COVID-19 medical discussion

[triplehorn 2664]

4 minutes ago, Horn Dog said:

As long as the side effects are minor then I don't have a problem with that.   Our understanding of vaccines is pretty good now, and they are not using live virus, just surface proteins or snippets of viral RNA,  so making a non-fatal vaccine should not be that difficult.  Now whether it works or not is another story, but I know that no vaccine doesn't work.   At least make it available to medical personnel.  They understand the risk/benefits and need it now.  If they wait 18-24 months, the vaccine will be useless.

One thing Dr. Fauci spoke about at yesterday's presser is that with this coronavirus, there is concern over a possible observed phenomenon where re-exposure to the bug after you form immunity can result in a fatal immune response when the lungs are involved.  In other words you drown from your own immune response targeting the lungs.  So that is something that is being carefully looked at and understood before rushing out with a vaccine.

[Anastasis 23475]

Any of the front line docs here getting an early impression on hydroxychloroquine.  Apparently NY has trial(s) in progress.  The ID guys have to have a gut feel by now for whether we are seeing the same signal seen in the french study. 

[Thetexashammer 1062]

36 minutes ago, Horn Dog said:

 

As long as the side effects are minor then I don't have a problem with that.   Our understanding of vaccines is pretty good now, and they are not using live virus, just surface proteins or snippets of viral RNA,  so making a non-fatal vaccine should not be that difficult.  Now whether it works or not is another story, but I know that no vaccine doesn't work.   At least make it available to medical personnel.  They understand the risk/benefits and need it now.  If they wait 18-24 months, the vaccine will be useless.

Just putting myself on the record, again, that a vaccine will be available sooner not later. Like, by fall.

One example of how they'll achieve this was mentioned by Fauci recently. Instead of waiting around to the end of Phase III trials to start producing vaccine, you can produce a billion samples beforehand. Simple, and it does nothing to compromise safety. There are a million tweaks like that one that will get you a vaccine a lot faster than the regular process. You can run phases concurrently, that's another tweak.

Keep in mind, you need an antibody to a surface protein on the virus. It's only a 30k base pair virus, it was sequenced months ago, it's not that hard to figure out how to copy the surface protein and create an immune response. I mean it's not easy but damn we have much better tools than we did even a decade ago.

 

[gmr548 16580]

1 hour ago, triplehorn said:

One thing Dr. Fauci spoke about at yesterday's presser is that with this coronavirus, there is concern over a possible observed phenomenon where re-exposure to the bug after you form immunity can result in a fatal immune response when the lungs are involved.  In other words you drown from your own immune response targeting the lungs.  So that is something that is being carefully looked at and understood before rushing out with a vaccine.

Do you have a link on that? I tried to google but it looks like Fauci only spoke briefly about vaccines yesterday?

[triplehorn 2664]

1 hour ago, Anastasis said:

Any of the front line docs here getting an early impression on hydroxychloroquine.  Apparently NY has trial(s) in progress.  The ID guys have to have a gut feel by now for whether we are seeing the same signal seen in the french study. 

So far, what I’ve learned second hand is little to no clinical improvement or benefit noted once you’re in an ICU setting on O2/vent and have pneumonia.

Early intervention/prophylaxis is where I’d be focused looking at right now.  But then assuming clear benefit, applying that is dependent on access to mass testing and rapid results turnaround.  Absent that, treatment would be rendered relatively useless due to rapid progression to bilateral pneumonia on average 5 days after symptom onset.  
 

Edited March 27, 2020 by triplehorn

[triplehorn 2664]

11 minutes ago, gmr548 said:

Do you have a link on that? I tried to google but it looks like Fauci only spoke briefly about vaccines yesterday?

I looked for it earlier today and haven’t found it yet.  His podium time yesterday was brief but very information dense.  It’s worth keeping an eye out for it.  Maybe a transcript pops up.

[gmr548 16580]

20 minutes ago, triplehorn said:

I looked for it earlier today and haven’t found it yet.  His podium time yesterday was brief but very information dense.  It’s worth keeping an eye out for it.  Maybe a transcript pops up.

https://www.ideastream.org/prepare-for-outbreak-surge-white-house-coronavirus-briefing-march-26-2020

Fauci starts at about 1:24:45 and speaks for a few minutes. at 1:28, he mentions that there are cases where potential vaccines end up making the disease worse and needing to avoid that being part of the vaccine testing timeline. That's the closest I could find.

[triplehorn 2664]

9 minutes ago, gmr548 said:

https://www.ideastream.org/prepare-for-outbreak-surge-white-house-coronavirus-briefing-march-26-2020

Fauci starts at about 1:24:45 and speaks for a few minutes. at 1:28, he mentions that there are cases where potential vaccines end up making the disease worse and needing to avoid that being part of the vaccine testing timeline. That's the closest I could find.

Thanks.  Fauci speaks to the principle of avoiding “enhancement” of an infection after receiving a vaccine against said infection.  no bueno.

Fauci is a no bullshittin truth teller.  Glad we have him.

Edited March 27, 2020 by triplehorn

[Mrs Whiggins 13050]

3 hours ago, triplehorn said:

 Maybe a transcript pops up.

 

3 hours ago, gmr548 said:

https://www.ideastream.org/prepare-for-outbreak-surge-white-house-coronavirus-briefing-march-26-2020

Fauci starts at about 1:24:45 and speaks for a few minutes. at 1:28, he mentions that there are cases where potential vaccines end up making the disease worse and needing to avoid that being part of the vaccine testing timeline. That's the closest I could find.

Here is a transcript from Dr. Fauci March 26:
 

Spoiler

 

Thank you Mr. Vice President. I'm going to change the topic just a little bit because there was questions that came up and I've been asked about this on a couple of media interactions regarding the interventions that we're talking about. And it's important because it's about something that I said yesterday, about what we would likely see. Whenever you put the clamps down and shut things down, you do it for two reasons: You do it to prevent the further spread -- as we call, mitigation -- but you also do it to buy yourself time to get better prepared for what might be a rebound. It may be a rebound that we get things really under control, and then you pull back, which ultimately we're going to have to do. Everybody in the world is going to have to do that.

You're either going to get a rebound, or it might cycle into the next season. So what are we going to do to prepare ourselves for that? One of the most important things is one that I mentioned several times from this podium, and that is to clarify a bit about the timeline for vaccines and would that have any real impact on what we would call "the rebound" or what we call a "cycling in the season." Certainly, for sure, a vaccine is not going to help us now, next month, the month after. But as I mentioned to you, we went into a phase one trial. And I keep referring to one vaccine; there's more than one. There's a couple of handfuls of vaccines at different stages of development, but they're all following the same course. And the course is: You first go into a phase one trial to see if it's safe and you have very few people, 45 people, within a certain age group -- all healthy, none at really any great risk of getting infected.

And the reason you do that is because you want to make sure that it's safe. Then the next thing you do -- and that takes about three months, easily, maybe more. So that's going to bring us into the beginning or middle of the summer. Then you go to a phase two trial, or what we say "two-three," which means we're going to put a lot of people in there. Now we hope that there aren't a lot of people getting infected, but it is likely there will be somewhere in the world where that's going on. So it's likely that we will get what's called an "efficacy signal," and we will know whether or not it actually works. If, in fact, it does, we hope to rush it to be able to have some impact on recycling in the next season.

And like I said, that could be a year to a year and a half. I'm not changing any of the dates that I mentioned. But one of the things that we are going to do that you need to understand -- that has been a stumbling block for previous development of vaccines -- and that is, even before you know something works, at risk, you have to start producing it. Because once you know it works, you can't say, "Great, it works. Now give me another six months to produce it." So we're working with a variety of companies to take that risk. We didn't take it with Zika. That's why, you know, we have a nice Zika vaccine but we don't have enough to do it because there's no Zika around. Same with SARS. So that's one of the things we're really going to push on is to be able to have it ready, if in fact, it works.

Now, the issue of safety -- something that I want to make sure the American public understand: It's not only safety when you inject somebody and they get maybe an idiosyncratic reaction, they get a little allergic reaction, they get pain. There's safety associated -- "Does the vaccine make you worse?" And there are diseases in which you vaccinate someone, they get infected with what you're trying to protect them with, and you actually enhance the infection. You can get a good feel for that in animal models. So that's going to be interspersed at the same time that we're testing. We're going to try and make sure we don't have enhancement. So the worst possible thing you do is vaccinate somebody to prevent infection and actually make them worse. Next, and finally, with regard -- I'll get you -- to your question.

Finally, with regard to therapies -- I mean, we keep getting asked about therapies. There's a whole menu of therapies that are going into clinical trial. As I've told you all and I'll repeat it again: The best way to get the best drug as quickly as possible is to do a randomized controlled trial so that you know is it safe and is it effective. If it's not effective, get it off the board and go to the next thing. If it is effective, get it out to the people that need it. So you're going to be hearing, over the next month or more, about different drugs that are going to go into these randomized controlled trials. And I feel confident, knowing about what this virus is and what we can do with it, that we will have some sort of therapy that'll give at least a partial, if not a very good protection in preventing progression of disease. And we'll be back here talking about that a lot, I'm sure. Thank you.

 

 

[wild_turkey 3167]

Fauci speaks to the principle of avoiding “enhancement” of an infection after receiving a vaccine against said infection.

There have apparently been problems with immune enhancement with previous vaccine attempts with other coronaviruses. The vaccine makes the infection worse for people who get it.

So a lot of people keep wanting them to rush out a vaccine even if it’s only 70% effective because a mediocre vaccine beats no vaccine, but the reality is that a bad vaccine has the potential to make the problem worse. We can’t risk injecting most of the country with a vaccine that makes things worse.

[Pasken 1309]

4 minutes ago, wild_turkey said:

So a lot of people keep wanting them to rush out a vaccine even if it’s only 70% effective because a mediocre vaccine beats no vaccine, but the reality is that a bad vaccine has the potential to make the problem worse. We can’t risk injecting most of the country with a vaccine that makes things worse.

 

It's pretty much how every movie about an infected outbreak begins.

[triplehorn 2664]

----> Masks 

I appreciate this expert's demeanor and presentation.  Solid.  It's coming from the national MD spokesperson in SoKo, the country arguably doing the best job top to bottom managing covid.  A lot of it is familiar to most of us by now.

~16min in : Masks rationale.  Really the highlight of the interview.

~22 min in: 20% of new infections today in SoKo are being imported via inbound foreign air travel 

~32 min: talks history and future of vaccines, references Dr. Fauci, and talks "repurposing" various drugs to treat Covid.  I'm still waiting to hear someone discuss the potential differences in outcomes between using CHQ/HCHQ for early intervention versus late intervention.  For now the emphasis still appears to be applying them to more advanced complicated cases.  fwiw, I think early app is where it's at.

 

[Hagbard Celine 10871]

Fantastic video.

[Nice Guy Eddie 13515]

Houston Methodist first to try blood transfusion test https://www-houstonchronicle-com.cdn.ampproject.org/c/s/www.houstonchronicle.com/news/houston-texas/amp/Houston-Methodist-first-in-the-nation-to-try-15164229.php

Quote

Houston Methodist Hospital Saturday night transfused the blood of a patient who has recovered from COVID-19 into a critically ill patient, the first hospital in the nation to try the experimental therapy.

A Houston individual who has been in good health for more than two weeks since being diagnosed donated the blood plasma for what’s known as convalescent serum therapy

 

[Anastasis 23475]

So here's the new french study. 

https://www.mediterranee-infection.com/wp-content/uploads/2020/03/COVID-IHU-2-1.pdf

 

[Anastasis 23475]

Relevant to ACE/ARB treatment. Some discussion of the mechanisms and interactions between the RAA system and COVID. 

https://www.nejm.org/doi/full/10.1056/NEJMsr2005760?

On the basis of the available evidence, we think that, despite the theoretical concerns and uncertainty regarding the effect of RAAS inhibitors on ACE2 and the way in which these drugs might affect the propensity for or severity of Covid-19, RAAS inhibitors should be continued in patients in otherwise stable condition who are at risk for, are being evaluated for, or have Covid-19 (see text box), a position now supported by multiple specialty societies (Table S2). Although additional data may further inform the treatment of high-risk patients with Covid-19, clinicians need to be cognizant of the unintended consequences of prematurely discontinuing proven therapies in response to hypothetical concerns that may be based on incomplete experimental evidence.69

Edited March 30, 2020 by Anastasis

[zork 629]

22 hours ago, Anastasis said:

So here's the new french study. 

https://www.mediterranee-infection.com/wp-content/uploads/2020/03/COVID-IHU-2-1.pdf

 

Westchester county, 1 hr N of NYC, Dr (Hasidic community Dr.)says he has treated 450-500 cases with 100% success:

Rudy interviews him pretty well getting him to give a lot of good detail including his dosages:  Interview starts about 2 minutes in. @Newdoc @ChiTownDoc

Spoiler

 

 

Edited March 31, 2020 by zork

[ChiTownDoc 21154]

10 minutes ago, zork said:

Westchester county, 1 hr N of NYC, Dr (Hasidic community Dr.)says he has treated 450-500 cases with 100% success:

Rudy interviews him pretty well getting him to give a lot of good detail including his dosages:  Interview starts about 2 minutes in. @Newdoc @ChiTownDoc

  Hide contents

 

 

I’m dead serious when I ask how you were able to make it through that interview?  I just couldn’t.  Rudy can barely get a sentence out and his questions are moronic.  ‘Why would your community be high risk?’  Lol.  Couldn’t watch. If you watch that and aren’t shaking your head, regardless of your political stance, I’m not sure what to tell you.   
 

I did read the paper about the regimen (azithromycin/chloroquine).  Anybody telling you they had 100% success with those 2 meds is totally full of shit.  U of C and NW have had some very minimal success.  100%?  Lol.  The success isn’t even attributable to the meds.  It may have just been that % if people are not affected or get better after X days.  Every ID doctor I spoke to says there’s minimal evidence it works and only 2 admit it might be worth a long shot.  A far cry from some miracle about to save us all.  Also the 4/5 well regarded ID docs who commented couldn’t figure out why the FDA approved choroquine.  Now the patients who need it for an actual indication like Lupus can’t get it.  Stupid all around.  

[zork 629]

1 minute ago, ChiTownDoc said:

I’m dead serious when I ask how you were able to make it through that interview?  I just couldn’t.  Rudy can barely get a sentence out and his questions are moronic.  ‘Why would your community be high risk?’  Lol.  Couldn’t watch. If you watch that and aren’t shaking your head, regardless of your political stance, I’m not sure what to tell you.   
 

I did read the paper about the regimen (azithromycin/chloroquine).  Anybody telling you they had 100% success with those 2 meds is totally full of shit.  U of C and NW have had some very minimal success.  100%?  Lol.  The success isn’t even attributable to the meds.  It may have just been that % if people are not affected or get better after X days.  Every ID doctor I spoke to says there’s minimal evidence it works and only 2 admit it might be worth a long shot.  A far cry from some miracle about to save us all.  Also the 4/5 well regarded ID docs who commented couldn’t figure out why the FDA approved choroquine.  Now the patients who need it for an actual indication like Lupus can’t get it.  Stupid all around.  

The Dr says zinc is one of the keys and that the hydroxychloroquine opens up the pathways that actually allow the zinc to be effective at blocking the coronavid, that the z-pack is mainly to keep the lungs from developing into the bacterial infection.  I don't have a visceral reaction to Rudy but realize some do.  

[Anastasis 23475]

All the best medical science is pushed out to clinicians and researchers through Hannity and Rudy. /noCR. 

I hope that the HCQ/A/Zn regimens shake out, but until it is demonstrated in a controlled study with random assignment it can only be considered a signal to be followed up on.  If physicians want to push the regimen out to patients in desperate situations, I have no problem with it.  But broad uptake really requires sound medical evidence.

[RayDog 682]

The evidence so far suggests that if it is a desperate situation, such as intubation is required, it is already too late for chloroquine to be effective. That apparent fact certainly leads to the mixed results we see.

And, given it appears that over 80% of cases recover on their own with mild or no symptoms, chloroquine may have no effect on those patients. Blind trials need to conducted with early stage patients to know for sure. 

[ChiTownDoc 21154]

33 minutes ago, zork said:

The Dr says zinc is one of the keys and that the hydroxychloroquine opens up the pathways that actually allow the zinc to be effective at blocking the coronavid, that the z-pack is mainly to keep the lungs from developing into the bacterial infection.  I don't have a visceral reaction to Rudy but realize some do.  

It may help with severity - I really hope it does.  But the best of the best out there don't have much hope for it.  I really hope they're wrong and I'm wrong.  The zinc makes some sense on a biological level - again, a reach.  But that orthodox community is so devastated with deaths and hospitalizations I have no idea what that doc is talking about?  I seriously know their relatives here in the orthodox community of Chicago and they're like wtf is this guy talking about?   Our family is dying left and right up there.  I'm really not trying to be an asshole.  We all hope some concoction will end all this shit. 

[Anastasis 23475]

54 minutes ago, RayDog said:

The evidence so far suggests that if it is a desperate situation, such as intubation is required, it is already too late for chloroquine to be effective. That apparent fact certainly leads to the mixed results we see.

I think that the front line clinicians can triage their patients sufficiently well and make the appropriate front line determinations. At this point they likely know exactly what the profile of the high risk cases looks like the minute the roll in the door. 

1 hour ago, RayDog said:

And, given it appears that over 80% of cases recover on their own with mild or no symptoms, chloroquine may have no effect on those patients. Blind trials need to conducted with early stage patients to know for sure. 

Blinding is not really the pivotal component.  What we need is random assignment with a suitable standard of care control group. 

[zork 629]

Whatever doctoring they are doing in Westchester NY, given the latest from JH webstats, it seems people should listen to them:  

9326 confirmed positive tests

10 deaths.  To this point and of course there are delayed stats to come.  

 

 

[SHOOTER12 8811]

On 3/14/2020 at 3:03 PM, EuroHorn said:

Scentscy?

Family of Chad Briscoe?

[SHOOTER12 8811]

On 3/14/2020 at 5:14 PM, triplehorn said:

on it.  I'm taking it daily though for presumptive active sars-cov-2 infection.

 

Sounds like Futureman is going to be getting a lot of referrals.

[Anastasis 23475]

Small chinese study on HCQ...

First American studies should be posting some results before end of week.

https://www.medrxiv.org/content/10.1101/2020.03.22.20040758v2

Aims: Studies have indicated that chloroquine (CQ) shows antagonism against COVID-19 in vitro. However, evidence regarding its effects in patients is limited. This study aims to evaluate the efficacy of hydroxychloroquine (HCQ) in the treatment of patients with COVID-19.

Main methods: From February 4 to February 28, 2020, 62 patients suffering from COVID-19 were diagnosed and admitted to Renmin Hospital of Wuhan University. All participants were randomized in a parallel-group trial, 31 patients were assigned to receive an additional 5-day HCQ (400 mg/d) treatment, Time to clinical recovery (TTCR), clinical characteristics, and radiological results were assessed at baseline and 5 days after treatment to evaluate the effect of HCQ.

Key findings: For the 62 COVID-19 patients, 46.8% (29 of 62) were male and 53.2% (33 of 62) were female, the mean age was 44.7 (15.3) years. No difference in the age and sex distribution between the control group and the HCQ group. But for TTCR, the body temperature recovery time and the cough remission time were significantly shortened in the HCQ treatment group. Besides, a larger proportion of patients with improved pneumonia in the HCQ treatment group (80.6%, 25 of 32) compared with the control group (54.8%, 17 of 32). Notably, all 4 patients progressed to severe illness that occurred in the control group. However, there were 2 patients with mild adverse reactions in the HCQ treatment group.

Significance: Among patients with COVID-19, the use of HCQ could significantly shorten TTCR and promote the absorption of pneumonia.

Edited April 1, 2020 by Anastasis

[Victor Lazlo 1777]

Zork posted this in the No Politics thread, but I thought it needed to be seen here, as the possible effects of ACE inhibitors and ARDs had been discussed earlier.

 

• Report post
•  
•  #2790Posted 1 hour ago

"Interesting Italy demographics, etc:

Quote

2. Demographic data

The average age of deceased and COVID-19 positive patients is 78 years (median 79, range 26-100, InterQuartile Range - IQR 73-85). There are 3088 women (30.8%). For 2 patients the age data was not available. The median age of COVID-19 positive deceased patients is more than 15 years higher than that of patients who contracted the infection (median age: patients who died 79 years - patients with infection 62 years). The graph shows the number of deaths by age group. Women who died after contracting COVID-19 infection are older than men (median ages: women 82 - men 78).

https://www.epicentro.iss.it/coronavirus/sars-cov-2-decessi-italia

 

Quote

3. Pre-existing pathologies

The graph presents the most common pre-existing chronic pathologies (diagnosed before contracting SARS-CoV-2 infection) in deceased patients. This figure was obtained in 909 deceased for which it was possible to analyze the medical records of hospitalization. The average number of pathologies observed in this population is 2.7 (median 3, Standard Deviation 1.6). Overall, 19 patients (2.1% of the sample) had 0 pathologies, 197 (21.6%) had 1 pathology, 223 had 2 pathologies (24.5%) and 470 (51.7%) had 3 or more pathologies . Prior to hospitalization, 28% of COVID-19 positive deceased patients followed ACE inhibitor therapy and 16% Sartani (angiotensin receptor blocker) therapy.

Number of pathologies

Pie chart with 4 slices.

positive COVID-2019 deceased patients

 

 

Numero di patologiepazienti deceduti COVID-2019 positivi2.1 %2.1 %21.6 %21.6 %24.5 %24.5 %51.8 %51.8 %

go to the link above for the graphs/charts, browser needs to translate."

 Prior to hospitalization, 28% of COVID-19 positive deceased patients followed ACE inhibitor therapy and 16% Sartani (angiotensin receptor blocker) therapy.

 

As the bold text shows, of the 909 deaths in the study, 28% were on ACE inhibitors and 16% on ARBs before hospitalization.

 

 

Edited April 1, 2020 by Victor Lazlo

[Brisketexan 105158]

14 minutes ago, Victor Lazlo said:

Zork posted this in the No Politics thread, but I thought it needed to be seen here, as the possible effects of ACE inhibitors and ARDs had been discussed earlier.

 

• Report post
•  
•  #2790Posted 1 hour ago

"Interesting Italy demographics, etc:

https://www.epicentro.iss.it/coronavirus/sars-cov-2-decessi-italia

 

go to the link above for the graphs/charts, browser needs to translate."

 Prior to hospitalization, 28% of COVID-19 positive deceased patients followed ACE inhibitor therapy and 16% Sartani (angiotensin receptor blocker) therapy.

 

As the bold text shows, of the 909 deaths in the study, 28% were on ACE inhibitors and 16% on ARBs before hospitalization.

 

 

Ok.  But correlation and causation and such.  I mean, older folks are much more likely to be on such meds.  They are also the more vulnerable group.  Is it the meds, or is it that folks who happen to be more highly represented in the at-risk category also take those meds more than the average member of the population?

It's like saying that 25% of the deceased had watched Matlock reruns in the past month.  That doesn't mean that Matlock kills you.  It means that this virus kills old people, who happen to be the demographic that most watches Matlock*.

* Murder, She Wrote reruns would also be acceptable here.

[Victor Lazlo 1777]

6 minutes ago, Brisketexan said:

Ok.  But correlation and causation and such.  I mean, older folks are much more likely to be on such meds.  They are also the more vulnerable group.  Is it the meds, or is it that folks who happen to be more highly represented in the at-risk category also take those meds more than the average member of the population?

It's like saying that 25% of the deceased had watched Matlock reruns in the past month.  That doesn't mean that Matlock kills you.  It means that this virus kills old people, who happen to be the demographic that most watches Matlock*.

* Murder, She Wrote reruns would also be acceptable here.

A couple of weeks ago, Dr. Fauci was asked about those types of meds in a press conference. He said that it was an issue that needed to be looked at and that he was hoping to get info from the Italians.

From the study results, I - like you  - am not sure it can tell us much about causation.

[triplehorn 2664]

The FDA-approved Drug Ivermectin inhibits the replication of SARS-CoV-2 in vitro

•Ivermectin is an inhibitor of the COVID-19 causative virus (SARS-CoV-2) in vitro.

•A single treatment able to effect ∼5000-fold reduction in virus at 48h in cell culture.

•Ivermectin is FDA-approved for parasitic infections, and therefore has a potential for repurposing.

•Ivermectin is widely available, due to its inclusion on the WHO model list of essential medicines.

 

[Armybrat 40851]

10 minutes ago, triplehorn said:

The FDA-approved Drug Ivermectin inhibits the replication of SARS-CoV-2 in vitro

•Ivermectin is an inhibitor of the COVID-19 causative virus (SARS-CoV-2) in vitro.

•A single treatment able to effect ∼5000-fold reduction in virus at 48h in cell culture.

•Ivermectin is FDA-approved for parasitic infections, and therefore has a potential for repurposing.

•Ivermectin is widely available, due to its inclusion on the WHO model list of essential medicines.

 

Plain English please.

[Anastasis 23475]

6 minutes ago, Armybrat said:

Plain English please.

people think they found stuff that works in test tubes and hope maybe it works one day in people. 

[gmr548 16580]

The FDA-approved Drug Ivermectin inhibits the replication of SARS-CoV-2 in vitro

•Ivermectin is an inhibitor of the COVID-19 causative virus (SARS-CoV-2) in vitro.

•A single treatment able to effect ∼5000-fold reduction in virus at 48h in cell culture.

•Ivermectin is FDA-approved for parasitic infections, and therefore has a potential for repurposing.

•Ivermectin is widely available, due to its inclusion on the WHO model list of essential medicines.

 

 

Pretty sure that's a dog heartworm med lol

 

Odd to me that there appears to be buzz around anti-parasitic drugs to deal with a coronavirus. I'm curious about that as a layman.

 

[triplehorn 2664]

19 minutes ago, Armybrat said:

Plain English please.

It's a medication that already has an established safety profile when people take it, hence the FDA approval for use to treat parasites.  It's potent at knocking out this covid virus with a single dose in a petri dish.  Need to see if that knockout dose translates into a safe effective dose in people.  Hopefully you don't have to take x10 the normal parasite dose in order to kill the virus.

But basic re-purposing an established med would be fast head start.

 

Edited April 4, 2020 by triplehorn

[strangulation! 1716]

Would tests on people be the next stage? Or would they need to test on certain animals and then progress to humans?

[triplehorn 2664]

21 minutes ago, strangulation! said:

Would tests on people be the next stage? Or would they need to test on certain animals and then progress to humans?

With this drug, they can go straight to human trials for Covid.  The article says that even relatively high dose of this med is safe in people from studies looking at dengue viral infection (which isn't particularly effective vs dengue)

"Importantly, recent reviews and meta-analysis indicate that high dose ivermectin has comparable safety as the standard low-dose treatment, although there is not enough evidence to make conclusions about the safety profile in pregnancy28,29. The critical next step in further evaluation for possible benefit in COVID-19 patients will be to examine a multiple addition dosing regimen that mimics the current approved usage of ivermectin in humans. "

There's also this important consideration:

"Ultimately, development of an effective anti-viral for SARS-CoV-2, if given to patients early in infection, could help to limit the viral load, prevent severe disease progression and limit person-person transmission."

With Covid, a lot appears to hinge on early detection and intervention.  If you wait until pneumonia has set in, the damage is done.  That's one area where testing limitations in availability and rapid results are still biting us in he butt.

[Anastasis 23475]

The lack of interim HCQ data from NY at this point is concerning. 

[triplehorn 2664]

8 hours ago, Anastasis said:

The lack of interim HCQ data from NY at this point is concerning. 

Compare looking at outcomes with early intervention vs intervention with complications present.  Selecting subjects for early intervention is a situation where the difference between efficacy or not will manifest in maybe 5 or less out of every 100 subjects who would otherwise end up in the ICU with pneumonia.  Showing that is more difficult than showing response between groups by selecting for subjects already having complications of infection.  

Since testing is a debacle, ideally we need a widely available med that anyone could take and that is safe enough to take even if you don't have confirmation of covid from a test (due to low availability and turnaround time).  That could allow rapidly attacking a virus with the greatest chance of success without waiting for confirmation.  It'd be ideal if a one-and-done single dose could work in people (as seen in vitro) as that would reduce med exposure to the vast majority of people who don't progress to complications.  You could refine recs for early intervention based on older age and/or existence of co-morbid medical conditions, or anyone with URI symptoms with airway restriction/dyspnea.

For now, the proven way to shut this bug down within weeks is extreme social distancing.  and everyone covering their nose and mouth with basically anything while in public.

[Newdoc 3448]

I haven't seen this website talked about here but it's hard to parse out what's been posted due to the almost CR levels of bitching in the main thread.   I will link an article that shows a calculated and relative increased risk of Covid mortality across age groups. It looks to be a pretty good analysis and reported the correct way, could help Joe Public under 60 yo to calm down the "we're all gonna die". He does absolutely state that mitigation factors are critical however.

How much risk does Covid represent.

 

Quote

This suggests that COVID-19 very roughly contributes a year’s worth of risk. There is a simple reality check on this figure. Every year around 600,000 people die in the UK. The Imperial College team estimates that if the virus went completely unchallenged, around 80% of people would be infected and there would be around 510,000 deaths.

So, roughly speaking, we might say that getting COVID-19 is like packing a year’s worth of risk into a week or two. Which is why it’s important to spread out the infections to avoid the NHS being overwhelmed.

Quote

This is because, both for COVID and in normal circumstances, much of the risk is held by people whom are already chronically ill. So for the large majority of healthy people, their risks of either dying from COVID, or dying of something else, are much lower than those quoted here. Although of course for every death there will be others who are seriously ill.

 

[gmr548 16580]

On 4/4/2020 at 7:22 PM, Newdoc said:

I haven't seen this website talked about here but it's hard to parse out what's been posted due to the almost CR levels of bitching in the main thread.   I will link an article that shows a calculated and relative increased risk of Covid mortality across age groups. It looks to be a pretty good analysis and reported the correct way, could help Joe Public under 60 yo to calm down the "we're all gonna die". He does absolutely state that mitigation factors are critical however.

How much risk does Covid represent.

 

 

That's a good way to look at it because it pretty succinctly sums up why most people don't need to panic, but also why we absolutely need to be taking distancing protocols very seriously. The odds of a relatively young, healthy person dying if you roll their annual risk into a week or two still isn't very high. A year's worth of critical cases coming into a hospital in the same timeframe would absolutely overwhelm the place and result in many unnecessary deaths due to care rationing.

People seem to have a really hard time understanding that both of those things are true.

[Txzen 498]

On 4/3/2020 at 9:03 PM, strangulation! said:

Would tests on people be the next stage? Or would they need to test on certain animals and then progress to humans?

Full disclosure, I'm a cancer research guy, not infectious disease. But certainly many of the animal models for human infectious diseases are fraught with limitations just like those in oncology. 

The Gilead drug remdesivir, for instance, looked good in vitro for Ebola, and pretty good in primate disease models models - but perhaps has not shown as much promise in the field. The primate models are so-called semi-permissive for Ebola (and also some respiratory viruses), meaning that the disease often doesn't quite take hold as well in monkeys or is not as sustained as it is in humans. So, testing of the drugs in these models often is early on after exposure to the infectious agent to show if it has an impact. 

Compare that to treating people in the field where Ebola has sprung up - people in all the various stages of disease, long after being infected with various levels of disease burden and the resulting complications of other systems involved. It's not so simple to make the leap from preclinical to clinical. 

It all highlights the need for the continued clinical trials of all of these agents alone or in combination, as is ongoing now. Sporadic reports of a few patients treated here or there is not conclusive evidence of efficacy. 

[naija 2868]

3 hours ago, gmr548 said:

That's a good way to look at it because it pretty succinctly sums up why most people don't need to panic, but also why we absolutely need to be taking distancing protocols very seriously. The odds of a relatively young, healthy person dying if you roll their annual risk into a week or two still isn't very high. A year's worth of critical cases coming into a hospital in the same timeframe would absolutely overwhelm the place and result in many unnecessary deaths due to care rationing.

People seem to have a really hard time understanding that both of those things are true.

That's the message that we have failed to get through and I think when it is all said and done, will be what others use as pushback that alot of the measures were too strenuous. And very smart people do not understand it. 

[naija 2868]

The guys that work on Cytokine Storm Syndrome are pushing it to explain the mortality of a subset of patients and the interleukin blockade drugs as a means of counteracting the syndrome. 

[Jiggy-Z 3433]

On 4/1/2020 at 1:17 PM, Brisketexan said:

Ok.  But correlation and causation and such.  I mean, older folks are much more likely to be on such meds.  They are also the more vulnerable group.  Is it the meds, or is it that folks who happen to be more highly represented in the at-risk category also take those meds more than the average member of the population?

It's like saying that 25% of the deceased had watched Matlock reruns in the past month.  That doesn't mean that Matlock kills you.  It means that this virus kills old people, who happen to be the demographic that most watches Matlock*.

* Murder, She Wrote reruns would also be acceptable here.

Do you even Diagnosis: Murder, bro?

[naija 2868]

Does anyone have a good place to see what fatalities have occurred amongst healthcare workers so far? I've heard of a couple of residents succumbing to it... but nothing official yet

[Anastasis 23475]

University of Michigan summary of HCQ data: https://www.med.umich.edu/asp/pdf/adult_guidelines/COVID-19_appendix.pdf

[PRONG HORN 3147]

[Skipper 6136]

This is pretty over my head but posting for medical professionals that might find it interesting.  Attia is a pretty sharp guy and his team is spending a ton of time reviewing all potential therapies out there so figure anything he thinks is worth posting is probably worth sharing:   https://peterattiamd.com/wp-content/uploads/2020/04/Exogenous-pulmonary-surfactant-as-a-potential-adjuvant-therapy-in-SARS-CoV-2-patients-experiencing-acute-respiratory-distress-syndrome_-3-1.pdf

[GringoSalado 1651]

Siap

https://www.statnews.com/2020/04/08/doctors-say-ventilators-overused-for-covid-19/

 

With ventilators running out, doctors say the machines are overused for Covid-19

By SHARON BEGLEY @sxbegle

APRIL 8, 2020

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HEALTH

With ventilators running out, doctors say the machines are overused for Covid-19

By SHARON BEGLEY @sxbegle

APRIL 8, 2020

A fuel cell stack testing engineer tests ventilator oxygen at Bloom Energy in Sunnyvale, Calif. The company has switched over to refurbishing ventilators as an increasing number of patients experience respiratory issues as a result of Covid-19.BETH LABERGE/POOL PHOTO VIA AP

Even as hospitals and governors raise the alarm about a shortage of ventilators, some critical care physicians are questioning the widespread use of the breathing machines for Covid-19 patients, saying that large numbers of patients could instead be treated with less intensive respiratory support.

If the iconoclasts are right, putting coronavirus patients on ventilators could be of little benefit to many and even harmful to some.

What’s driving this reassessment is a baffling observation about Covid-19: Many patients have blood oxygen levels so low they should be dead. But they’re not gasping for air, their hearts aren’t racing, and their brains show no signs of blinking off from lack of oxygen.

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That is making critical care physicians suspect that blood levels of oxygen, which for decades have driven decisions about breathing support for patients with pneumonia and acute respiratory distress, might be misleading them about how to care for those with Covid-19. In particular, more and more are concerned about the use of intubation and mechanical ventilators. They argue that more patients could receive simpler, noninvasive respiratory support, such as the breathing masks used in sleep apnea, at least to start with and maybe for the duration of the illness.

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“I think we may indeed be able to support a subset of these patients” with less invasive breathing support, said Sohan Japa, an internal medicine physician at Boston’s Brigham and Women’s Hospital. “I think we have to be more nuanced about who we intubate.”

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That would help relieve a shortage of ventilators so critical that states are scrambling to procure them and some hospitals are taking the unprecedented (and largely untested) step of using a single ventilator for more than one patient. And it would mean fewer Covid-19 patients, particularly elderly ones, would be at risk of suffering the long-term cognitive and physical effects of sedation and intubation while being on a ventilator.

None of this means that ventilators are not necessary in the Covid-19 crisis, or that hospitals are wrong to fear running out. But as doctors learn more about treating Covid-19, and question old dogma about blood oxygen and the need for ventilators, they might be able to substitute simpler and more widely available devices.

An oxygen saturation rate below 93% (normal is 95% to 100%) has long been taken as a sign of potential hypoxia and impending organ damage. Before Covid-19, when the oxygen level dropped below this threshold, physicians supported their patients’ breathing with noninvasive devices such as continuous positive airway pressure (CPAP, the sleep apnea device) and bilevel positive airway pressure ventilators (BiPAP). Both work via a tube into a face mask.

In severe pneumonia or acute respiratory distress unrelated to Covid-19, or if the noninvasive devices don’t boost oxygen levels enough, critical care doctors turn to mechanical ventilators that push oxygen into the lungs at a preset rate and force: A physician threads a 10-inch plastic tube down a patient’s throat and into the lungs, attaches it to the ventilator, and administers heavy and long-lasting sedation so the patient can’t fight the sensation of being unable to breathe on his own.

 

In this video, we look at how ventilators work, and how they are used to treat patients with Covid-19.

But because in some patients with Covid-19, blood-oxygen levels fall to hardly-ever-seen levels, into the 70s and even lower, physicians are intubating them sooner. “Data from China suggested that early intubation would keep Covid-19 patients’ heart, liver, and kidneys from failing due to hypoxia,” said a veteran emergency medicine physician. “This has been the whole thing driving decisions about breathing support: Knock them out and put them on a ventilator.”

To be sure, many physicians are starting simple. “Most hospitals, including ours, are using simpler, noninvasive strategies first,” including the apnea devices and even nasal cannulas, said Greg Martin, a critical care physician at Emory University School of Medicine and president-elect of the Society of Critical Care Medicine. (Nasal cannulas are tubes whose two prongs, held beneath the nostrils by elastic, deliver air to the nose.) “It doesn’t require sedation and the patient [remains conscious and] can participate in his care. But if the oxygen saturation gets too low you can achieve more oxygen delivery with a mechanical ventilator.”

The question is whether ICU physicians are moving patients to mechanical ventilators too quickly. “Almost the entire decision tree is driven by oxygen saturation levels,” said the emergency medicine physician, who asked not to be named so as not to appear to be criticizing colleagues.

That’s not unreasonable. In patients who are on ventilators due to non-Covid-19 pneumonia or acute respiratory distress, a blood oxygen level in the 80s can mean impending death, with no room to give noninvasive breathing support more time to work. Physicians are using their experience with ventilators in those situations to guide their care for Covid-19 patients. The problem, critical care physician Cameron Kyle-Sidell told Medscape this week, is that because U.S. physicians had never seen Covid-19 before February, they are basing clinical decisions on conditions that may not be good guides.

“It’s hard to switch tracks when the train is going a million miles an hour,” said Kyle-Sidell, who works at a New York City hospital. “This may be an entirely new disease,” making ventilator protocols developed for other conditions less than ideal.

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As doctors learn more about the disease, however, both frontline experience and a few small studies are leading him and others to question how, and how often, mechanical ventilators are used for Covid-19.

The first batch of evidence relates to how often the machines fail to help. “Contrary to the impression that if extremely ill patients with Covid-19 are treated with ventilators they will live and if they are not, they will die, the reality is far different,” said geriatric and palliative care physician Muriel Gillick of Harvard Medical School.

Researchers in Wuhan, for instance, reported that, of 37 critically ill Covid-19 patients who were put on mechanical ventilators, 30 died within a month. In a U.S. study of patients in Seattle, only one of the seven patients older than 70 who were put on a ventilator survived; just 36% of those younger than 70 did. And in a study published by JAMA on Monday, physicians in Italy reported that nearly 90% of 1,300 critically ill patients with Covid-19 were intubated and put on a ventilator; only 11% received noninvasive ventilation. One-quarter died in the ICU; 58% were still in the ICU, and 16% had been discharged.

Older patients who do survive risk permanent cognitive and respiratory damage from being on heavy sedation for many days if not weeks and from the intubation, Gillick said.

To be sure, the mere need for ventilators in Covid-19 patients suggests many in the studies were so critically ill their chances of survival were poor no matter what care they received.

But one of the most severe consequences of Covid-19 suggests another reason the ventilators aren’t more beneficial. In acute respiratory distress syndrome, which results from immune cells ravaging the lungs and kills many Covid-19 patients, the air sacs of the lungs become filled with a gummy yellow fluid. “That limits oxygen transfer from the lungs to the blood even when a machine pumps in oxygen,” Gillick said.

As patients go downhill, protocols developed for other respiratory conditions call for increasing the force with which a ventilator delivers oxygen, the amount of oxygen, or the rate of delivery, she explained. But if oxygen can’t cross into the blood from the lungs in the first place, those measures, especially greater force, may prove harmful. High levels of oxygen impair the lung’s air sacs, while high pressure to force in more oxygen damages the lungs.

Related: 

A system to allocate scarce ventilators and ICU beds gains traction for not counting any group out

In a letter last week in the American Journal of Respiratory and Critical Care Medicine, researchers in Germany and Italy said their Covid-19 patients were unlike any others with acute respiratory distress. Their lungs are relatively elastic (“compliant”), a sign of health “in sharp contrast to expectations for severe ARDS.” Their low blood oxygen might result from things that ventilators don’t fix. Such patients need “the lowest possible [air pressure] and gentle ventilation,” they said, arguing against increasing the pressure even if blood oxygen levels remain low. “We need to be patient.”

“We need to ask, are we using ventilators in a way that makes sense for other diseases but not for this one?” Gillick said. “Instead of asking how do we ration a scarce resource, we should be asking how do we best treat this disease?”

Researchers and clinicians on the front lines are trying. In a small study last week in Annals of Intensive Care, physicians who treated Covid-19 patients at two hospitals in China found that the majority of patients needed no more than a nasal cannula. Among the 41% who needed more intense breathing support, none was put on a ventilator right away. Instead, they were given noninvasive devices such as BiPAP; their blood oxygen levels “significantly improved” after an hour or two. (Eventually two of seven needed to be intubated.) The researchers concluded that the more comfortable nasal cannula is just as good as BiPAP and that a middle ground is as safe for Covid-19 patients as quicker use of a ventilator.

“Anecdotal experience from Italy [also suggests] that they were able to support a number of folks using these [non-invasive] methods,” Japa said.

To be “more nuanced about who we intubate,” as she suggests, starts with questioning the significance of oxygen saturation levels. Those levels often “look beyond awful,” said Scott Weingart, a critical care physician in New York and host of the “EMCrit” podcast. But many can speak in full sentences, don’t report shortness of breath, and have no signs of the heart or other organ abnormalities that hypoxia can cause.

“The patients in front of me are unlike any I’ve ever seen,” Kyle-Sidell told Medscape about those he cared for in a hard-hit Brooklyn hospital. “They looked a lot more like they had altitude sickness than pneumonia.”

Because U.S. data on treating Covid-19 patients are nearly nonexistent, health care workers are flying blind when it comes to caring for such confounding patients.  But anecdotally, Weingart said, “we’ve had a number of people who improved and got off CPAP or high flow [nasal cannulas] who would have been tubed 100 out of 100 times in the past.” What he calls “this knee-jerk response” of putting people on ventilators if their blood oxygen levels remain low with noninvasive devices “is really bad. … I think these patients do much, much worse on the ventilator.”

That could be because the ones who get intubated are the sickest, he said, “but that has not been my experience: It makes things worse as a direct result of the intubation.” High levels of force and oxygen levels, both in quest of restoring oxygen saturation levels to normal, can injure the lungs. “I would do everything in my power to avoid intubating patients,” Weingart said.

One reason Covid-19 patients can have near-hypoxic levels of blood oxygen without the usual gasping and other signs of impairment is that their blood levels of carbon dioxide, which diffuses into air in the lungs and is then exhaled, remain low. That suggests the lungs are still accomplishing the critical job of removing carbon dioxide even if they’re struggling to absorb oxygen. That, too, is reminiscent of altitude sickness more than pneumonia.

The noninvasive devices “can provide some amount of support for breathing and oxygenation, without needing a ventilator,” said ICU physician and pulmonologist Lakshman Swamy of Boston Medical Center.

One problem, though, is that CPAP and other positive-pressure machines pose a risk to health care workers, he said.  The devices push aerosolized virus particles into the air, where anyone entering the patient’s room can inhale them. The intubation required for mechanical ventilators can also aerosolize virus particles, but the machine is a contained system after that.

“If we had unlimited supply of protective equipment and if we had a better understanding of what this virus actually does in terms of aerosolizing, and if we had more negative pressure rooms, then we would be able to use more” of the noninvasive breathing support devices, Swamy said.

About the Author

Sharon Begley

Senior Writer, Science and Discovery

Sharon covers science and discovery.

 sharon.begley@statnews.com

 @sxbegle

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