Role of Vitamin D in COVID-19: Active or Passive?

Bess Dawson-Hughes


J Clin Endocrinol Metab. 2021;106(12):e5260-e5261. 

In This Article

Abstract and Introduction


Amidst a raging pandemic, Nogues et al. developed and implemented a protocol to determine whether treatment with calcifediol compared with no calcifediol altered the course of 838 coronavirus disease 2019 (COVID-19) patients admitted to a hospital in Barcelona, Spain.[1] This was not a classical randomized, controlled trial, but rather a real-world examination of outcomes of patients assigned (on a bed availability basis) to 1 of 8 COVID wards, 3 of which had chosen not to administer calcifediol and 5 that had chosen to do so. Other practices in the 8 wards were standardized. Some patients did not have serum 25-hydroxyvitamin D (25(OH)D) measurements upon admission for reasons related to staff availability. The supplemented patients had significantly fewer transfers to the intensive care unit (adjusted odds ratio, 0.13 [95% CI, 0.07–0.23]) and lower mortality rates (adjusted odds ratio, 0.52 [95% CI, 0.27–0.99]) than the unsupplemented patients, findings that have important implications for the in-hospital management of COVID-19 patients globally.

25(OH)D was measured in 678 of the 838 patients upon admission to the hospital. It was notable that the median 25(OH)D level was 13 [interquartile values 8, 24] ng/mL in the calcifediol-treated group and 12 [8,19] ng/mL in the untreated control group. How might we interpret the significance of these very low 25(OH)D levels at the time of hospitalization? Was low 25(OH)D a predisposing factor to serious COVID-19 infection or was it a marker of inflammation associated with acute illness? The answer has implications for patient care.