. [6] reported olfactory dysfunction in 74% (53/72) of patients. In our study, olfactory dysfunction was reported in the 28 out of 74 symptomatic patients (37.83%). Our results are comparable with above mentioned studies. In contrast Mao et al. [12] reported the incidence of hypogeusia in 5.6% and hyposmia in 5.1%. Giacomelli et al. [13] reported a study on 59 patients, 20 (33.9%) reported at least 1 taste or olfactory disorder and 11 (18.6%) both. Vaira et al. [14] reported chemosensory dysfunction in 19.4% out of 320 patients.
Wide variation in above reported literature may be attributed to pathophysiology of nCoV-2 infection. Suzuki et al. [16] in 2008 reported Corona virus as pathogen to cause post viral Olfactory Dysfunction. Peng Zhou et al. [17] identified the role of Angiotensin converting enzyme 2 (ACE2) in the pathogenesis of SARS-CoV-2. Brann DH et al. [18] studied and explained the role of 2 genes: ACE2 and TMPRSS in olfactory epithelial support cells, stem cells, and nasal respiratory epithelium explaining the possible mechanism of anosmia in COVID-19 patients. These 2 genes play a potential role in transport of SARS-CoV-2 into the cell. Netland et al. [19] also reported the potential role of SARS-CoV receptor (human ACE 2) in trans- neuronal spread of virus to olfactory bulb region. Yanan Cao et al. [20] reported expression quantitative trait loci (eQTLs) variants of the ACE2 gene which can be a cause for ACE2 polymorphisms and ACE2 expression levels between Asian and European populations. It can be one of possible aetiology in variety of expression in olfactory dysfunction in different countries or races. However its exact aetiology is a matter of further detailed research to confirm ACE 2 receptors role.
Recovery in olfactory dysfunction with assessment by QD-NOS was seen in 19/28 (67.86%) at 1 week, rest 9 recovered from olfactory dysfunction by the end of total 14 days, so complete recovery of olfactory dysfunction was seen in 100% of patients by 14 days. Lechien et al. reported 72.6% of patients recovered olfactory function within the first 8 days following the resolution of the disease. Timothée Klopfenstein et al. also reported ansomia recovery in 80% of patients recovered within 14 days. Lee et al. [21] reported recovery in 80% of Patients with post-viral olfactory loss within 1 year.
Lechien et al. [8] observed olfactory dysfunction was not significantly associated with Nasal discharge or nasal obstruction. In our study, 8/28- olfactory dysfunction group (28.57%) had associated posterior nasal discharge and 3/28 (10.7%) patients had associated rhinorrhea. However this association was found not to be statistically significant.
Lechien et al. [8] and Klopfenstein et al. [9], both observed diarrhoea in > 5 0% of patients. But as per our data, no patient with olfactory dysfunction had associated diarrhoea complaint.
In 12 patients of COVID-19 with Hypertension and in 7 patients of COVID-19 with Diabetes Mellitus 2, olfactory dysfunction was seen in 4 patients (33.33%) and 5 patients (71.42%) respectively. Because of small sample size, it was not possible to evaluate statistically correlation between COVID-19 with associated co-morbidity Hypertension /Diabetes and Olfactory dysfunction.
Dysgeusia was present in 20/152 patients (13.15%). At 7th day evaluation, recovery in dysgeusia was seen in 13/20 (65%). Recovery was noticed in rest of the patients at 14th day follow up. Giacomelli et al. [13] observed taste dysfunction in 10.2% of subjects.
The strength of our study is that it is a prospective study of the true cohort of COVID-19 patients in Indian population as all patients with RT-PCR confirmed COVID-19 were admitted in our hospital irrespective of presence/absence of symptoms. So our study group is a true representation of COVID-19 cohort which eliminates the bias of not including or missing out asymptomatic/mildly symptomatic patients who don’t need admission in hospital. Our study limitations are small sample size and being an observational study, our study didn’t benefit in improvement in treatment. However, to best of our knowledge this is the first Indian single centre cohort study of confirmed COVID-19 patients to evaluate olfactory and gustatory dysfunction.