Context COVID-19 is a major health problem because of saturation of intensive care units (ICU) and mortality. Vitamin D has emerged as a potential treatment able to reduce the disease severity. Objective To elucidate the effect of calcifediol [25OHD3] treatment on COVID-19-related outcomes. Design Observational cohort study from March to May, 2020. Setting Patients admitted to COVID-19 wards of Hospital del Mar, Barcelona, Spain. Patients A total of 930 patients with COVID-19 were included. Ninety-two were excluded due to previous calcifediol intake. Intervention Of the remaining 838, a total of 447 received calcifediol (532ug on day one plus 266ug on day 3, 7, 15, and 30) whereas 391 were not treated at the time of hospital admission (Intention-to-Treat). Of the latter, 53 patients were treated later during ICU admission and were allocated in the treated group in a second analysis. In healthy subjects, calcifediol is about 3.2-fold more potent on a weight basis than cholecalciferol. Main Outcome Measures ICU admission and mortality. Results ICU assistance was required by 102 (12.2%) participants. Out of 447 patients treated with calcifediol at admission, 20 (4.5%) required ICU, compared to 82 (21%) out of 391 non-treated (p-value<0.0001). Logistic regression of calcifediol treatment on ICU admission, adjusted by age, gender, linearized 25OHD levels at baseline, and comorbidities showed that treated patients had a reduced risk to require ICU (OR 0.13 [95% CI 0.07;0.23]). Overall mortality was 10%. In the Intention-to-Treat analysis, 21 (4.7%) out of 447 patients treated with calcifediol at admission died compared to 62 patients (15.9%) out of 391 non-treated (p=0.0001). Adjusted results showed a reduced mortality risk with an OR 0.21 [95% CI 0.10; 0.43]). In the second analysis, the obtained OR was 0.52 [95% CI 0.27;0.99]. Conclusions In patients hospitalized with COVID-19, calcifediol treatment significantly reduced ICU admission and mortality.

The results do not support the hypothesis that leptin increases cardiovascular risk by increasing left ventricular mass index or blood pressure. Other mechanisms, related to atherosclerosis, could explain the increased risk of cardiovascular diseases observed with high leptin levels.

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