Vitamin D is a secosteroid hormone which may have beneficial role in reducing COVID-19 adverse outcomes by first regulating the renin angiotensin system (RAS). Recent studies on animal in which acute respiratory distress syndrome (ARDS) was induced, showed that vitamin D lead to pulmonary permeability reduction by modulating RAS activity as well as the expression of the angiotensin-2 converting enzyme (ACE2). During COVID-19, downregulation of ACE2 leads to cytokine storm in the host, causing ARDS. In contrast, an experimental study conducted on mice in which ARDS was induced chemically, revealed that vitamin D admiration contributed to mRNA and ACE2 proteins levels improvement, ADRS milder symptoms as well as less lung damage. Additionally, vitamin D had shown antiviral effects on several previous studies, that though to be exerted either by antimicrobial peptides induction which subsequently had direct antiviral action or through immunomodulatory and anti-inflammatory effects. In addition, vitamin D stabilizes physical barriers which prevent viruses from reaching tissues susceptible to infection. Finally, previous studies demonstrated that hypovitaminosis D is accompanied by various comorbidities including diabetes mellitus, hypertension, chronic cardiovascular and respiratory diseases, and cancers, all medical conditions that are considered risk factors of COVID-19 infection deterioration and even high mortality rate. The objective of this study is to evaluate whether supplementation with high-dose vitamin D improves the prognosis of patients diagnosed with COVID-19 compared to a standard dose of vitamin D.
Study Type
OBSERVATIONAL
Enrollment
116
Teachers Hospital
Cairo, Please Select, Egypt
Duration of hospitalization
Length of hospital stay
Time frame: Two weeks
In-hospital mortality
Death during hospitalization
Time frame: Two weeks
Clinical status improvement using six category ordinal scale
Change in six category ordinal scale. The categories were defined as follows: 1) patient discharged, 2) hospitalization not requiring supplemental oxygen, 3) hospitalization requiring supplemental low-flow oxygen, 4) hospitalization requiring high-flow supplemental oxygen, 5) hospitalization requiring invasive mechanical ventilation, 6) death.
Time frame: Two weeks
Change in gas exchange
Difference between ratio of partial pressure of arterial oxygen (PaO2) to the fraction of inspired oxygen (FiO2) at baseline, and before discharge
Time frame: Two weeks
Time to increase in oxygenation
Time to increase in SpO2/FiO2 of 50 or greater compared to the baseline SpO2/FiO2)
Time frame: 48 hours
Change in Lactate dehydrogenase (LDH) levels
Change in levels of Lactate dehydrogenase (LDH) between baseline and before discharge
Time frame: Two weeks
Change in C-reactive protein (CRP) levels
Change in levels of C-reactive protein (CRP) between baseline and before discharge
Time frame: Two weeks
Change in serum ferritin levels
Change in levels of serum ferritin between baseline and before discharge
Time frame: Two weeks
Occurrence of secondary infection
Occurrence of sepsis
Time frame: Two weeks
Occurrence of at least one severe adverse event
Any serious or severe adverse event that might happens during hospital stay
Time frame: Two weeks
Need for mechanical ventilator or intensive care unit (ICU) support
Admission to ICU or usage of mechanical ventilator
Time frame: Two weeks
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