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Cytokine storm patients......
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Last: 4 yr ago by jagvocate
Reading this thread is like listening to Jimbo and Saban talk football strategies. The collaboration, intelligence and ingenuity is inspiring. Thanks to all the medical community is doing!
Spoke with our local Genentech rep. He confirmed what PatrriotAg said. There is no shortage of Actemra. FYI. Trying to get it asap.
Had another patient die this morning. Not my first and they weren't expected to survive but it always sucks. We're batting about .500 with regards to saving those requiring intubation thus far which is pretty good as far as this disease goes.
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
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Sorry to hear. Can't express it enough, thanks for all the work you're doing fighting this fight.
Thank you for being on the front line and doing what you do! Sorry you have to deal with losing patients.Infection_Ag11 said:
Had another patient die this morning. Not my first and they weren't expected to survive but it always sucks. We're batting about .500 with regards to saving those requiring intubation thus far which is pretty good as far as this disease goes.
Keep fighting Doc(s)! We love you guys and gals!
GIG EM.
GIG EM.
I don't know how you do it, but thank you!
We have procured a dose of Actemra for my pt. But can't get the drug till Monday. Sadly I don't think she will see Monday.
Marcus Aurelius said:
We have procured a dose of Actemra for my pt. But can't get the drug till Monday. Sadly I don't think she will see Monday.
I am so sorry to hear that. Keep pressing on Hero
Infection_Ag11 said:
Had another patient die this morning. Not my first and they weren't expected to survive but it always sucks. We're batting about .500 with regards to saving those requiring intubation thus far which is pretty good as far as this disease goes.
I'm so sorry, keep up the good fight!
Are you noticing anything about the pts that are able to come of the vent, age, etc? Or is it pretty much a crap shoot once it progresses to that point?
AgsMyDude said:Infection_Ag11 said:
Had another patient die this morning. Not my first and they weren't expected to survive but it always sucks. We're batting about .500 with regards to saving those requiring intubation thus far which is pretty good as far as this disease goes.
I'm so sorry, keep up the good fight!
Are you noticing anything about the pts that are able to come of the vent, age, etc? Or is it pretty much a crap shoot once it progresses to that point?
If you have significant underlying lung disease, heart failure, are morbidly obese or >80 you're pretty much toast if you get intubated. We can overcome kidney failure and liver disease in younger patients sometimes as long as your heart works reasonably well.
The ones we're saving are generally in the 30-70 range, reasonably healthy for their age with good lung compliance and who don't develop bacterial super infections/hospital acquired infections. And even the it takes 7-10 days to extubate them.
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
To all the Docs. You are Patriots and Hero's.
It may not feel like it but times like this is your finest hour to lay people like myself. Don't lose faith in setbacks.
It may not feel like it but times like this is your finest hour to lay people like myself. Don't lose faith in setbacks.
Hooper Drives the Boat
Marcus Aurelius said:
We have procured a dose of Actemra for my pt. But can't get the drug till Monday. Sadly I don't think she will see Monday.
I wonder if a rheumatologist or infusion clinic would loan you a dose then let you repay. I'm not in a position to do it anymore but someone might if your pharmacy is willing.
That's a pain point with a lot of these speciality products. They overnight from a few places instead of coming from your normal wholesaler.
Valuable info and exchange of ideas here. These patients are the sickest of the sick. Hopefully the collaboration present will lead to a higher success rate for everyone. These are new times and the real time info here and across the physician spectrum regardless of location, I believe, will ultimately pay off!
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
What constitutes reasonably healthy for a 30 year old? Thats a pretty broad age range.Infection_Ag11 said:AgsMyDude said:Infection_Ag11 said:
Had another patient die this morning. Not my first and they weren't expected to survive but it always sucks. We're batting about .500 with regards to saving those requiring intubation thus far which is pretty good as far as this disease goes.
I'm so sorry, keep up the good fight!
Are you noticing anything about the pts that are able to come of the vent, age, etc? Or is it pretty much a crap shoot once it progresses to that point?
If you have significant underlying lung disease, heart failure, are morbidly obese or >80 you're pretty much toast if you get intubated. We can overcome kidney failure and liver disease in younger patients sometimes as long as your heart works reasonably well.
The ones we're saving are generally in the 30-70 range, reasonably healthy for their age with good lung compliance and who don't develop bacterial super infections/hospital acquired infections. And even the it takes 7-10 days to extubate them.
Most deaths due to coronavirus are preceded by a fulminating pulmonary deterioration that is associated with a sudden onset "cytokine storm". In the cytokine storm, a number of cytokines are elevated, including a set of cytokines typical of an innate immune response, viz, IL-6, TNF, IL1, MCP, IL10 amongst others.
-6,
Why IL6 was chosen for therapeutic targeting over TNF and IL-1 (for which FDA approved agents exist) is not clear.
The mechanism of cytokine production and pulmonary deterioration is most likely explained by an uncommonly encountered immunologic phenomenon referred to as "disease enhancement", which is known to occur for the two COVID-related coronaviruses, SARS and MERS. Disease enhancement occurs when an individual develops an antibody response to a virus, however, instead of the patient resolving the infection as a result of antibody production, the antibodies initiate an inflammatory response within the innate immune system that targets distal lung parenchyma. Activated type M1 macro****es and monocytes mediate the pulmonary inflammation as antibodies opsonize the viral particles, then bind to Fc receptor gamma 1 (CD64) the high affinity Fc receptor. This in turn results in macro****e activation and severe pulmonary inflammation. (Liu et al, JCI 2019).
if you cannot get IL6, you may wish to try a TNF blocker or an IL1 blocker which are both on the market.
We are not aware of a major role for gamma interferon, so this would not be a preferred approach.
If you can get acmes to convalescent serum that would be the next step. if you cannot get convalescent serum, suggest trying IVIG at 2 gm/kg given in two divided doses, 12-24 hours apart. this will block the CD64 receptor nonspecifically, thereby potentially mitigating macro****e activation and IL6 production. in addition IVIG has been shown to reduce IL-6 production. High dose steroids to blunt cytokine production have been associated with an absence of clinical benefit and risk of infection according to italian and chinese physicians.
If your patient is not on hydroxychoroquine and azithromycin suggest starting it, as it may help reduce viral loads during convalescence.
Good luck with your patient.
-6,
Why IL6 was chosen for therapeutic targeting over TNF and IL-1 (for which FDA approved agents exist) is not clear.
The mechanism of cytokine production and pulmonary deterioration is most likely explained by an uncommonly encountered immunologic phenomenon referred to as "disease enhancement", which is known to occur for the two COVID-related coronaviruses, SARS and MERS. Disease enhancement occurs when an individual develops an antibody response to a virus, however, instead of the patient resolving the infection as a result of antibody production, the antibodies initiate an inflammatory response within the innate immune system that targets distal lung parenchyma. Activated type M1 macro****es and monocytes mediate the pulmonary inflammation as antibodies opsonize the viral particles, then bind to Fc receptor gamma 1 (CD64) the high affinity Fc receptor. This in turn results in macro****e activation and severe pulmonary inflammation. (Liu et al, JCI 2019).
if you cannot get IL6, you may wish to try a TNF blocker or an IL1 blocker which are both on the market.
We are not aware of a major role for gamma interferon, so this would not be a preferred approach.
If you can get acmes to convalescent serum that would be the next step. if you cannot get convalescent serum, suggest trying IVIG at 2 gm/kg given in two divided doses, 12-24 hours apart. this will block the CD64 receptor nonspecifically, thereby potentially mitigating macro****e activation and IL6 production. in addition IVIG has been shown to reduce IL-6 production. High dose steroids to blunt cytokine production have been associated with an absence of clinical benefit and risk of infection according to italian and chinese physicians.
If your patient is not on hydroxychoroquine and azithromycin suggest starting it, as it may help reduce viral loads during convalescence.
Good luck with your patient.
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
Sorry i forgot to mention that Sanofi has another FDA approved IL6 antibody sarilumb. you may wish to try getting that drug.
Remdisivir is in clinical trials, and although initially promising, we have not been impressed with its efficacy in COVID patients, although the n is small.. Colleagues i have spoken to are not that impressed either.
to get remdisivir now your patient has to be at a site participating in the randomized trial (to my knowledge)
Remdisivir is in clinical trials, and although initially promising, we have not been impressed with its efficacy in COVID patients, although the n is small.. Colleagues i have spoken to are not that impressed either.
to get remdisivir now your patient has to be at a site participating in the randomized trial (to my knowledge)
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
Feel like we brought someone back from the brink with tocilizumab. Gave the patient 400 mg yesterday and another dose 12 hours later, in just 24 hours O2 requirements down from 100% FiO2 to 60% on the vent, down to 1 pressor from 3 and can now tolerate volume removal with CRRT so lungs sound better.
Long way to go but this guy would be our sickest to survive if he does. I've very bullish on the IL-6 inhibitors right now based on our experiences and the other anecdotal reports across the world. Hopefully the studies will show benefit because this would open a whole new door for post-viral cytokine release patients.
Long way to go but this guy would be our sickest to survive if he does. I've very bullish on the IL-6 inhibitors right now based on our experiences and the other anecdotal reports across the world. Hopefully the studies will show benefit because this would open a whole new door for post-viral cytokine release patients.
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
Good news. I think it's the most promising drug for these folks.
This mimics the findings in about 3-4 other countries.
We are at war, I really wish the weapons to fight could get released. Tocilizumab is a death fighter, the worst case on it is a highly probable result without it.
We are at war, I really wish the weapons to fight could get released. Tocilizumab is a death fighter, the worst case on it is a highly probable result without it.
Sirolumab also sounds promising, and remdesivir for for severe patients who are about to get intubated or just got tubed. More than 10-12 days out from symptom onset it anecdotally seems like the benefit is lost which seems to make sense given the mechanism. The IL-6 inhibitors essentially act as salvage therapy for the cytokine storm.
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
Have any of the docs on here tried the TNF or Jak inhibitors?
And docs, y'all are heroes and prayed for everyday.
And docs, y'all are heroes and prayed for everyday.
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
Yelnick McWawa said:
The links in the three posts above mine are very good reads for an average shlub like me. Thank y'all so much for posting.
So let's say the particular medication discussed in the first release turns out to be truly effective...how long does it realistically take to get those meds distributed and into the hands of doctors treating relevant patients?
There's an important step before distribution.
Hell yes!!! Great job everyone. Hoping and praying for all patients.Infection_Ag11 said:
Feel like we brought someone back from the brink with tocilizumab. Gave the patient 400 mg yesterday and another dose 12 hours later, in just 24 hours O2 requirements down from 100% FiO2 to 60% on the vent, down to 1 pressor from 3 and can now tolerate volume removal with CRRT so lungs sound better.
Long way to go but this guy would be our sickest to survive if he does. I've very bullish on the IL-6 inhibitors right now based on our experiences and the other anecdotal reports across the world. Hopefully the studies will show benefit because this would open a whole new door for post-viral cytokine release patients.
There are current or upcoming studies for a variety of inflammatory cascade targets including GM-CSF, TREM-1, CD137, JAK1, JAK2, TLR 2, 3, 4, 7, 9...IL1, 6, 7, 18, 28. We're throwing everything at it, hopefully something sticks.Quote:
Why IL6 was chosen for therapeutic targeting over TNF and IL-1 (for which FDA approved agents exist) is not clear.
94chem said:Yelnick McWawa said:
The links in the three posts above mine are very good reads for an average shlub like me. Thank y'all so much for posting.
So let's say the particular medication discussed in the first release turns out to be truly effective...how long does it realistically take to get those meds distributed and into the hands of doctors treating relevant patients?
There's an important step before distribution.
It they're already approved for something else itll speed things up because the drug manufacturing process already exists at commercial scale. But experimental drugs have probably not been made in mass quantities so itll take time to ramp up. Maybe months.
All of antibodies (drugs that end in -mab) are even slower to produce than oral drugs because the process to produce them is very complex and also has to be sterile.
My guess is that Roche/genetech is working as hard as possible to ramp up Actemra production.
I would love to see some of the manufacturers help each other mass produce these but I don't know if they will share the details or if the FDA would allow it.
NawlinsAg01 said:There are current or upcoming studies for a variety of inflammatory cascade targets including GM-CSF, TREM-1, CD137, JAK1, JAK2, TLR 2, 3, 4, 7, 9...IL1, 6, 7, 18, 28. We're throwing everything at it, hopefully something sticks.Quote:
Why IL6 was chosen for therapeutic targeting over TNF and IL-1 (for which FDA approved agents exist) is not clear.
Thanks Doc! And I figured as much, you folks will do anything to save lives and we appreciate it.
God bless!
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
Could use more good news like thisInfection_Ag11 said:
Feel like we brought someone back from the brink with tocilizumab. Gave the patient 400 mg yesterday and another dose 12 hours later, in just 24 hours O2 requirements down from 100% FiO2 to 60% on the vent, down to 1 pressor from 3 and can now tolerate volume removal with CRRT so lungs sound better.
Long way to go but this guy would be our sickest to survive if he does. I've very bullish on the IL-6 inhibitors right now based on our experiences and the other anecdotal reports across the world. Hopefully the studies will show benefit because this would open a whole new door for post-viral cytokine release patients.
dermdoc said:NawlinsAg01 said:There are current or upcoming studies for a variety of inflammatory cascade targets including GM-CSF, TREM-1, CD137, JAK1, JAK2, TLR 2, 3, 4, 7, 9...IL1, 6, 7, 18, 28. We're throwing everything at it, hopefully something sticks.Quote:
Why IL6 was chosen for therapeutic targeting over TNF and IL-1 (for which FDA approved agents exist) is not clear.
Thanks Doc! And I figured as much, you folks will do anything to save lives and we appreciate it.
God bless!
If nothing else this pandemic has again revealed how incredible human ingenuity and willpower really is. Every once in a while we see a global event that tests our limits as a species and we seem to consistently rise to the challenge.
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
Another drug, Leronlimab, seems to also help with cytokine storms.
It's a very new drug and just moved to Phase 2 trials. The manufacturer is trying to push this forward as quickly as possible.
https://texags.com/forums/84/topics/3104737
It's a very new drug and just moved to Phase 2 trials. The manufacturer is trying to push this forward as quickly as possible.
https://texags.com/forums/84/topics/3104737
"If you will not fight for right when you can easily win without blood shed; if you will not fight when your victory is sure and not too costly; you may come to the moment when you will have to fight with all the odds against you and only a precarious chance of survival. There may even be a worse case. You may have to fight when there is no hope of victory, because it is better to perish than to live as slaves." - Sir Winston Churchill
The word on toci is that it enables rapid improvements in about 1/4 to 1/3 of patients.
We have seen remarkable improvements with toci even in transplant recipients who are on systemic immunosuppression
We have seen remarkable improvements with toci even in transplant recipients who are on systemic immunosuppression
No material on this site is intended to be a substitute for professional medical advice, diagnosis or treatment. See full Medical Disclaimer.
Marcus Aurelius said:
We have procured a dose of Actemra for my pt. But can't get the drug till Monday. Sadly I don't think she will see Monday.
I hope your patient has managed to pull through the weekend, and the Actemra is able to help her.
Is this cytokine storm the same mechanism that kills flu patients? Is there any chance that we learn something from this pandemic that causes less flu deaths in the future?
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