Role of the inflammatory markers and distinguishing them

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Summary:

Do we have a causative association of symptoms with the specific inflammatory markers in an infection?
We know the inflammatory markers are markedly elevated during covid infection (may be for any infection)

The typical of them are CRP, D-dimer, Ferritin, IL6, LDH, PCT over and above the traditional ESR and abnormal/subnormal platelets counts etc.

I want to know, are these markers typically associated to any particular symptom like fever, bodyache, malaise, loss of taste/smell, pneumonia etc?

Suppose we have two groups of people infected with cov2 virus. Let us say, one group has elevated IL-6, CRP, D-dimer & ferritin and not so elevated in other markers. The other group has elevated IL-6, CRP, LDH & PCT and not so elevated markers in others. Something like that...

What will be the diagnosis in these two cases? How do we interpret the marker levels vis-a-vis the disease?
 

Answers and Replies

  • #2
Ygggdrasil
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There was a recent paper that investigated this issue:

Multi-omics resolves a sharp disease-state shift between mild and moderate COVID-19
https://www.cell.com/cell/fulltext/S0092-8674(20)31444-6

Abstract:
We present an integrated analysis of the clinical measurements, immune cells and plasma multi-omics of 139 COVID-19 patients representing all levels of disease severity, from serial blood draws collected during the first week of infection following diagnosis. We identify a major shift between mild and moderate disease, at which point elevated inflammatory signaling is accompanied by the loss of specific classes of metabolites and metabolic processes. Within this stressed plasma environment at moderate disease, multiple unusual immune cell phenotypes emerge and amplify with increasing disease severity. We condensed over 120,000 immune features into a single axis to capture how different immune cell classes coordinate in response to SARS-CoV-2. This immune-response axis independently aligns with the major plasma composition changes, with clinical metrics of blood clotting, and with the sharp transition between mild and moderate disease. This study suggests that moderate disease may provide the most effective setting for therapeutic intervention.
 
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  • #3
Astronuc
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There is some new controversy on the inflammatory response to COVID-19.

From NYTimes via MSN - An Explanation for Some Covid-19 Deaths May Not Be Holding Up
https://www.msn.com/en-us/health/he...-may-not-be-holding-up/ar-BB1aO4OH?li=BBnb7Kz

In a number of recent studies, some researchers say, an agent suspected of causing the storms might not be the culprit or that such storms might not happen in the way doctors believed. Not everyone agrees.
The (cytokine) storm idea has so far centered on one cytokine, interleukin-6, or il-6. The belief that it might be the culprit in certain Covid deaths began with reports from China early in the course of the pandemic. Doctors there said a patient who fared poorly had high levels of il-6. The doctors tried using drugs that block il-6, and the patient recovered. Similar reports followed there and in Italy.
Now rigorous studies are failing to find that anti il-6 drugs are effective. Other studies are finding that il-6 levels are not even highly elevated in Covid patients compared to levels in other critically ill patients.
Inflammation from a variety of immune system overreactions may play a role, researchers said. One piece of evidence is that the steroid, dexamethasone, which broadly suppresses the immune system, can reduce the death rate.
Dr. Bruce Walker, an immunologist who is director of the Ragon Institute of Massachusetts General Hospital, M.I.T. and Harvard, and who was not involved in the new studies, cites another possibility from a study he coauthored. The authors found that "the virus can destroy germinal centers, places in lymph nodes where antibodies are produced. The result can be fewer antibodies and less effective ones."
 

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