Introduction
A new coronovirus (CoV) infection was reported to begin in late 2019 in Wuhan, Hubei, China, which the World Health Organization (WHO) called COVID-19 on February 11, 2020 (1). On March 11, 2020, COVID-19 infection was declared a pandemic by WHO due to the global logarithmic increase of cases (2). Studies have reported that crude mortality rates worldwide due to the COVID-19 outbreak vary between 5.6% and 15.2%. The risk of death was found to be higher for elderly individuals and those with comorbid conditions such as hypertension and diabetes mellitus. In an article reviewing 46,248 cases, hypertension, diabetes mellitus, cardiovascular disease and respiratory morbidity were specified to be the most common comorbidities (3).
Vitamin D deficiency is an important problem of global public health which all age groups face. More than one billion people all over the world are estimated to have vitamin D deficiency. Vitamin D is a pluripotent hormone modulating the adaptive and innate immune response(4). The risk of infection by several mechanisms can be reduced by vitamin D. Vitamin D induces cathelicidins and defensins that can lower viral replication rate. It also increases the concentration of anti-inflammatory cytokines, as well as the concentration of pro-inflammatory cytokines that cause pneumonia and lung damage (1). In previous studies, vitamin D deficiency has been shown to increase respiratory infections risk including respiratory syncytial virus (RSV), tuberculosis and flu, and is a risk factor for acute respiratory distress syndrome (ARDS) (4).
The SARS-CoV-2 virus among the COVID-19 patients, enters host cells by binding to receptors of angiotensin-converting enzyme 2 (ACE2) in the respiratory tract of infected patients (5). The primary targets of coronaviruses are type-II pneumocytes and there is high expression of ACE2 receptors in these cells. The level of surfactant can be reduced due to dysfunction of Type-II pneumocytes, increasing surface tension in COVID-19 (6). It has been shown that surfactant synthesis in alveolar type-II cells is stimulated by 1,25-dihydroxyvitamin D metabolites (7). To protect the lung against acute injury and prevent the vitamin D deficiency which is regarded as a COVID-19 pathogenic factor, Vitamin D agonist calcitriol modulates expression of the renin -angiotensin system members such as ACE2 in tissue of lung (8). Vitamin D is a secosteroid with a wide range of immunomodulatory, anti-inflammatory, of antifibriotic and antioxidant effects. Inflammatory cytokine expression [eg, IL-la, IL-la, tumor necrosis factor-α] is inhibited by vitamin D and there is association between its deficiency and over-expression of Thl cytokines (9). Epidemiological studies have reported an association between vitamin D deficiency and acute lung injury and viral respiratory infections (10). Consequently, the immune response against respiratory virus infections should be improved by a sufficient level of 25 (OH) D in serum (11). 1,25-dihydroxy vitamin D3 increases the absorption of Ca from duodenum and phosphorus from ileum. It also prevents the loss of calcium in the kidneys and increases bone resorption.
In this study, we aimed to determine the prevalence and clinical importance of vitamin D deficiency in children and adolescent patients who were hospitalized with the diagnosis of COVID-19.