I have added a topic to my website ibshypo.com/index.php/covid... describing a remakable study showing COVID-19 patients have impaired T4 to T3 conversion but normal T4 secretion. I wasn't able to format it for posting on the forum, hence the link.
I believe this gives us an incredible opportunity to demonstrate the limitations of TSH assays. We measure how much TSH there is but not its activity, how much it stimulates deiodinase and secretion.
I hope to (gently) lobby thyroid researchers in the hope a team will carry out a study of the effects of TSH in COVID-19 patients on peripheral deiodinase. Who knows? We might even end up with TSH assays that are useful for all patients, especially those whose TSH does not respond adequately when thyroid hormone levels fall.
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jimh111
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In some ways I'm not surprised that covid is a form of nonthyroidal illness. But its reach into the whole of the body's immune response system and its tendency to activate human responses which then overwhelm the body is new and will likely give totally new responses to counteract this. It's a new virus which is here for ever, but it will reduce its potency so as to optimise its survival and not kill too many infected people. Ultimately I think it will join flu as a common possibly seasonal occurrence,
I agree ... a nurse who looks after covid patients has told a family member that they think the virus has weakened now because people are recovering quicker and they are not having any long term problems.
Ironically our improved treatment of COVID-19 might reduce the rate of these less lethal adaptations. As well as being a curse on society it also presents an opportunity to gain a better understanding of TSH action, especially as COVID-19 research is attracting funding.
So far no links between hypothyroidism and susceptibility to COVID-19 have been found.
COVID-19 causes TSH and fT3 to fall, as in other forms of NTI. You can see this in colourful graphs 'b' and 'c' in Fig. 5 from this study ncbi.nlm.nih.gov/pmc/articl... . The numbers 1, 2, 3, 4 along the bottom refer to days 1, 4, 7, 10 after admission. TSH and fT3 return to normal after recovery from COVID-19.
Graph 'f' in Fig. 5 is striking because it shows that patients had much lower vitamin D levels than controls. This and other studies tend to show that vitamin D deficiency is most likely linked to catching COVID-19 and having a worse outcome. I would strongly recommend everyone takes sufficient vitamin D to avoid deficiency.
But someone with already low-ish TSH wouldn't have been diagnosed as hypothyroid, esp if T4 in range. I'm glad that yet another study shows low vit D is implicated, which NHS seems to be largely ignoring. Rising PTH is also interesting.
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