Abstract
ABSTRACT.The risk of acute respiratory tract infections is particularly pronounced in patients deficient in 25-hydroxyvitamin D (25(OH)D). With respect to COVID-19, there are conflicting evidence on the association of 25(OH)D levels with disease severity. We undertook this study to evaluate the 25(OH)D status in COVID-19 patients admitted in Karachi, Pakistan, and associated vitamin D deficiency with primary outcomes of mortality, length of stay, intubation, and frequency of COVID-19 symptoms. A total of 91 patients were evaluated for 25(OH)D status during their COVID-19 disease course. 25-hydroxyvitamin D levels were classified as deficient (< 10 ng/mL), insufficient (10–30 ng/mL), or sufficient (> 30 ng/mL). The study population comprised 68.1% males (N = 62). The mean age was 52.6 ± 15.7 years. Vitamin D deficiency was significantly associated with intensive care unit (ICU) admission (RR: 3.20; P = 0.048), invasive ventilation (RR: 2.78; P = 0.043), persistent pulmonary infiltrates (RR: 7.58; P < 0.001), and death (RR: 2.98; P < 0.001) on univariate Cox regression. On multivariate Cox regression, only death (RR: 2.13; P = 0.046) and persistent pulmonary infiltrates (RR: 6.78; P = 0.009) remained significant after adjustment for confounding factors. On Kaplan Meier curves, vitamin D deficient patients had persistent pulmonary infiltrates and a greater probability of requiring mechanical ventilation than patients with 25(OH)D ≥ 10 ng/mL. Mechanical ventilation had to be initiated early in the deficient group during the 30-day hospital stay (Chi-square: 4.565, P = 0.033). Patients with 25(OH)D ≥ 10 ng/mL also demonstrated a higher probability of survival than those with 25(OH)D concentrations < 10 ng/mL. 25-hydroxyvitamin D deficient population had longer hospital stays and worse outcomes.
Highlights
Vitamin D deficiency has been associated with a greater risk of respiratory tract infections.[1]
Of the cases 69.2% were managed in isolation wards and the remaining in intensive care units (ICUs)
Our findings limit generalizability and power. Another major limitation of this study is the additional confounders that may account for the differences in 25(OH)D status and outcomes, which impacts the validity of the findings
Summary
Vitamin D deficiency has been associated with a greater risk of respiratory tract infections.[1] The receptors for 25(OH)D are expressed on macrophages (and dendritic cells) and are known to regulate the transcription process, including some genes encoding antimicrobial peptides and may play a role in warding off respiratory infections.2 25-hydroxyvitamin D is known to protect from free radical–mediated oxidative injury. Other mechanisms that vitamin D levels could impact the morbidity and mortality of SARS-COV-2 may include minimizing the pro-inflammatory response in these patients including selective separation of inflammatory cytokines; inducing the innate and acquired antiviral immune response and/or local conversion of 25(OH)D to 1,25-(OH)2D by an increase expression of CYP27B1 enzyme in lung epithelial cells. Whereas Abrishami et al.[4] found significant associations of 25(OH)D deficiency with decreased survival and increased total lung involvement. We undertook this study to evaluate the role of 25(OH)D status in COVID-19 patients, and the
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