Despite the high number of coronavirus disease-19 (COVID-19) cases from India, there are few reports from India describing the clinical epidemiology of COVID-19. This study aimed to describe the clinical/epidemiological characteristics and outcomes of asymptomatic vs. symptomatic COVID-19 patients. This was a retrospective chart review of all admitted patients with COVID-19 above 18 years with a history of travel within one month of the admission. The patients were categorized into asymptomatic and symptomatic. The symptomatic patients were further classified into mild, moderate and severe. The demographic profile, risk factors, clinical features, laboratory parameters, treatment details and outcome of all patients were recorded. The clinical and laboratory parameters were compared between symptomatic patients and asymptomatic patients. Of the 127 recruited patients, 75 were asymptomatic. Of the 52 symptomatic patients, 41 patients were classified as a mild illness. The mean age of the patients was 44.5 ± 15 years. A total of 73 patients had one or more risk factors. The male patients were more commonly found to be symptomatic compared to female patients. Neutrophil-lymphocyte ratio, C-reactive protein and lactate dehydrogenase were significantly elevated in symptomatic patients. A total of five individuals required supplemental oxygen therapy, and one of them required mechanical ventilation. All the patients had favourable outcomes. Asymptomatic and mild illness form a significant proportion of positive patients and have excellent outcomes without therapeutic interventions.
The recent clinical trial reports pertaining to the efficacy of chloroquine and hydroxychloroquine against COVID-19 albeit yet to be validated with larger clinical trials, have sparked much interest globally to evaluate whether this anti-malarial drug can be repurposed for the treatment of COVID-19. In addition to its anti-viral activity, the anti-inflammatory activity of chloroquine may also contribute to its efficacy. Based on our data obtained from an animal infection model of melioidosis (a disease caused by the bacteria Burkholderia pseudomallei), treatment with chloroquine can result in the phosphorylation and consequent inhibition of glycogen synthase kinase-3β (GSK3β). This serine/threonine protein kinase is now recognised as a point of convergence for host inflammatory response. In view of this, it is plausible that the mechanism for the anti-inflammatory effect of chloroquine against COVID-19 involves inhibition of host GSK3β.