Vitamin D deficiency is frequently reported in patients with SARS-CoV-2 infection. The aim of this study was to correlate serum concentrations of 25OH-vitamin D with clinical parameters of lung involvement in elderly patients hospitalized with COVID-19.
Sixty-five consecutive patients with COVID-19 (mean age 76 ± 13 years) were retrospectively analyzed and compared with sixty-five subjects controlled by sex and age (CNT).
The following clinical parameters were collected: type of lung involvement, respiratory parameters (PaO2, LIKE THIS2, PaCO2, PaO2/ FiO2), Laboratory parameters (including 25OH-vitamin D, dimer D, C-reactive protein), as well as the duration of hospitalization and the duration of COVID-19 symptoms.
The results revealed that serum vitamin D levels were found to be significantly lower in COVID-19 patients than in CNT (mean 7.9 vs 16.3 ng / mL, p = 0.001) and a statistically significant positive correlation was observed. between serum levels of vitamin D and PaO2(P = 0.03), SO2(P = 0.05) and PaO2/ FiO2(P = 0.02).
A statistically significant negative correlation was found between serum levels of vitamin D and dimer D (p = 0.04), C-reactive protein (p = 0.04), and the percentage of O2In a venturi mask (p = 0.04).
A negative correlation was also observed between serum vitamin D levels and the severity of radiological lung involvement, as assessed by computed tomography: in particular, vitamin D was found to be significantly lower in patients with COVID-19 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 serum vitamin D levels were found in elderly patients with COVID-19 who died during hospitalization, compared with those who survived (mean 3.0 vs 8.4 ng / ml, p = 0.046).
The researchers conclude that this study confirms that serum 25OH-vitamin D deficiency is associated with more severe lung involvement, longer duration of disease, and a risk of death, in elderly COVID-19 patients.
Detection of low vitamin D levels also in younger patients with COVID-19 with fewer comorbidities suggests vitamin D deficiency as a crucial risk factor at any age.
The report states that the results are likely to be related to the role of the biologically active metabolite of vitamin D. [1,25(OH)2-D] which as a steroid hormone participates in the regulation of the growth and differentiation of various types of immune cells.
This study has some limitations, including the small number of patients analyzed and the large variability of the data: for this reason, the correlation coefficients are relatively small. Therefore, robust, randomized, clinical trials involving a larger number of patients are needed.
Background of the research
This is the latest in a deluge of studies linking vitamin D deficiency with the severity of COVID-19. Researchers and health professionals are calling on governments around the world to add vitamin D supplements to their anti-virus strategies.
Vitamin D has been associated with COVID-19 infection, in terms of increased risk of developing disease, increased severity of the disease, increased frequency of hospitalization in intensive care units, and increased risk of death.
The results of the current study are quite similar to those of a recent study reporting serum vitamin D levels <50 nmol / L (<20 ng / mL) in 61% of hospitalized patients (mean age 76 years). . They observed a significantly higher prevalence of vitamin D deficiency (<50 nmol / L) in patients in need of intensive treatments than in those who did not have it (81% of patients).
Similarly, another study reported 25OHD deficiency in 67% of patients with mild SARS-CoV-2 disease, but in 80% of patients who needed mechanical ventilation.
A recent systematic review looked at seven studies on the severity of COVID-19, intensive care treatment, and mortality (1368 patients were included) and detected a mean vitamin D level of 22.9 nmol / L (9, 16 ng / mL), higher but similar to our cohort of patients (7.9 ng / mL). Patients with good prognosis had significantly higher vitamin D levels compared with those with poor prognosis.
A low PaO2 / FiO2 ratio was detected as an independent risk factor for death in patients with COVID-19. Our study detected a statistically significant positive correlation between serum 25OHD levels and PaO2 / FiO2 values. This observation is consistent with the results of another study that reported a high prevalence of hypovitaminosis D in patients with COVID-19 with a low PaO2 / FiO2 ratio.
It is not entirely understood how vitamin D interferes with the progression of COVID-19, but this report seeks to elucidate some pathways.
“1.25 (OH) 2-D plays an antiviral role, regulating the inflammatory response by modulating toll receptor expression and NK cell function and suppressing overexpression of proinflammatory cytokines. 1.25 (OH) 2-D also enhances defense by inducing the release of antimicrobial peptides, such as catelicidin, which leads to viral destruction and elimination and facilitates the recruitment of monocytes, macrophages, neutrophils, and dendritic cells. (…)
“Therefore, 1,25 (OH) 2-D can regulate innate / adaptive responses and can interfere with dendritic cell maturation and its ability to present antigen to T cells, changing the profile of T cells of the proinflammatory Th1 and Th17 subsets of Th2 and Treg subsets, thus inhibiting proinflammatory processes. (…)
“In addition to immunomodulatory and antiviral effects, 1,25 (OH) 2-D modulates the renin-angiotensin system, which also plays a key role in the pathogenesis of COVID-19. ACE2 appears to be the major host cell receptor that mediates SARS-CoV-2 infection: the virus binds to ACE2 through its ear glycoprotein to enter the cell, thereby reducing ACE2 expression. (…)
“Vitamin D suppresses renin at the transcriptional level and, consequently, angiotensin expression, and increases ACE2 expression, possibly restoring the physiological concentration of ACE2 regulated by the virus. (…)
“In the lung, various types of alveolar cells express the ACE2 receptor. These cells play an important role in the production of surfactant, capable of regulating alveolar surface tension. SARS-CoV-2 can infect cells by binding ACE2 and suppressing surfactant production.Loss of alveolar cells causes lung damage and respiratory failure due to loss of pulmonary surfactant.This damage could be prevented by vitamin D. (…)
“Interestingly … vitamin D deficiency is associated with an increased risk of thrombotic events. As is well known, patients with COVID-19 frequently suffer from microthrombotic complications, which can contribute to worsening lung disease and death. main histological findings of the autopsy sequential alveolar damage, characterized mainly 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