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Posted On: 04/02/2024 5:24:31 AM
Post# of 148870
In fact, RANTES increased substantially in the 700mg group but did modestly fall in the 350mg group.
Yes, IL6 modestly decreased in the 350mg group, but did not budge in either the 700mg or 700mg HM group
CRP doesn't budge in any group
in contrast to
ENRAGE which is clearly reduced in all the 350mg group and the 700mg HM group.
In fact, there is no other marker that behaves quite like ENRAGE in this heat map. It is the only one which is reduced in both 700 and 350.
There is another which is elevated in 350 and 700, and that should also be a contender for measurement of primary/secondary endpoint. That would be brain derived neurotrophic factor. Why not measure that with its elevation, disease dissipates?
The questioin arises then, Why are we messing around with CRP if it doesn't move?
My answer to this is because it probably does move in the more inflamed population of HIV much more than it does in NASH patients. CRP is a marker of acute inflammation and not so much a marker of chronic inflammation. NASH is a chronic disease and would be better represented by a marker of chronic inflammation like ESR. I bet if that biomarker was followed, we would have seen a reduction in ESR with 350 and 700.
Since NASH is an ongoing disease, CRP would not be all that out of the ordinary to start out with and after leronlimab, only steatosis and fibrosis would have been reduced, but not CRP so much.
With the sickness found in these HIV patients, Dr. Lalezari may already know that these individuals have elevated CRP to begin with. He may have already witnessed firsthand that CRP is reduced with leronlimab administration. The elevated CRP in these patients would represent an acute illness / exacerbation on top of the chronic disease of HIV. The subsequent reduction in CRP would reflect leronlimab's nullifying effect on the inflammation resulting from the restoration of the native balance / ratio of immunoregulatory mechanisms which handle the disease.
Yes, IL6 modestly decreased in the 350mg group, but did not budge in either the 700mg or 700mg HM group
CRP doesn't budge in any group
in contrast to
ENRAGE which is clearly reduced in all the 350mg group and the 700mg HM group.
In fact, there is no other marker that behaves quite like ENRAGE in this heat map. It is the only one which is reduced in both 700 and 350.
There is another which is elevated in 350 and 700, and that should also be a contender for measurement of primary/secondary endpoint. That would be brain derived neurotrophic factor. Why not measure that with its elevation, disease dissipates?
The questioin arises then, Why are we messing around with CRP if it doesn't move?
My answer to this is because it probably does move in the more inflamed population of HIV much more than it does in NASH patients. CRP is a marker of acute inflammation and not so much a marker of chronic inflammation. NASH is a chronic disease and would be better represented by a marker of chronic inflammation like ESR. I bet if that biomarker was followed, we would have seen a reduction in ESR with 350 and 700.
Since NASH is an ongoing disease, CRP would not be all that out of the ordinary to start out with and after leronlimab, only steatosis and fibrosis would have been reduced, but not CRP so much.
With the sickness found in these HIV patients, Dr. Lalezari may already know that these individuals have elevated CRP to begin with. He may have already witnessed firsthand that CRP is reduced with leronlimab administration. The elevated CRP in these patients would represent an acute illness / exacerbation on top of the chronic disease of HIV. The subsequent reduction in CRP would reflect leronlimab's nullifying effect on the inflammation resulting from the restoration of the native balance / ratio of immunoregulatory mechanisms which handle the disease.
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