A growing number of concordant reports support a protective role for vitamin D in reducing at least the risk/severity of respiratory tract infections (RTIs), especially in the influenza and COVID-19 context.
Major clinical reports show that vitamin D deficiency contribute to acute respiratory distress syndrome (ARDS) SARS-CoV-2 and that case-fatality rates increase with age and the highest SARS-CoV-2 serum concentrations.
Targeted 25(OH)D serum concentration measurements and vitamin D supplementation is strongly suggested have important patient and public health benefits.9 The positive role of vitamin D replacement therapy (vDRT) in reducing risk and severity in COVID-19 patients is supported by several clinical evidences and RCTs are undergoing, however, previous experiences of RCT related to vDRT are available from other lung viral infection studies and even in mechanically ventilated adult intensive care unit (ICU) patientsThese important observations are corroborated by several biological/molecular mechanisms through vitamin D can generally reduce risk of infections and downregulate the immune/inflammatory reaction.
Indeed, functional vitamin D receptors (VDR) are highly-expressed in B-lymphocytes and T-lymphocytes and mainly in monocytes/macrophages, justifying a role in modulating both innate and adaptive immune responses.
These important observations are corroborated by several biological/molecular mechanisms through vitamin D can generally reduce risk of infections and downregulate the immune/inflammatory reaction.
Indeed, functional vitamin D receptors (VDR) are highly-expressed in B-lymphocytes and T-lymphocytes and mainly in monocytes/macrophages, justifying a role in modulating both innate and adaptive immune responses.
We will analyse and discuss such available clinical evidences on the light of vitamin D molecular actions and the need to supplementation in COVID-19 patients.
Vitamin D is a steroidal hormone (D hormone) and may influence the immune response in COVID-19 in show Figure
Vitamin D enters the body through dietary consumption (about 20% of vitamin D3) or is synthesised by the skin (80%) from 7-dihydro-cholesterol (provitamin D or chlecalciferol) after exposure to type B ultraviolet (UVB) which varies seasonally.
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