Abstract
Abstract Background Vitamin D is recognized to be an immune regulator. Also, it is known to have antiviral effects by several mechanisms, including reducing inflammatory cytokines. Objectives To examine the 25-hydroxyvitamin D (25(OH)D) status for assessing the severity of COVID-19. Methods This study consisted of 596 patients confirmed as SARS-CoV-2 infection and 59 healthy individuals. The cases separated into non-severe group, severe survival, and severe non-survival group. 25(OH)D and other laboratory parameters were evaluated retrospectively. Results In all COVID-19 groups 25(OH)D levels were low compared to controls (p<0.05). 25(OH)D concentrations were lowest in patients in severe non-survival groups than those in other SARS-CoV-2 infection groups (p<0.05). Multivariate regression analysis exhibited that decreasing 25(OH)D was associated with an increased likelihood of non-severe, severe survival and severe non-survival disease. There were significant associations between 25(OH)D and certain inflammatory and hemostatic parameters (p<0.05, for all). Conclusions 25(OH)D deficiency was observed among patients with COVID-19. Declined steadily 25(OH)D levels make a huge contribution to the scale of the progression of the disease. Correlations support that 25(OH)D may be a substantial tool for utilizing the severity of the disease and estimating the survival. Also, supplementation of 25(OH)D might slow down the course of the COVID-19.
Highlights
The world is struggling with coronavirus infection which was nominated as coronavirus disease 2019 (COVID-19) [1]
In the light of above reasons, we investigated 25(OH)D status and its relationships with other laboratory parameters in COVID-19
COVID-19 ensues from the infection originated by acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [2]
Summary
The world is struggling with coronavirus infection which was nominated as coronavirus disease 2019 (COVID-19) [1]. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) elicits the infection of COVID-19. It was initially identified in subjects in Wuhan province in China [2]. It has widely disseminated overrun the world and has pronounced a pandemic by the world Health Organization (WHO) [1]. As of 16 August 2020, there have been 21,260,760 confirmed cases of COVID-19, including 761.018 deaths, reported to WHO [3]. The pathophysiology of COVID-19 is not great brought into light, it constitutes a complicated interplay through SARS-CoV-2 and immune system. SARS-CoV-2 is recognized to lead an acute lung harm which ends in aggressive inflammation triggered by viral replication [4]. It is known to have antiviral effects by several mechanisms, including reducing inflammatory cytokines
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