Vitamin D deficiency is frequently reported in patients with SARS-CoV-2 infection. The aim of this study was to correlate the 25OH vitamin D serum concentrations with clinical parameters of lung involvement, in elderly patients admitted to hospital with COVID-19.
Sixty-five consecutive COVID-19 patients (mean age 76 ± 13 years) were retrospectively analyzed and compared with sixty-five gender- and age-adjusted control subjects (CNT).
The following clinical parameters were collected: type of pulmonary involvement, respiratory parameters (PaO2, SO2, PaCO2, PaO2/ FiO2), Laboratory parameters (including 25OH vitamin D, D-dimer, C-reactive protein), as well as the duration of hospitalization and the duration of COVID-19 symptoms.
Results showed that significantly lower vitamin D serum levels were found in COVID-19 patients than in CNT (median 7.9 versus 16.3 ng / ml, p = 0.001) and a statistically significant positive correlation was observed between vitamin D serum levels and PaO2(P = 0.03), SO2(P = 0.05) and PaO2/ FiO2(P = 0.02).
A statistically significant negative correlation was found between vitamin D serum levels and D-dimer (p = 0.04), C-reactive protein (p = 0.04) and percentage O2In a venturi mask (p = 0.04).
A negative correlation was also observed between vitamin D serum levels and severity of radiological lung involvement, evaluated by computed tomography: in particular, vitamin D was found to be significantly lower in COVID-19 patients with multiple lung consolidations (p = 0.0001) or diffuse / severe interstitial lung involvement than in those with mild involvement (p = 0.05).
Finally, significantly lower vitamin D serum levels were found in elderly COVID-19 patients who died during hospitalization compared with those who survived (median 3.0 vs 8.4 ng / ml, p = 0.046).
The researchers conclude that this study confirms that 25OH vitamin D serum deficiency is associated with more severe lung involvement, longer disease duration, and risk of death in older COVID-19 patients.
The detection of low vitamin D levels also in younger COVID-19 patients with fewer comorbidities further indicates vitamin D deficiency as a major risk factor at any age.
The report states that the results are probably linked to the role that the biologically active metabolite of vitamin D plays [1,25(OH)2-D] that as a steroid hormone is involved in regulating growth and differentiation of different immune cell types.
This study has some limitations, including the small number of patients analyzed and the large data variation: for this reason, the correlation coefficients are relatively small. Therefore, robust design of randomized clinical trials was required, including a greater number of patients.
Research background
This is the latest in an avalanche of studies linking vitamin D deficiency to COVID-19. Researchers and health professionals are urging world governments to add vitamin D supplementation to their virus-fighting strategies.
Vitamin D is associated with COVID-19 infection in terms of higher risk of disease development, higher severity of diseases, higher frequency of hospitalization in the intensive care unit and higher risk of death.
The results of the present study are very similar to those of a recent study in which vitamin D serum levels <50 nmol / L (<20 ng / ml) were reported in 61% of patients in the hospital (mean age 76 years) . They observed a significantly higher incidence of vitamin D deficiency (<50 nmol / l) in patients requiring intensive care than in those without (81% of patients).
Similarly, another study reported 25OHD deficiency in 67% of patients with mild SARS-CoV-2 disease, but in 80% of patients requiring mechanical ventilation.
In a recent systematic review, seven studies on COVID-19 severity, intensive care and mortality (1368 patients included) were analyzed and an average vitamin D level of 22.9 nmol / L (9.16 ng / ml) was detected. , higher, but similar to that of our group of patients (7.9 ng / ml). Patients with a good prognosis have significantly higher vitamin D levels compared to those with a poor prognosis.
A low PaO2 / FiO2 ratio was detected as an independent risk factor for death in COVID-19 patients. Our study found a statistically significant positive correlation between 25OHD serum levels and PaO2 / FiO2 values. This observation is consistent with the results of another study reporting a high incidence of hypovitaminosis D in COVID-19 patients with a low PaO2 / FiO2 ratio.
How vitamin D interferes with the progression of COVID-19 is not fully understood, but this report aims to elucidate some avenues.
“1,25 (OH) 2-D plays an antiviral role, regulating the inflammatory response by modulating toll-like receptor expression and NK cell function, and suppressing under-expression of pro-inflammatory cytokines. 1.25 (OH ) 2-D also enhances the defense by inducing antimicrobial peptide release, such as catalyzidine leading to viral destruction and clearance and facilitating the recruitment of monocytes, macrophages, neutrophils and dendritic cells.
“Therefore, 1,25 (OH) 2-D can regulate the congenital / adaptive responses and may worsen with the maturation of dendritic cells and their ability to present antigen to T cells, which increases the T profile of the pro- inflammatory Th1 shifts and Th17 substructures to Th2 and Treg substructures, which inhibit the pro-inflammatory processes.
“In addition to the immunomodulatory and antiviral effects, 1,25 (OH) 2-D modulates the renin-angiotensin system, which also plays a crucial role in the pathogenesis of COVID-19. ACE2 appears to be the major host receptor for SARS infection. -CoV-2: the virus attaches to ACE2 through its peak glycoprotein to enter the cell, which reduces the expression of ACE2.
“Vitamin D suppresses renin at the transcriptional level and consequently angiotensin expression, increasing ACE2 expression, possibly restoring the physiological concentration of ACE2 which is downregulated by the virus.
“In the lung, several alveolar cell types express the ACE2 receptor. These cells play an important role in the production of surfactant, which can regulate the alveolar surface tension. SARS-CoV-2 can infect the alveolar cells through ACE2 binding and the production of surfactant.The loss of alveolar cells leads to lung damage and respiratory failure due to the loss of pulmonary wetting agent.This damage can be prevented by vitamin D.
“Interestingly, vitamin D deficiency is associated with a higher risk of thrombotic events. As is well known, patients with COVID-19 often suffer from microthrombotic complications, which can contribute to worse lung disease and death. The main histological findings of the autopsy reports sequential alveolar damage, mainly characterized by focal capillary microthrombosis. “
Source: Nutrients
Cutolo. M., et al
“Vitamin D and lung outcomes in elderly patients with COVID-19”
https://doi.org/10.3390/nu13030717