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.