Vitamin D deficiency is commonly reported in patients with SARS-CoV-2 infection. The aim of this study was to correlate serum levels of 25OH-Vitamin D with clinical parameters of lung involvement in elderly patients hospitalized 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-dependent controls (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 duration of hospitalization and duration of COVID-19 symptoms.
Results showed that significantly lower serum vitamin D 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 serum vitamin D 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 serum vitamin D levels and the severity of radiological pulmonary involvement, evaluated by computed tomography: in particular, vitamin D was found significantly lower in COVID-19 patients with multiple lung consolidations (p = 0.0001) or diffuse / severe interstitial lung involvement than in patients with mild involvement (p = 0.05).
Finally, significantly lower serum vitamin D levels were found in elderly COVID-19 patients who died during hospitalization, compared to those who survived (median 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 disease, longer disease duration, and risk of death in elderly COVID-19 patients.
The detection of low vitamin D levels also in younger COVID-19 patients with less co-morbidity further suggests that vitamin D deficiency is a critical risk factor at any age.
The report states that the results are likely related to the role played by vitamin D’s biologically active metabolite [1,25(OH)2-D] which, as a steroid hormone, is involved in the regulation of growth and differentiation of different 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, robustly designed randomized clinical trials with a greater number of patients are needed.
Research background
This is the latest in a deluge of studies linking vitamin D deficiency and the severity of COVID-19. Researchers and health professionals are calling on the governments of the world to add vitamin D supplementation to their virus control strategies.
Vitamin D has been associated with COVID-19 infection, in terms of a higher risk of disease development, higher disease severity, higher frequency of hospitalization in the intensive care unit and higher risk of death.
The results of the current study are quite similar to those of a recent study reporting vitamin D serum levels <50 nmol / l (<20 ng / ml) in 61% of hospitalized patients (mean age 76 years). They saw a significantly greater prevalence of vitamin D deficiency (<50 nmol / l) in patients requiring intensive care treatment than in patients 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.
A recent systematic review analyzed seven studies of COVID-19 severity, intensive care treatment and mortality (1368 patients enrolled) and found a mean vitamin D level of 22.9 nmol / l (9.16 ng / ml) , higher but comparable to that of our cohort of patients (7.9 ng / ml). Patients with a good prognosis had 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 in agreement with the results of another study reporting a high prevalence of hypovitaminosis D in COVID-19 patients with a low PaO2 / FiO2 ratio.
How vitamin D interferes with the progression of COVID-19 isn’t entirely clear, but this report aims to clarify some pathways.
1,25 (OH) 2-D plays an antiviral role and regulates the inflammatory response by modulating toll-like receptor expression and NK cell function and suppressing overexpression of pro-inflammatory cytokines. 1,25 (OH) 2-D improves the defense also by inducing antimicrobial peptide release, such as cathelicidin, which leads to viral destruction and clearance and facilitates the recruitment of monocytes, macrophages, neutrophils and dendritic cells.
Therefore, 1,25 (OH) 2-D can regulate innate / adaptive responses and interfere with dendritic cell maturation and their ability to present antigen to T cells, shifting the T cell profile from the pro- inflammatory Th1 and Th17 subsets to Th2 and Treg subsets, inhibiting the pro-inflammatory processes.
In addition to its immunomodulatory and antiviral effects, 1,25 (OH) 2-D modulates the renin-angiotensin system, which also plays a critical role in the pathogenesis of COVID-19. ACE2 appears to be the major host cell receptor responsible for SARS-CoV infection. -2: The virus attaches to ACE2 through its peak glycoprotein to enter the cell, reducing ACE2 expression.
Vitamin D suppresses renin at the transcriptional level and, consequently, the expression of angiotensin, and increases ACE2 expression, potentially restoring the physiological concentration of ACE2 that is lowered by the virus.
“In the lungs, different alveolar cell types express the ACE2 receptor. These cells play an important role in producing surfactant, which is able to regulate alveolar surface tension. SARS-CoV-2 can infect the alveolar cells by ACE2 binding and the production of the loss of alveolar cells leads to lung damage and respiratory failure due to the loss of pulmonary surfactant. This damage can be prevented by vitamin D.
“Interestingly … vitamin D deficiency is associated with a higher risk of thrombotic events. As is known, patients with COVID-19 often suffer from microthrombotic complications, which can contribute to worsening lung disease and death. autopsies report sequential alveolar damage, mainly characterized by focal capillary microthrombosis. “
Source: Nutrients
Cutolo. M., et al
“Vitamin D and Pulmonary Results in Older COVID-19 Patients”
https://doi.org/10.3390/nu13030717