文章基本信息

标题：Comment on Sobczyk, M.K.; Gaunt, T.R. The Effect of Circulating Zinc, Selenium, Copper and Vitamin K 1 on COVID-19 Outcomes: A Mendelian Randomization Study. Nutrients 2022, 14, 233
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作者：Rob Janssen ; Cees Vermeer ; Jona Walk 等
期刊名称：Nutrients
电子版ISSN：2072-6643
出版年度：2022
卷号：14
期号：5
DOI：10.3390/nu14051112
语种：English
出版社：MDPI Publishing
摘要：Sobczyk and Gaunt genetically predicted circulating zinc, selenium, copper, and vitamin K 1 levels—instead of directly measuring nutrients in blood—and hypothesized that these levels would associate with SARS-CoV-2 infection and COVID-19 severity [ 1]. We have concerns about their conclusions regarding vitamin K in COVID-19. Major study limitations were that the genetic instruments had not demonstrated reliable association with the measured exposure (plasma vitamin K 1) and that the authors used the same genome-wide association study for instrument discovery and effect estimation. Moreover, even direct quantification of blood vitamin K 1 concentrations is not a valid method for quantifying vitamin K 1 status, since this assessment only reflects a snapshot of recent vitamin K 1 intake, is sensitive to triglyceride concentrations, and gives little information about the vitamin K 1 utilization in tissue. There are also differences between vitamins K 1 and K 2 in half-life time, tissue distribution, and bioavailability [ 2]. Vitamin K 2 has a much longer half-life and may, therefore, be important particularly during acute illness, where vitamin K reserves are being used and become less available in peripheral tissues. Consumption of vitamin K 2 is usually too low to accurately quantify their plasma concentration. Due to these factors, most experts in the field advocate measuring levels of inactive circulating vitamin-K-dependent proteins to assess the combined deficiency of vitamins K 1 and K 2. In our studies, we used PIVKA- II and dp- ucMGP as measures of hepatic and extrahepatic vitamin K status, respectively [ 3, 4, 5]. Particularly extrahepatic vitamin K status is severely compromised in COVID-19, and high dp-ucMGP levels are associated with increased mortality [ 4, 5]. Another debatable assumption made by Sobczyk and Gaunt is that the baseline vitamin K status—at the moment of SARS-CoV-2 contraction—is a predictive factor for the disease course of subsequently developing COVID-19 [ 1]. An alternative explanation for the poor vitamin K status in COVID-19 patients is high vitamin K expenditure during the disease. Interestingly, observations in individuals using vitamin K antagonists as anticoagulant drugs support our theory that it is mainly increased vitamin K utilization during the infection, rather than poor baseline vitamin K status, that is responsible for the extrahepatic vitamin K deficiency we found in our studies [ 6, 7]. Given that Sobczyk and Gaunt may not have accurately predicted overall extrahepatic vitamin K status, and that they estimated pre-COVID rather than vitamin K levels during the infection, we are of the opinion that their genetic data analysis is interesting but cannot be used to decide whether vitamin K supplementation has a role in COVID-19.