Nobody seems to be talking about the actual reason Chinese doctors found chloroquine (and HCQ) interesting and it has nothing to do with it's immunosuppressing effect:
Their conclusion was that chloroquine could indeed allow zinc to enter the cell and then inhibit replication (and therefore that the treatment needed to be administered early).
Nobody seems to be talking about a very easy way to verify chloroquine (and HCQ) efficiency by just using the same method used in China:
Cross-check the list of patients infected with Lupus (lupus erythematosus) and with chronic HCQ treatment (they take it for years) with the list of known infected COVID19 patients.
In China (and specifically in Wuhan), this is how they (team of Dr Zhang Zhan) found out about the efficiency of HCQ. They noticed that there were no patients with chronic HCQ treatment for lupus (lupus erythematosus) infected with covid19. This was in peoples Hospital of Wuhan University (source: https://www.jqknews.com/news/388543-The_novel_coronavirus_pn...)
This alone would be enough to prove some efficiency even as prophyalxis (as they are advocating officially in India). This should be quite trivial to check with the current amount of confirmed infection.
In principle that would be a great thing to check but due to lack of clinical systems interoperability it's not at all trivial to check. Surescripts and the various pharmacy chains have data on who has been taking chloroquine but researchers will still have to get access, and then do a bunch of record linkage work to compare outcomes. In the hardest hit areas I suspect healthcare providers have also fallen behind on data entry so there's going to be a data quality problem.
An interesting hint could come from this pre-print study: https://www.biorxiv.org/content/10.1101/2020.03.29.014407v1
They tried different administration modalities of HCQ to in-vitro infected cells: some cells got nothing (control), some got HCQ only before infection, some got HCQ only after infection, some got HCQ both before and after infection. THe cells that got HCQ only before or only after infection had just slightly better outcome than control (they appear as heavily infected), while cells that received HCQ both before and after contagion were in much healthier conditions. If that would be the same in vivo as in vitro, that would entail that it would be possible to use HCQ as prophylaxis, given that the patients never stop taking the drug. Of course the caveat is "IF that would be the same in vivo as in vitro", that they didn't (yet) tested.
> Their conclusion was that chloroquine could indeed allow zinc to enter the cell and then inhibit replication (and therefore that the treatment needed to be administered early).
Where does the "if it inhibits replication it needs to be administered early" line come from? I've seen it elsewhere too, but why wouldn't inhibit replication lead to => continually declining amounts in the body => easier recovery at any stage?
Nobody is going to point out that of the 11 patients, "8 had significant comorbidities associated with poor outcomes (obesity: 2; solid cancer: 3; hematological cancer: 2; HIV-infection: 1)"?
I don't even understand what the point of this study was except as a rebuttal to the prior study. I mean, if people thought the prior study was cherry picking results. I don't even know what I'd call this...
There's _some_ anecdotal evidence that it _may_ work if treated early. Hopefully there are some real studies that are being done on that.
That is frightening. Increasing the mutation rate must carry a large unknown risk. Also surely the first thing to mutate will be self-defeating resistance to that drug...
I have no medical expertise, but there's something that is confusing me. From what I read, typically, you get the virus, then an opportunistic bacterium gives you pneumonia, and that's what you die from. But this study seems to be saying "someone else found these meds reduced the virus and we didn't". But the meds are more or less antibiotics, aren't they? So could the explanation simply be that while the virus is the same, the bacteria are not, in the two tests?
My understanding is what you said is true for influenza and to a lesser extent colds. Those virus tend infect the upper respiratory system. COVID19 though can infect the lower lungs and directly causes pneumonia. And viral pneumonia is no joke even before COVID19.
I am not in any way qualified in the medical domain but these methods look similar to the other Study that was viewed as flawed that showed it did work. Seems there is no solid data either way.
Well this one seems more rigorous. They monitored concentration in blood for 4 days, they checked viral presence two following days at the end. They don't mention viral load though and I don't know if they have a threshold for cycles in QPCR to estimate that.
This kind of paper is not here to say here is the proof it works or it does not work, it is meant to say: this what we had with us, this how we did it, this is the results we observed and whether or not it validates the hypothesis stated.
Wonder when the Indian Council of Medical Research will release more papers - there were a few patients who responded positively under their suggested treatment plan:
> “We used a combo of Lopinavir and Ritonavir drugs which are usually given as a second line of treatment for HIV with drugs meant for curing malaria and swine flu. We administered this line of treatment to a 70-year-old Italian woman, who had come as a tourist to Rajasthan, who tested positive and was being treated by us, as well as another Italian, who is 69-year-old,” said Dr Sudhir Bhandari.
> ... “The team of doctors under the leadership of Dr Sudhir Bhandari, Principal of SMS Medical College held consultations with the ICMR and tried a combination medicines given for malaria, swine flu (Tamiflu) along with drugs for HIV and it worked well. All three persons including the Italians were cured this way,” said Rohit Kumar Singh, additional chief secretary, health of Rajasthan government.
> ... The three persons who tested positive were administered a combination of 200mg Lopinavir and 50 mg of Ritonavir twice a day besides Oseltamivir and Chloroquine that are given to the swine flu and malaria patients.
> However, the doctors at the SMS Hospital warned that this was only an emergency treatment and the HIV medicines were used only as an emergency measure that could help in regaining normalcy.
Update: The Indian Council of Medical Research has also given the go ahead to try out plasma therapy for the really serious, and some hospitals and institute are waiting for clearance of the same from the Drug Controller General of India:
> ... Blood for the plasma therapy will be collected from recovered patients at SCTIMST and the medical colleges and donated to critical patients with sanction from Blood Transfusion Council. Plasma would be separated from blood and taken to other hospitals under refrigeration.
> ... When a person suffers from COVID-19, antibodies are created in his or her body as defence. Such B lymphocytes would be present in plasma. After a patient recovers from the disease, these antibodies remain in blood to prevent another attack by the virus. The plasma collected from such people and given to another patient would have antibodies which target the virus and prevent the recipient from slipping into a more serious condition. According to researches, plasma taken from one donor would have sufficient doses for two patients.
COVID-19 attacks hemoglobin and that is how it damages the lungs. With your hemoglobin unable to exchange oxygen with blood in the lungs, it causes terrible damage.
Chloroquine prevents the virus from affecting hemoglobin, or reduces the effect. This is also how Chloroquine treats malaria.
The problem with a study on severe cases is that the damage is already done and the hemoglobin is already compromised.
It is best to start treatment with chloroquine prior to reaching the severe stage. By the time you are severe you’ve gotten permanent lung damage and the immune system is in a race condition unable to keep up with the virus.
If you want to detour into tinfoil hat territory, you could posit that these studies on severe patients were designed knowing it would show low or no efficacy, because it’s too late to protect the patient’s hemoglobin.
Azithromycin slows ribosonal RNA replication in bacteria. It is unclear how it helps with a Covid.
Antivirals are much more promising for severe cases, but even they can’t heal ground glass in the lungs.
COVID-19 is not a normal respiratory infection. It seems to prevent your RBCs from holding onto O2 and CO2 mimicking high altitude sickness. The disease acts like HAPE (high altitude pulmonary edema). The damage and inflammation is coming from the blood's inability to properly perform gas exchange in the lungs. Other damage could actually be coming from ventilators with pressure set too high (lungs of patients are mechanically normal, atypical for ARDS). Patient oxygen stats are also weird, they're hypoxic, but not necessarily short of breath.
> Chloroquine prevents the virus from affecting hemoglobin
This virus attacks the cells that live in the throat and lungs. The "spike" as far as I'm aware does not attach to haemoglobin.
> damage is already done and the hemoglobin is already compromised.
Its the lungs that are damaged, not the blood. The reason why people die is because they drown in thier own fluids, as the cells walls of the lungs are broken down by the patient's immune system.
If Chloroquine was effective, it would stop the virus reproducing. This would lead to a detectable change in viral load.
Sure, it could already be to late by then, the damage is done. But, the viral load would have a measurable change. These studies don't really show anything conclusive.
This means that its unlikley to work as a prophylactic as its not actually stopping the virus from attaching or reproducing.
> Azithromycin
Thats there to stop any opportunistic bacteria from causing more damage. Typically when someone is admitted to ICU for covid they have a lower than expected white cell count.
> Antivirals are much more promising
yes because they actually disrupt the virus replicating. Chloroquine doesn't appear to do that. This is the problem with making drugs. Something that works in the petridish doesn't always work in the body. This is why Gilead's new wonder drug wasn't in production, because it was designed to target ebola, but didn't really work.
> If you want to detour into tinfoil hat territory, you could posit that these studies on severe patients were designed knowing it would show low or no efficacy, because it’s too late to protect the patient’s hemoglobin.
I would think it is still useful because from what I've read, this protocol is often used for severe cases at the moment, so it's useful to know if it has no impact.
Isn't that paper highly theoretical at this point since it's based on computer simulations? Are there any studies on actual humans confirming the virus's effect on hemoglobin?
If that hypothesis correct then we should be able to test it with blood transfusions, or possibly hyperbaric oxygen therapy (HBOT). HBOT can be used to treat patients with severe carbon monoxide poisoning. Even though their hemoglobin is unavailable, enough oxygen dissolves into the blood to prevent ischemia.
"COVID-19 attacks hemoglobin and that is how it damages the lungs."
COVID-19 is not the virus, it is a disease cause by SARS-CoV-2.
And no, SARS2 does not "attack hemoglobin". The lungs are filled with fluid from an overly zealous cytokine response and the bacterial infections that follow.
An in-vitro pre-print study ( https://www.biorxiv.org/content/10.1101/2020.03.29.014407v1 ) showed that administering Hydroxychloroquine only after Covid-19 infection is not helping much, while administering it both before the infection and after the infection gives great outcomes. They tried different administration modalities of HCQ to in-vitro infected cells: some cells got nothing (control), some got HCQ only before infection, some got HCQ only after infection, some got HCQ both before and after infection. THe cells that got HCQ only before or only after infection had just slightly better outcome than control (they appear as heavily infected), while cells that received HCQ both before and after contagion were in much healthier conditions. If that would be the same in vivo as in vitro, that would entail that it would be possible to use HCQ as prophylaxis, given that the patients never stop taking the drug. Of course the caveat is "IF that would be the same in vivo as in vitro", that they didn't (yet) tested.
The lack of productive discussion around a potential treatment tells us more about our bad decision-making under anxiety conditions than it does about the efficacy or not of the medical proposal. Although I posted a preprint of the French micro-study to HN a few weeks ago when this first became a topic of discussion, I now regret doing so due to the subsequent public confusion and imho very irresponsible promotion of it as a harm-free prophylactic by Trump.
Imagine a treatment that would being people back to life. Surely if you saw that 11 times you would believe it worked. In fact, after n = 1, you would be so amazed you'd be thinking there is a trick. The point is that, while N is important, the N needed to uncover a signal differs wildly with the outcome you're trying to affect, specifically the outcome's variance. If one of these drug cocktails 'works' (which has many different definitions in clinical research), the signal may be obvious enough that n = 11 is enough to hone in on a promising treatment for further study. It's complicated.
Generally speaking, a criticism of a study that focuses only on something like this is uninteresting -- while it _may_ be a valid criticism, it is not always (many valid studies have very small samples!), and so stating it unsupported is actually more like evidence that you don't know how to critically evaluate a study. As Zeynep Tufekci said: 'Anybody immediately responds to a correlation with “but correlation does not imply causation” probably doesn’t know what they’re talking about. Don’t have much to say, throw around smart sounding cocktail phrase.'
TL;DR: China says "hey, this stuff might work". French doctor conducts two very sketchy rapid-fire studies, then starts promoting himself on TV, including on Dr. Oz. No red flags there, right?
Pretty much every virologists I listened to said "this stuff might work", because it's entirely plausible that it might work.
> That's a long read, but it's pretty damning.
It actually isn't. All it says is that the evidence is poor and done by people with questionable reputation. It doesn't say "it doesn't work". What if it does work, but only in the early stages, when symptoms aren't severe (yet)? You wouldn't know.
Chloroquine and hydroxychloroquine are somewhat dangerous drugs and are therefore far more likely to only be given as a "last resort" rather than as a "precautionary measure", given their unproven status.
What are the odds that a reputable person is going to put their reputation on the line, doing such a dangerous trial on patients that aren't at high risk? Early on, a disreputable person is way more likely to do it. There won't be any good evidence for a while, in the meantime it's all a gamble.
This study is important, but limited in its scope. It shouldn't poison the well.
Unfortunately, I'm one of those people. My last refill ran out last week, and my pharmacist doesn't think I can get a refill anytime soon :-(
Fortunately my condition is not life threatening or severe, but it's something I've been living with for many years, and the HCQ was just finally getting it under control, so it's a bummer that there is so much hoarding going on before we even know if it really works for Covid-19.
Also, it is not a risk free medication. While it's generally safe, my doctor makes me get frequent lab work & a vision test because the side effects can be pretty bad for a small minority of people.
Thank you, i'm sure they are incompetent idiots that could not prevent their patients to die, after all they have graduated from a third world country and are probably not capable doctors. /s
[IANAD] hydroxychloroquine is an immunosuppressant and shouldn't be combined even with vaccines ( https://www.medicinenet.com/hydroxychloroquine/article.htm#w... ), so using it when immune system is really fighting an infection may happen to be very antiproductive unless it is a case of COVID triggered cytokine storm (hyperinflammation) when such immunosuppressant is probably what you'd really want. May be it is a reason why in come cases of COVID it works and in some doesn't.
"However, in hyperinflammation, immunosuppression is likely to be beneficial. Re-analysis of data from a phase 3 randomised controlled trial of IL-1 blockade (anakinra) in sepsis, showed significant survival benefit in patients with hyperinflammation, without increased adverse events.8
A multicentre, randomised controlled trial of tocilizumab (IL-6 receptor blockade, licensed for cytokine release syndrome), has been approved in patients with COVID-19 pneumonia and elevated IL-6 in China "
Notable fact is that majority of the deaths of the second wave (the deadliest, which in addition to children/weak/elderly was also strongly hitting healthy 25-35 years old) of Spanish flu was due to cytokine storm.
Yes, obviously in case of hyperinflammation doctor are giving immunosuppressing drugs, HCQ or other depending on the stocks (and of course the patient history and other drugs given prior). They are very capable people in most cases, urgentists are often very knowledgable, and reanimation doctors are probably the best at interfering/preventing coktail effect. They are not available in all cases, but they try to be there for the most important ones.
No one, no scientist is saying with certainty that HCQ does not work at all. However, the maxim is primum non nocere. Are HCQ effects important enough to use it in every case when you can do otherwise? Well, according to the last Raoult study on 80 mild cases, no. 3 hospitalisation, 1 death for 80 cases is around the same result as German/S.K. mild cases who are given no treatment at all (a bit superior, even, but n=80 is clearly not enough).
Maybe HCQ reduce contagiosity. In this case, is HCQ more efficient than interferon? I know that i would prefer interferon as my liver and kidneys can take more hit than my heart atm (i already have a medication that cause tachycardia when i overdose it a little + some minor heart issues).
Is HCQ more efficient than rinovir? this particular article seems to say that it's not but why should i trust this article more than Raoult and some French articles? Should i take everything (interferon, rinovir, HCQ, CQ) and hope for the best? Or, since i can afford to as i live in a rich country, should i wait the different study results?
[+] [-] Cantbekhan|6 years ago|reply
1) Chloroquine (and HCQ) is a zinc ionophore: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4182877/
2) Zinc seems to inhibit RNA polymerase of Coronaviruses in vitro https://www.researchgate.net/publication/47794995_Zn_Inhibit...
Their conclusion was that chloroquine could indeed allow zinc to enter the cell and then inhibit replication (and therefore that the treatment needed to be administered early).
Nobody seems to be talking about a very easy way to verify chloroquine (and HCQ) efficiency by just using the same method used in China:
Cross-check the list of patients infected with Lupus (lupus erythematosus) and with chronic HCQ treatment (they take it for years) with the list of known infected COVID19 patients.
In China (and specifically in Wuhan), this is how they (team of Dr Zhang Zhan) found out about the efficiency of HCQ. They noticed that there were no patients with chronic HCQ treatment for lupus (lupus erythematosus) infected with covid19. This was in peoples Hospital of Wuhan University (source: https://www.jqknews.com/news/388543-The_novel_coronavirus_pn...)
This alone would be enough to prove some efficiency even as prophyalxis (as they are advocating officially in India). This should be quite trivial to check with the current amount of confirmed infection.
These details were all explained in this medcram vid: https://www.youtube.com/watch?v=Eeh054-Hx1U
[+] [-] unknown|6 years ago|reply
[deleted]
[+] [-] nradov|6 years ago|reply
[+] [-] ruggi|6 years ago|reply
[+] [-] majormajor|6 years ago|reply
Where does the "if it inhibits replication it needs to be administered early" line come from? I've seen it elsewhere too, but why wouldn't inhibit replication lead to => continually declining amounts in the body => easier recovery at any stage?
[+] [-] OniBait|6 years ago|reply
I don't even understand what the point of this study was except as a rebuttal to the prior study. I mean, if people thought the prior study was cherry picking results. I don't even know what I'd call this...
There's _some_ anecdotal evidence that it _may_ work if treated early. Hopefully there are some real studies that are being done on that.
[+] [-] raphlinus|6 years ago|reply
Note this is by Derek Lowe of "Things I won't work with" fame, an extremely informative series about entertainingly dangerous chemicals.
And here's a new piece of candy for people who want to get their hopes up about a promising treatment: https://stm.sciencemag.org/content/early/2020/04/03/scitrans...
(h/t Helen Branswell of STAT news, who is very much worth following, who retweeted Timothy Sheahan)
[+] [-] dang|6 years ago|reply
[+] [-] robocat|6 years ago|reply
That is frightening. Increasing the mutation rate must carry a large unknown risk. Also surely the first thing to mutate will be self-defeating resistance to that drug...
[+] [-] unknown|6 years ago|reply
[deleted]
[+] [-] perl4ever|6 years ago|reply
[+] [-] Gibbon1|6 years ago|reply
[+] [-] jfnixon|6 years ago|reply
https://erj.ersjournals.com/content/36/3/646
[+] [-] sunsu|6 years ago|reply
[+] [-] unknown|6 years ago|reply
[deleted]
[+] [-] uncoder0|6 years ago|reply
[+] [-] archgoon|6 years ago|reply
[+] [-] malpighien|6 years ago|reply
[+] [-] arrrg|6 years ago|reply
[+] [-] podgaj|6 years ago|reply
It is one thing to inhibit the virus, but zinc is needed to reduce the over active immune response,
[+] [-] webmobdev|6 years ago|reply
> “We used a combo of Lopinavir and Ritonavir drugs which are usually given as a second line of treatment for HIV with drugs meant for curing malaria and swine flu. We administered this line of treatment to a 70-year-old Italian woman, who had come as a tourist to Rajasthan, who tested positive and was being treated by us, as well as another Italian, who is 69-year-old,” said Dr Sudhir Bhandari.
> ... “The team of doctors under the leadership of Dr Sudhir Bhandari, Principal of SMS Medical College held consultations with the ICMR and tried a combination medicines given for malaria, swine flu (Tamiflu) along with drugs for HIV and it worked well. All three persons including the Italians were cured this way,” said Rohit Kumar Singh, additional chief secretary, health of Rajasthan government.
Source: https://www.nationalheraldindia.com/india/three-coronavirus-...
> ... The three persons who tested positive were administered a combination of 200mg Lopinavir and 50 mg of Ritonavir twice a day besides Oseltamivir and Chloroquine that are given to the swine flu and malaria patients.
> However, the doctors at the SMS Hospital warned that this was only an emergency treatment and the HIV medicines were used only as an emergency measure that could help in regaining normalcy.
Source: https://www.nationalheraldindia.com/india/covid-19-magic-med...
[+] [-] webmobdev|6 years ago|reply
> ... Blood for the plasma therapy will be collected from recovered patients at SCTIMST and the medical colleges and donated to critical patients with sanction from Blood Transfusion Council. Plasma would be separated from blood and taken to other hospitals under refrigeration.
> ... When a person suffers from COVID-19, antibodies are created in his or her body as defence. Such B lymphocytes would be present in plasma. After a patient recovers from the disease, these antibodies remain in blood to prevent another attack by the virus. The plasma collected from such people and given to another patient would have antibodies which target the virus and prevent the recipient from slipping into a more serious condition. According to researches, plasma taken from one donor would have sufficient doses for two patients.
Source: https://english.manoramaonline.com/news/kerala/2020/04/09/ke...
[+] [-] rpiguy|6 years ago|reply
https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surf...
Chloroquine prevents the virus from affecting hemoglobin, or reduces the effect. This is also how Chloroquine treats malaria.
The problem with a study on severe cases is that the damage is already done and the hemoglobin is already compromised.
It is best to start treatment with chloroquine prior to reaching the severe stage. By the time you are severe you’ve gotten permanent lung damage and the immune system is in a race condition unable to keep up with the virus.
If you want to detour into tinfoil hat territory, you could posit that these studies on severe patients were designed knowing it would show low or no efficacy, because it’s too late to protect the patient’s hemoglobin.
Azithromycin slows ribosonal RNA replication in bacteria. It is unclear how it helps with a Covid.
Antivirals are much more promising for severe cases, but even they can’t heal ground glass in the lungs.
[+] [-] praeter|6 years ago|reply
https://vimeo.com/402537849
https://twitter.com/EricLeeMD/status/1245054768185303041?s=1...
https://twitter.com/cameronks/status/1243582723945566208?s=1...
https://www.cureus.com/articles/29004-acetazolamide-nifedipi...
[+] [-] KaiserPro|6 years ago|reply
This virus attacks the cells that live in the throat and lungs. The "spike" as far as I'm aware does not attach to haemoglobin.
> damage is already done and the hemoglobin is already compromised.
Its the lungs that are damaged, not the blood. The reason why people die is because they drown in thier own fluids, as the cells walls of the lungs are broken down by the patient's immune system.
If Chloroquine was effective, it would stop the virus reproducing. This would lead to a detectable change in viral load.
Sure, it could already be to late by then, the damage is done. But, the viral load would have a measurable change. These studies don't really show anything conclusive.
This means that its unlikley to work as a prophylactic as its not actually stopping the virus from attaching or reproducing.
> Azithromycin
Thats there to stop any opportunistic bacteria from causing more damage. Typically when someone is admitted to ICU for covid they have a lower than expected white cell count.
> Antivirals are much more promising
yes because they actually disrupt the virus replicating. Chloroquine doesn't appear to do that. This is the problem with making drugs. Something that works in the petridish doesn't always work in the body. This is why Gilead's new wonder drug wasn't in production, because it was designed to target ebola, but didn't really work.
[+] [-] tonfa|6 years ago|reply
I would think it is still useful because from what I've read, this protocol is often used for severe cases at the moment, so it's useful to know if it has no impact.
[+] [-] nodamage|6 years ago|reply
[+] [-] nradov|6 years ago|reply
[+] [-] podgaj|6 years ago|reply
COVID-19 is not the virus, it is a disease cause by SARS-CoV-2.
And no, SARS2 does not "attack hemoglobin". The lungs are filled with fluid from an overly zealous cytokine response and the bacterial infections that follow.
[+] [-] gmaster1440|6 years ago|reply
[+] [-] deadmetheny|6 years ago|reply
[+] [-] ruggi|6 years ago|reply
[+] [-] sdiq|6 years ago|reply
Not a study but just another anecdote. Using zinc this time round rather than azithromycin.
[+] [-] snapetom|6 years ago|reply
[+] [-] klipt|6 years ago|reply
Politicians should shut up about unproven medicines and leave it to the professionals to actually practice, you know, evidence based medicine.
[+] [-] anigbrowl|6 years ago|reply
[+] [-] libpcap|6 years ago|reply
[deleted]
[+] [-] sna1l|6 years ago|reply
[+] [-] dang|6 years ago|reply
https://news.ycombinator.com/newsguidelines.html
[+] [-] kilbuz|6 years ago|reply
[+] [-] michael_storm|6 years ago|reply
[+] [-] crygin|6 years ago|reply
[+] [-] SrslyJosh|6 years ago|reply
https://respectfulinsolence.com/2020/04/03/zelenko-smith-aba...
That's a long read, but it's pretty damning.
TL;DR: China says "hey, this stuff might work". French doctor conducts two very sketchy rapid-fire studies, then starts promoting himself on TV, including on Dr. Oz. No red flags there, right?
[+] [-] gridlockd|6 years ago|reply
> That's a long read, but it's pretty damning.
It actually isn't. All it says is that the evidence is poor and done by people with questionable reputation. It doesn't say "it doesn't work". What if it does work, but only in the early stages, when symptoms aren't severe (yet)? You wouldn't know.
Chloroquine and hydroxychloroquine are somewhat dangerous drugs and are therefore far more likely to only be given as a "last resort" rather than as a "precautionary measure", given their unproven status.
What are the odds that a reputable person is going to put their reputation on the line, doing such a dangerous trial on patients that aren't at high risk? Early on, a disreputable person is way more likely to do it. There won't be any good evidence for a while, in the meantime it's all a gamble.
This study is important, but limited in its scope. It shouldn't poison the well.
[+] [-] rodgerd|6 years ago|reply
Great.
[+] [-] transreal|6 years ago|reply
Fortunately my condition is not life threatening or severe, but it's something I've been living with for many years, and the HCQ was just finally getting it under control, so it's a bummer that there is so much hoarding going on before we even know if it really works for Covid-19.
Also, it is not a risk free medication. While it's generally safe, my doctor makes me get frequent lab work & a vision test because the side effects can be pretty bad for a small minority of people.
[+] [-] tgafpc2|6 years ago|reply
[+] [-] orwin|6 years ago|reply
[+] [-] trhway|6 years ago|reply
https://www.thelancet.com/journals/lancet/article/PIIS0140-6...
"However, in hyperinflammation, immunosuppression is likely to be beneficial. Re-analysis of data from a phase 3 randomised controlled trial of IL-1 blockade (anakinra) in sepsis, showed significant survival benefit in patients with hyperinflammation, without increased adverse events.8 A multicentre, randomised controlled trial of tocilizumab (IL-6 receptor blockade, licensed for cytokine release syndrome), has been approved in patients with COVID-19 pneumonia and elevated IL-6 in China "
Notable fact is that majority of the deaths of the second wave (the deadliest, which in addition to children/weak/elderly was also strongly hitting healthy 25-35 years old) of Spanish flu was due to cytokine storm.
[+] [-] orwin|6 years ago|reply
No one, no scientist is saying with certainty that HCQ does not work at all. However, the maxim is primum non nocere. Are HCQ effects important enough to use it in every case when you can do otherwise? Well, according to the last Raoult study on 80 mild cases, no. 3 hospitalisation, 1 death for 80 cases is around the same result as German/S.K. mild cases who are given no treatment at all (a bit superior, even, but n=80 is clearly not enough).
Maybe HCQ reduce contagiosity. In this case, is HCQ more efficient than interferon? I know that i would prefer interferon as my liver and kidneys can take more hit than my heart atm (i already have a medication that cause tachycardia when i overdose it a little + some minor heart issues). Is HCQ more efficient than rinovir? this particular article seems to say that it's not but why should i trust this article more than Raoult and some French articles? Should i take everything (interferon, rinovir, HCQ, CQ) and hope for the best? Or, since i can afford to as i live in a rich country, should i wait the different study results?