Since the beginning of the pandemic there has been a lot of science and media coverage of the phenomenon known as The Cytokine Storm, a severe hyper-immune response to the SARS-CoV-2 virus that in some patients results in organ damage.
A new paper published in the Lancet reveals that there is NO cytokine mediated pathway in an acute Covid-19 infection.
They reviewed 25 Covid studies documenting patient cytokine levels, and 12 studies featuring diagnoses where it is known that the cytokine mediated pathway exists - Acute Respiratory Distress Syndrome (ARDS), Sepsis and post CAR-T therapy.
It had been originally hypothesised that in the hyper inflammation phase of acute Covid-19 infection there is a massive release of IL-6 (the main cytokine) and it is this that causes ARDS, acute renal failure, acute heart failure and acute liver failure.
In the review they found that the ARDS, Sepsis and post CAR-T therapy patients had IL-6 levels of between 500 to 4000. The acute Covid-19 patients had IL-6 levels of on average 36.
So they looked at the other cytokines and again saw a much lower level. This time of IL-8, TNF, IFN and IL-10.
BUT they found that the CRP, LDH and Ferritin was a little higher in the Covid-19 patients and the D-Dimer much higher.
A “Covid-19 phenotype” so that in the acute phase of the infection blood tests are done which look at the D-Dimer, CRP, Ferritin, LDH and lymphocytes (the white cells which fight viral infections), and not the cytokines.
The organs that are affected in Covid-19 are mainly the lungs, brain, kidneys, heart, gastro intestinal tract and the endothelial cells. The researchers feel that the resulting damage to these organs are by direct invasion by the virus and not a hyper-inflammatory response.
They then went on to say that this would explain why the drug Tocilizumab has not worked very well in hospitalised patients - Tocilizumab is an anti IL-6 medication and would only be effective if there was a cytokine mediated pathway.
Also there is the fact that the use of the steroid medication Dexamethasone has proved beneficial BUT the RECOVERY trial shows that the best results from using this at > 7 days and is essentially preventing lung fibrosis - and not what was initially thought quelling the cytokine storm.
How does this help us with Long Covid? Currently I am not sure it does unfortunately, but it means that hopefully research will now be directed correctly.
Incidentally If you have a loved one who becomes acutely unwell with Covid-19 and attends the hospital make sure they get their CRP, White cell count, LDH, Ferritin and D-Dimer done as a bare minimum even if it looks like they are not going to be admitted