Correlation between Serum Vitamin D3 levels and severity of COVID-19, experience from a COVID-19-dedicated tertiary care hospital from Western India

The COVID-19 pandemic caused by a novel coronavirus (SARS-CoV-2) is characterized by significant morbidity and mortality with no current specific treatment. Preclinical research suggests that the SARS-CoV-2 virus enters cells via the angiotensin-converting enzyme 2 (ACE2). [1] Coronavirus replication downregulates ACE2, causing the renin-angiotensin system (RAS) to become dysfunctional and producing a cytokine storm with increased production of pro-inflammatory cytokines. This increases the risk of pneumonia, sepsis, acute respiratory distress syndrome and heart failure. [2] Research shows that vitamin D plays a role in balancing RAS, in reducing lung damage through the anti-inflammatory effect which is seen with higher vitamin D levels ranging from 20 to 60 ng/mL. [3] [4] [5] Vitamin D deficiency is one of India's most underdiagnosed and undertreated nutritional deficiencies. [6] Many studies have found that lacking vitamin D or vitamin D receptors causes altered innate and adaptive immune functions. [7, 8] Vitamin D supplementation is a potentially exciting treatment for COVID-19 infection but scientifically, with a low level of evidence until now. [9] Some studies have confirmed the Context: It is postulated that 25(OH)D deficiency is associated with a worse prognosis of COVID-19. Aims: We aimed to find out whether baseline serum 25-hydroxy vitamin D levels were correlated with COVID-19 disease severity or not in Indian population. Settings and Design: It is a prospective observational study. Methods and Material: We prospectively recruited 200 COVID-19-positive adult patients and measured their baseline vitamin D levels on admission and prospectively followed their clinical course for their outcome and correlated the association. Statistical Analysis Used: The continuous data were represented as mean (±SD) or median (IQR), while the categorical data were represented as proportions. Parametric data were analysed using unpaired T-test and ANOVA for two and more than two groups, and for categorical, nonparametric data, Chi-square test were applied. A two-sided P value of <0.05 was considered as statistically significant with 95% confidence interval. Results: Eighty-six per cent (172/200) of patients had hypovitaminosis D (<30 ng/mL). The prevalence of 25(OH) severe deficiency, deficiency and vitamin D insufficiency was 23%, 41% and 22%, respectively. Clinical severity was graded as asymptomatic (11%), mild (14%), moderate (14.5%), severe (37.5%) and critical (22%). Sixty per cent of patients had clinically severe or critical disease requiring oxygen support with eleven per cent (n = 22) mortality overall. Age (P: 0.001), HTN (P: 0.049) and DM (P: 0.018) were negatively associated with clinical severity. No linear association was found between vitamin D levels and clinical severity. Low vitamin D levels had a significant inverse association with inflammatory markers like neutrophil-lymphocyte ratio (NLR, P: 0.012) and IL-6 (P:..