| Autor: |
Sreelatha, Souparnika, Devang, Nayana, Marathe, Aradhana |
| Zdroj: |
Current Nutrition & Food Science; 2022, Vol. 18 Issue: 7 p610-617, 8p |
| Abstrakt: |
Background: Intravascular thrombosis and pulmonary fibrosis in COVID-19 patients with pneumonia are significantly associated with the severity of the disease. Vitamin K is known to balance the coagulation mechanisms and also prevent calcification and fibrosis of the extrahepatic soft tissues. This narrative review focuses on the role of vitamin K as a linking factor for thrombotic as well as pulmonary complications of COVID-19. Materials and Methods: Article search was performed in databases of WHO, PubMed, Scopus and Clinical Trial Registry using appropriate keywords. Original articles included very few observational studies which showed a reduced level of vitamin K as well as activated extrahepatic vitamin K Dependent Proteins (VKDP) in COVID-19 patients when compared to healthy controls. Chronic treatment with vitamin K Antagonists did not reduce the risk of in-hospital death. Docking study was performed using Swiss dock, and it demonstrated a significant interaction between menaquinone and SARS-CoV-2 main protease (SARS-CoV-2 Mpro). Results and Discussion: Deficiency of vitamin K in COVID-19 can be due to excessive use of antagonists or defective ingestion or absorption. This triggers an imbalance in the normal coagulation- anticoagulation mechanism by channeling the available vitamin K to the liver, thereby causing a deficiency of the same in extrahepatic tissues, thus finally leading to thrombosis. This also prevents carboxylation and activation of extrahepatic VKDP required to prevent the calcification of soft tissues, thus leading to lung fibrosis. Conclusion: Supplementation of vitamin K should be considered as a potentially modifiable risk factor in severe COVID-19. Randomized control trials are highly recommended to provide clearer evidence on the same. |
| Databáze: |
Supplemental Index |
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