fascinating LeftYahoo, thank you, landmark article in NEJM on micro-emboli in C-19
these 7 patients with C19 had not been intubated, whereas some of the ARDS influenza patients had been, but still, the differences seemed to be profound,
that C-19 patients had endothelialitis which is inflammation of the lining of the smallest blood vessel walls , severe enough to lead to occlusion and clots. We know from other publications as well that this is leading to micro-clots in many organs throughout the body as well as heart attacks.
similar features have now been reported in repeated publications on C-19.
this is why I have commented before to The Yankee that there needs to be a plan after the phase 3 reports a positive result, which I am sure that it will, to design a trial looking at patients who are unwell, but prior to needing intubation, who specifically are at risk of micro-emboli and cardiac complications and also those at risk of pulmonary damage. As long term survivors will suffer a lot and be a huge drain on their pocket and the health care system.
the really interesting thing about this paper, is that the specific indices described as being abnormal due to C-19 and not due to influenza ARDS are of course, not surprisingly, exactly the sort of things that the Prof Si will be looking at, so we should have some answers from the phase 3, albeit in a sicker population of patients, ie with RemL reversing these endpoints, vs not in the placebo group. Remember the 25 or more secondary endpoints listed in Clinical Trial.gov.... Some can probably address the micro-emboli question.
this is incredibly important as micro-emboli create secondary inflammation which the body has to deal with, and if not cleared completely, there will be residual scarring, life long in all those young (and old) people. Estimates are that 20-30% of infected may be at risk of significant pulmonary or other complications although we don’t know how many really because so far the micro-emboli have only been looked for in post-mortem cases to my knowledge. There is so much we still don’t know.
RemL has the potential to reverse all this at the time of infection and to prevent it from occurring by reducing the inflammation in the first place, by the multifactorial effects on the inflammatory cascade. No other single drug that we yet have, eg including anti-angiogenics, would be as effective, IMO.
exciting times ahead.
hopefully we will see something about this, probably not with the initial results in September (hoping that we get some results then) but when translational results are first presented.
these are sorely needed.
thanks LeftYahoo
only MO DYOR
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