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 pulmonary 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 control subjects by sex and age (CNT).
The following clinical parameters were collected: type of lung damage, respiratory parameters (PaO2, ASA2, 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 showed that significantly lower serum vitamin D levels were found in patients with COVID-19 than in CNT (median 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 damage, 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 damage than in those with mild impairment (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 (median 3.0 versus 8.4 ng / ml). , p = 0.046).
The researchers concluded that this study confirms that serum 25OH-vitamin D deficiency is associated with more severe lung damage, longer duration of disease, and a risk of death in elderly patients with COVID-19.
Detection of low vitamin D levels in younger COVID-19 patients with fewer comorbidities further suggests vitamin D deficiency as a crucial risk factor at any age.
The report states that the results are likely related to the role of the biologically active metabolite of vitamin D. [1,25(OH)2-D] that because the steroid hormone is involved in regulating the growth and differentiation of different types of immune cells.
This study has some limitations, including the small number of patients analyzed and the high variability of the data: for this reason, the correlation coefficients are relatively small. Therefore, robustly designed randomized clinical trials, including a larger number of patients, are needed.
Research context
This is the latest in a flood of studies linking vitamin D deficiency to COVID-19 severity. Researchers and health professionals are calling on governments around the world to add vitamin D to their anti-virus strategies.
Vitamin D has been associated with COVID-19 infection in terms of an increased risk of developing the disease, a higher severity of the disease, a higher frequency of hospitalization in intensive care units and a higher risk of death.
The results of the current study are quite similar to those of a recent study that reported 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 requiring intensive care than in those without (81% of patients).
Similarly, another study reported a 25OHD deficiency in 67% of patients with mild SARS-CoV-2 disease, but in 80% of patients requiring mechanical ventilation.
A recent systematic review looked at seven studies of COVID-19 severity, intensive care, and mortality (including 1368 patients) and detected a mean vitamin D level of 22.9 nmol / L (9.16 ng / mL). , higher but similar to that of our cohort of patients (7.9 ng / ml). Patients with a good prognosis had significantly higher levels of vitamin D compared to those with a 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 reports a high prevalence of hypovitaminosis D in patients with low PaO2 / FiO2 COVID-19.
How vitamin D interferes with the progression of COVID-19 is not fully understood, but this report aims to elucidate some pathways.
“1,25 (OH) 2-D plays an anti-viral role, regulating the inflammatory response by modulating receptor expression similar to the rate and function of NK cells and suppressing overexpression of pro-inflammatory cytokines. 1,25 (OH)) 2-D also improves defense by inducing the release of antimicrobial peptides such as catelicidin that lead 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 interfere with dendritic cell maturation and their ability to present antigen to T cells, changing the profile of T cells from pro-inflammatory Th1 and Th17 subsets. Th2 and Treg subsets, thus inhibiting pro-inflammatory 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 main receptor of the host cell that mediates SARS-CoV-2 infection: the virus attaches to ACE2 through its peak glycoprotein to enter the cell, thus reducing ACE2 expression. (…)
‘Vitamin D suppresses transcriptional renin and, consequently, angiotensin expression and increases ACE2 expression, possibly restoring the physiological concentration of ACE2 down-regulated by the virus. (…)
“In the lungs, several types of alveolar cells express the ACE2 receptor. These cells play an important role in the production of the surfactant, capable of regulating alveolar surface tension. SARS-CoV-2 can infect alveolar cells by binding to ACE2 and can suppress surfactant production. Loss of alveolar cells results in lung damage and respiratory failure due to loss of lung surfactant. This damage could 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 frequently suffer from microthrombotic complications, which can contribute to aggravation of lung disease and death. The main histological findings of the autopsy report a sequential alveolar involvement, characterized mainly by focal capillary microthrombosis. “(…)
Source: Nutrients(…)
Cutolo. M., et al
“Vitamin D and pulmonary outcomes in elderly patients with COVID-19”(…)
https://doi.org/10.3390/nu13030717