Mielestäni tämä artikkeli on paljon tietoa antava. Tämä tosin on vuodelta 2021 eikä vielä tämän vuoden uusinta tietoa ole kukaan ehtinyt kaikeiti analysoida artikkeliksi asti.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8229409/
Relation of Serum Copper Status to Survival in COVID-19
Abstract: The trace element copper (Cu) is part of our nutrition and essentially needed for several cuproenzymes that control redox status and support the immune system. In blood, the ferroxidase ceruloplasmin (CP) accounts for the majority of circulating Cu and serves as transport protein. Both Cu and CP behave as positive, whereas serum selenium (Se) and its transporter selenoprotein P (SELENOP) behave as negative acute phase reactants. In view that coronavirus disease (COVID-19) causes systemic inflammation, we hypothesized that biomarkers of Cu and Se status are regulated inversely, in relation to disease severity and mortality risk.
....
. A combined biomarker as ratio of SELENOP over CP, as suggested for assessing thyroid hormone activity in hepatocytes [67], would then provide a most sensitive estimate for survival odds. Yet, our results indicate that at least for the hepatic acute phase reactants CP and SELENOP, the regulation is more complex than expected, as no consistent inverse regulation over time is observed. Either there are more important confounders affecting both transport proteins, or the postulated hypoxia and hyperinflammatory syndrome was not present in the non-survivors analysed, or the missing acute phase response detected via SELENOP and CP is indicative of a failing liver.
In view that the
hepatic biosynthesis of both CP and SELENOP is also stringently
regulated by thyroid hormone [67,68],
it may be speculated that the unexpected lack of inverse regulation may
be related to critical illness and the euthyroid sick or low-T3
syndrome that may develop in severely diseased COVID-19 patients [69].
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