What has Science Established ?
I want to try to punch above my weight (and be a troll) and contest this
Dr. Kathryn Hibbert, director of the medical intensive care unit at Massachusetts General Hospital … said it will take weeks or months to get results and doctors and patients will need to wait for the results of the clinical trials before knowing which Covid-19 patients — if any — should be getting remdesivir.
“I think we should be extremely cautious about responding too enthusiastically to early data that has not been thoroughly vetted,” Hibbert said. “In the scientific community, over decades, we’ve established that critical review of clinical trials is the best way to determine if the data is strong enough to inform clinical decisions.”
I think the verb “establishd” is doing a lot of work here. Scientists have established two sorts of things.
One is the set of empirical results, styized facts and well supported theories. It is reasonable to accept that science has established that information can not be transmitted faster than the speed of light and that DNA (and topically for some viruses RNA are genentic materials.
The other is that scientists have established rules for what can be published peer reviewed journals (and rules for peer review) and Congress has established a Pure Food and Drug Act which authorizes the FDA to establish rules for which pharmaceuticals can be sold. There is a difference between natural laws and, you know, ordinary laws. Both are binding and both have been established, but one set is discovered and the other set is made.
Let me take the following claim literlly “critical review of clinical trials is the best way to determine if the data is strong enough to inform clinical decisions.” Notice there is no qualifier on “the data”. Thus the statement implies that, when treating an individual patient, one must ignore data not from a clinical trial. This includes all diagnostic tests of the patient. Taken literally, Hibbert asserts that Doctors should consider only clinical trials and ignore all other data. This is nonsense and clearly she didn’t mean that.
I am quite sure that what she meant was [when considering a new drug] “critical review of clinical trials is the best way …”. I am also sure that she means this because she has the law on her side.
I think this rule was established by Congress (as interpreted by the FDA). It is absolutely not the rule in general. It is not the rule governing off label prescription. It is not the rule governing the design of automobile engines or the writing of computer code. It is the law regulating new drugs.
Now what does “strong enough to inform” mean ? The claim, if it means anything, is that evidence weaker than some threshold should be ignored entirely. This is absolutely inconsistent with any sort of rational forecasting or rational choice.
And here “established” means that those with the power to decide have so decided. It isn’t proven in the way it is proven that penicillin kills (some) bacteria. Now it might be that there is a case which can be made and CNN didn’t have time for it. Indeed, I think it proven that phase III trials are needed, because roughly two thirds of them fail, that is give disappointing results. This means that hopes based on evidence (usually including small controlled phase II trials) were proven to be false.
However, one chance in three that it works is not always negligible. In particular it sure shouldn’t be neglected when deciding what to do with Remdesivir and Covid 19. When dealing with a pandemic, there is no safe option. Notably, only lunatics demand proof that lockdowns work before ordering them. There are no large sample clinical trials of lockdown vs placebo. In this case, better safe than sorry is correctly interpreted as do what is safer not collect data and do nothing else until you know everything. Deciding to do nothing but collect data is deciding without knowing what to do. This is obvious to everyone but Trump and maniac followers (accepted by 81% of US addults asked in a poll). Yet when the question is whether to use Remdesivir, the answer is that science has established that Remdesivir shouldn’t be used for “weeks or months. ” This makes no sense.
It isn’t even an accurate description of current law and policy. In fact, there is an expanded access program so many patients do not have to wait weeks or months.
Now on the Chicago data. Yes there was no control group. but there are baseline data. It is known that roughly two thirds of ventilated Covid 19 patients die. The data from Chicago are clearly overwhelmingly statistically significant. They would be accepted as solid evidence by economists. It is only because gneuinely controlled trials are possible in medicine that they are considered to be the only evidence strong enough to guide decisions. Also, and always, because they are required by the FDA.
But mainly, Dr Hibbert accepts no difference between proposed treatments of a non fatal disorder, proposed new treatments when existing treatments usually work, proposed treatments when the alterntive is certain death (not the case at all with Covid 19) and proposed treaatments of an contagious disease such that time is of the essence.
The “established” rules include no consideration of costs and benefits and, most importantly, allow no consideration of the cost of delay.
I think the argument about proper medical practice made by the director of the medical intensive care unit at Massachusetts General Hospital is clearly wrong.
I think the problem is, as usual, a false dichotomy: are phase III (that is large) controlled trials pointless or necessary before anything can be done ? If one accepts that weaker data should inform clinical decisions, one does not have to conclude that phase III trials are worthless. It is possible to decide how to treat patients using the weaker data while conducting a phase III trial. This is happening, so it must be possible. It is possible to believe that phase III trials should be conducted without also believing that people with a week to live just have to wait weeks or months because it has been so “established”.
I see no comments yet. I am going to continue to rant down here in comments, because I think the post is already too long.
” “We have seen patients who’ve received remdesivir who’ve had remarkable recoveries and we’ve seen patients who’ve not received remdesivir and had remarkable recoveries,” said Hibbert, also an instructor at Harvard Medical School. “Overall, patients are doing well and have made recoveries, even the sickest of the sick.” ”
The claim that overall patients are doing well and have made recoveries even the sickest of the sick is not at all consistent with the data in the published literature. In the peer reviewed literature one reads things like 66% of ventilated patients go on to die. I think the statement is plainly false, just not true, known to be false, and therefore a lie. In any case, it sure isn’t solid data and yet Hibbert is telling CNN this and knows clinicians will hear her claim and might be infludenced by it. There are two completely different standards of evidence, one for dismissing things other than clinical trials and one for asserting something other than “patients have to wait”. In any case, I think I can assert that that the quoted claim above is false I am confident that it is a false claim about the experience at the MGH. The aim of the iie is to influence the practice of medicine.
Doctors ‘need to question their assumptions’
Since most patients recover from Covid-19, she said, physicians need to be careful before they ascribe a patient’s improvement to any particular treatment.
“As human beings, we are so conditioned to tie an intervention with outcomes and establish a causal relationship between those two things,” she said. “I change a patient’s meds and the next day they look better, and it could be because I changed their meds, or it could be they were destined to get better anyways for other reasons.”
Hibbert is setting up a straw man. She was asked about leaked data from U Chicago. This is not about an impression. This is a death rate of 2 out of 113 among patients with severe Covid 19. It also includes that most patients have been released from the hospital. Hibbert is just not responding to the data she was asked to discuss. She is instead responding to a straw man. I ask can she come up with an explanation of the data other than benefits from Remdesivir. Not have they “established” that a control group is needed, but rather is there a possible problem due to using outcomes other places as a pseudo control group which is so extreme that it can explain the pattern.
Her assumption is that the burden of proof is on the claim that a treatment works. This is true of current US law. It is not a valid statement about the scientific method. The claim that some data does not amount to proof of P because there are other possible explanations is normally be accompanied by such an alternative explanation. In science one is supposed to present hypotheses consistent with available data. This does not mean that if people can think of only one, then they know it is the truth (absolute proof does not exist). In law things are different. In criminal law some evidence is inadmisable. The defence does not need to explain it. It doesn’t count. In the FDA approval process, evidence other than results of phase III clinical trials is inadmissable, That doesn’t mean that a scientist may ignore or dismiss it. It is a question of what the law is and should be. An applied policy question not a scientific question.
What we know about the state of coronavirus treatments, vaccines and antibody tests
What we know about the state of coronavirus treatments, vaccines and antibody tests
She added that doctors need to question their assumptions.
”Our gut feeling is so influenced by what’s in front of us and the last patient we treated that it’s pretty dangerous to make decisions based on that gut feeling,” she said. “The whole reason to run trials is our guts are notoriously misleading. That’s the entire rationale for a science and evidence-based approach.”
Here she was asked to respond to data not to a gut feeling. Her argument is an example of the most common error of thought which is more common than any valid method of thought — the false dichotomy. She asserts that there are two factors which might influence are beliefs — the results of randomized controlled trials and gut feelings.She asserts that the Chicago data are gut feelings. This is simply false.
Now what are the possible consequences of Hibbert’s rhetoric, invalid arguments and her lie ? She said patients have to wait. If a patient on a ventilator follows her advice (given her emminence) and waits for the results of the phase III trial and does not ask for access to the expanded access program, that patient will probably die (I quote the 0.66 from the NEJM). If the patient does get Remdesivir, based on current evidence, it is reasonable to assert that the patient will probably live (not 111/113 or even pool Chicago and the NEJM compassionate use record but best estimate given available data greater than 0.5). I think her reckelss assertions would cause deaths if the wrong people took them seriously.
This will also happen if doctors defer to their estemed colleague at the MGH and decide that their patients have to wait so they don’t apply for expanded use.
I need to calm down. It might be better for me to not post this comment.
update: I came back to delete the comment, but I see I am too late.
Too late. Give me a chance to read both. I have already C&Ped this portion so as to add it back later if you delete it.
Too late indeed. I am back. I was trying to figure out how to edit comments and then delete the comment part which you copied.
I feel bad about saying extremely harsh things about someone who is actually fighting Covid 19 while I lie in my bed and type. but, well, there you have it and I can’t make you delete it.
I will just add an apology for trolling as my second comment.
Penicillin doesn’t kill bacteria. It blocks bacterial growth by inhibiting cell wall biosynthesis. Allows your immune system to kill the bacteria.
Many of us are bouncing around offering opinions. Would you offer one also? I believe you may know more than most of us together. I apologize for putting you on the spot.
“Thus the statement implies that, when treating an individual patient, one must ignore data not from a clinical trial. This includes all diagnostic tests of the patient.”
Where do you get that? A major reasons for demanding clinical data is to be able to interpret what the diagnostic tests mean. There’s a reason doctors consider a 103F fever alarming but show only minor concern for one of 99F and might consider a temperature of 98.6F “normal”. Those characterizations are precisely based on clinical data.
Diagnostic tests and observations then get fed back in as clinical data. Doctors are supposed to be observant and report their results. That’s why it was an ophthalmologist who raised an alarm about a respiratory disease in Wuhan.
“The claim, if it means anything, is that evidence weaker than some threshold should be ignored entirely.”
Where do you get that? No one says to ignore it entirely, just to keep it in perspective. Practicing medicine is about playing the odds, except you don’t what cards are in the deck and which are the high valued ones. You’ll play better if you pay attention to the studies based on lots of games rather than just the cards you play. Just because you’ve been seeing a lot of fives and won with a hand containing sevens, that doesn’t mean that’s all there is to the game.
If you read anything about clinical practice, you’d know that doctorsr in ERs in NYC are prescribing chloroquine and azithromycin off label, for example. Those doctors on the front lines haven’t been seeing much of an effect or we’d have seen a preprint on Medrxiv and a formal publication. If you’ve been following academic medicine for the past few months, you’d realize that the barrier to publication is having a few hours to write things up and upload them to Medrxiv.
Medicine isn’t economics where they start out with tax cuts for the rich and work backwards from there and let the bulk of the citizenry get by on less and less.
Perhaps not chloroquine and maybe hydroxychloroquine plus a Zipak (Azithromycin). What does much of am impact mean? One of 10 times it works or maybe 4 of 10 times? Anecdotally, hydroxychloroquine plus zinc (lozenge?) was given to a patient (neighbors father) who had COVID 19 and it worked for him. I can not tell you what stage of the virus infection he was in. What is the alternative. You are crabbing at Robert and are not offering any solution other than wait for the clinical trials. Since you brought it up, what impact has been experienced from administering Hydrochloroquine in NY? U of Michigan and U of Colorado are using it with limited success. My background is manufacturing pharma and healthcare supplies under GMP, USDA, and FDA regs.
I am skeptical because most antivirals do not work all that well. AZT by itself improves survival in AIDS a bit but not a lot. Acyclovir speeds up healing of Herpex simplex, but it does not cure. Perhaps most relevantly, oseltamivir shortens the duration of the flu by one day which is good but no homerun. Obviously, one must approach each situation, each drug, and each patient with an open mind, and I certainly hope that an effective treatment is in our grasp. However, there are many times when doctors published very optimistic preliminary results pan did not pan out.
Thanks for information.
Mark you are reasoning by anology. The data (withiut a control group) from Chicago is clearly much more relevant.
Sars Cov2 is not at all like HIV or Herpes. Both go dormant HIV with a DNA copy spliced into a chromosome and Herpes with it’s circular double stranded genome acting as a miny chromosome. When dormant they are invulnerable. Coronaviruses don’t do that. They replicate constantly (except not if there is remdesivir around) and are exposed to the immune system. Most covid 19 patients recove, that is, are cured by time.
Also Azt had a huge effect. By itself it saved thousands of lives (I am thinking of preventing transmission to fetuses who are born free of HIV
Influenza is more like Sars Cov2 but the result shows that the normal course is hard to beat. Severe Covid 19has an estimated mortality rate of 66%. 34% survival is easier to beat that 99.9 % survival.
Especially if the over 98% survival (so far) in Chicago holds up and is replicated.
I think people did not click the link. We really should all read the Statnews article which we are discussing https://www.statnews.com/2020/04/16/early-peek-at-data-on-gilead-coronavirus-drug-suggests-patients-are-responding-to-treatment/ The evidence is striking.
penicillin does kill bacteria. This is non technical but it contains citations https://www.bioprocessonline.com/doc/penicillin-kills-bacteria-via-death-peptide-0001
Where my claims “come from” are the quoted passage in the post. I chose to take literally the statement ” “In the scientific community, over decades, we’ve established that critical review of clinical trials is the best way to determine if the data is strong enough to inform clinical decisions.””
Note there is no qualiier on “the data”. no indication that the statement about “the data” does not apply to some data (such as a patients’ temperature). As writen the quoted statement is absurd. I do not think that you can contest my interpretation while sticking to the dictionary definitions of words and the rules of English grammar. You can assert that she clearly didn’t mean what she said literally. But she said what she said, I quoted it, and I noted its logical implications.
Not solid enough to inform clinical treatment implies it should be ignored. It’s what she said. It is not at all what she does (if she followed the advice she gave she would no longer have a licence to practice Medicine let alone be chief of a service at the MGH).
The discussion was of Remdesivir. Discussion of hydroxychloroquine is off topic. I trust you know about the evidence she semi dismisses. I expect that you have another explanation of the leaked data than the hypothesis that remdesivir helps. I am very eager to read your confrontation with the (leaked) information.
I am not opposed to clinical trials. I just re-read my post. I have trouble believing that you read it. I wrote many times that I believe that phase III clinical trials are necessary. I don’t see how you could have failed to notice. Your discussion of cards and the advantages of cntrolled trials is really off topic. It doesn’t address the evidence I discussed (from Chicago) and it doesn’t address my recommendation which is, bascally, the current policy except with even more extended access also to people with moderate Covid 19 who are not on ventilators.
The barrier proposed by Dr Hibbert is not wait until there is something on Medrxiv. She is dismissing two articles published in the New England Journal of Medicine as not good enough to inform clinical practice. She is also dismissing the (leaked) data from Chicago. That is not on Medxiv because researches in a phase III trial must coordinate what they say to the public. But the facts are facts.
“In the scientific community, over decades, we’ve established that critical review of clinical trials is the best way to determine if the data is strong enough to inform clinical decisions.”
There is something strange there. The part to which I object is “to inform clinical decisions”. I can start with her words and write a sentence with which I agree
“critical review of clinical trials is the best way to determine ” which of two therapies is better. So when* it is possible, it should be used.
Until then (and then might be one week from now) doctors have to treat patients using a less reliable process, which is nonetheless better than guessing or sitting around doing nothing waiting for the results of the trial.
I chose to take “inform clinical practice” literally, and to interpret “the data” as referring to the data, not some subset of the data. This was uncharitable and almost uncivil. The statement taken literally is absurd.
I want to understand why she said it. I have a guess. I think it is clear that “inform clinical practice” means “approve a new pharmaceutical” or “declare that use of a pharmaceutical is standard of care”.
In context “clinical practice” doesn’t mean “what practicing clinicians do” . It means two things. One is what pharmaceutical companies are allowed to do and the other is what doctors have to do to avoid malpractice liability.
In the post, I discuss how the FDA’s interpretation of the Pure Food and Drug Act is treated like a natural law, or maybe part of the scientific method. It’s just a law. Also it was recently changed by the Twenty First Century Cures Act and then again by the Right to Try Act
But I think that standard of care is also roughly as important. It is vitally important to doctors in the USA that there be official written standards of care. They are their only protection against malpractice suits. Sticking to them is rational. However, I also think that it is not maximizing patients’ expected welfare. The standards are changed on a schedule. They are written basically updating using the results of clinical trials. The change is basically mandatory (enforced by malpractice lawyers and civil juries). The point is that there is no requirement that the old standard be proven better than the new proposed standard. the burden of proof is on the new approach. This is not science — questions are not left open — specific instructions are written down.
I think the logic is the logic of defensive medicine not of caution or scientific rigor or anything else.
so I think I can make sense of the quote. One is that the FDA will not approve Remdesivir based on leaked data from a trial without a control group. Second that it is not wise to question the FDA, for they are powerful and rigid. Third it isn’t time to say that doctors should do something, because if one says that, then they will be sued for not doing it.
But it sure doesn’t mean that clinicians should (or ethically can) ignore the leaked data when deciding whether to try to get expanded access for their patients.
* I stress that by “when” I mean when. I don’t mean if. I think it might be possible soon after April 27 2020 when the first trials are scheduled to be completed. But there are patients who are now alive, who might be saved by Remdesivir, and who won’t be alive then, so decisions about care have to be made now — the decision might be stick to standard of care, but that is a decision and clearly a very risky one.
Read your link. Didn’t know that. However, what it actually says is that penicillin doesn’t kill bacteria, but some bacteria die as a result of penicillin treatment because they express a peptide that they make. If you knock out peptide expression, penicillin doesn’t kill the knockout cells. Ergo, penicillin itself doesn’t kill cells.
I need to re-read your post carefully before weighing in. Will try to do that today.
I would surmise you are a pretty busy person. I do not believe “I” have posted anything on hydroxychloroquine or Remdesivir in a while. The former appears to help in the beginning phases, the latter appears to work in all phases as informed taken from various articles. The former is being used at various hospitals with a limited degree of success from what I have learned anecdotally from others whom had it used on relatives and from conversing with family relations
Robert and PGL have taken this to a different level which is interesting to me as someone who has worked in healthcare pilot production projects for couple of major companies. It was an interesting dialogue had when people were waiting on product off of the pilot because it actually worked.
I was looking for your thoughts and opinion.
What puzzles me is the approach of waiting for clinical trial approval and a protocol to be established when there are few if any alternatives.
My overall impression is that you have become obsessed with the comments of one person. I’m not sure what a Talmudic exegesis of each line accomplishes that couldn’t have been accomplished in fewer words and without the personal attacks.
You posted this: “Her assumption is that the burden of proof is on the claim that a treatment works. This is true of current US law. It is not a valid statement about the scientific method. The claim that some data does not amount to proof of P because there are other possible explanations is normally be accompanied by such an alternative explanation. In science one is supposed to present hypotheses consistent with available data.”
First of all, science doesn’t deal in proof, it deals with the weight of facts and evidence. A scientific hypothesis is one that is testable and potentially falsifiable by experiment.
Second, in my field, the burden of proof rests with the person making the claim. Accordingly, the burden of proof for the claim that a drug has efficacy rests with those making the claim. The null hypothesis is that it doesn’t.
The price of allowing use of an ineffective drug isn’t necessarily zero. Using an ineffective drug may mean the patient doesn’t receive more effective therapy. Also, most drugs have some side effects; see, e.g. hydroxychloroquine and heart arrhythmia. Finally, an off-label use of a drug in finite supply can affect the availability of that drug for patients for whom the drug has clear benefit; see, e.g., hydroxychloroquine and lupus.
Are there other points you’d like me to address?
It occurs to me that doctors often prescribe small daily doses of aspirin for elderly patients who seem candidates for heart attacks and strokes. The thought is not that aspirin will certainly prevent such problems in all patients, but that statistically patients taking aspirin are likelier to survive such attacks — a couple of percent more likely.
I’m wondering if this might not be analogous to the use of Remdesivir with Covid 19 patients — that it isn’t a guaranteed cure for everyone but definitely helps some, and the possible benefits outweigh the possible bad side effects. Of course, we haven’t had rigorous studies showing the impact of Remdesivir over 5-year periods on hundreds of thousands of would be patients, and won’t I guess for another five or six or ten years. And I suspect a dose of Remdesivir costs more than the 2 cents a day aspirin …
Unlike hydroxychloroquine and COVID-19, there actually is a sound mechanistic basis for believing that daily aspirin can moderate risk for heart attack and stroke.
As a scientist I have a single question. Can anybody do better than Pr Raoult?
Pr Raoult is working in Marseille. Hydroxychloroquine + azythromycine has been used there very successfully. As of today, the results are:
2970 cases treated.
In the remaining part of France:
That is an improvement of 3200 % !
The use of hydroxychloroquine against viral infection is not new:
What is firmly established is that no one can do better over a 2970 large sample. We do not really have time for more studies, anything that can reduce the death toll by 3200 % is welcome, period.
Furthermore, what is firmly established in field epidemiology is how to stop an epidemic:
– Detect and quarantine the infected and their neighbors.
– Treat the infected.
– Disinfect cities and buildings.
How do you think Ebola epidemics were stopped? With ventilators, ER services, drugs, vaccines? No, they were stopped with a basic but efficient methodology. So stop arguing about the size of the sample and start to implement simple proven methods.
We are bombarded by papers predicting that or that if we lock down the whole World. All the published papers are using compartmental models (SIR, SIER, etc…) that assume healthy, infectious, infected are all well mixed, no airbone contagion or contagion by a soiled surface.
When you put the population into quarantine, this hypothesis fails, therefore any conclusion you may get with your model is just speculation…
A multi agents model taking into account both relationship and spatial network as well as the simple fact that infection occurs by both touching soiled surfaces or breathing around an individual 9 meters away ( increased cross section of infection) is far overdue.
Such a model would look like that:
Welcome to Angry Bear, mostly an economics blog. First time comments and commenters always go to moderation to eliminate spam, spammers, and advertising. A bit of an introduction. Amongst us in this post/thread, you will find professors of economics, medical research professors, doctors, laymen like myself(pharma and healthcare supply manufacturing) etc. The US is a litigious country and establishing protocol prevents a doctor from being sued. The use of Hydroxychloroquine in the US is off label and its usage has not been established for COVID 19 as well as the Gilead drug which is in trials.
I am familiar with Pr Raoult findings having read a paper describing what he achieved. I also know it is being used in various university hospitals with some success. My opinion is anecdotal and should not be used as proof although I have pushed this extensively. I know the others have also read similar documents and have more statements to make about its success and dangers.
With that being said, I will hit the approve button and you are free to comment.
I saw this also. “It is very important to administer the hydroxychloquine at the onsets of the first symptoms, not when the case is too severe. If the virus has already facilitated the entrance of the bacteria, it is useless.”
“This Expert Will Cure Your Excitement for Hydroxychloroquine
“These drugs should never be used as first-line defense to prevent any disease.”
Nonetheless, many doctors have used the drug when it seems as if options for patients were running out. Anecdotally, some physicians in the United States and abroad have acknowledged some success in using HCQ in the fight against the coronavirus. Under pressure from the Trump administration, the Food and Drug Administration and Department of Health and Human Services have passed measures to ramp up its use in hospitals—and several clinical trials are simultaneously underway to determine HCQ’s efficacy.
To better understand HCQ, its origins, and its potential risks, I spoke to Dr. Remington Nevin, a Vermont-based doctor who runs the Quinism Foundation, which advocates greater awareness of the neurological risks tied to quinoline, the broader category of drugs that HCQ falls under. Before establishing the foundation, Dr. Nevin spent 14 years in the military as an epidemiologist, where he saw the effects of another quinoline, mefloquine, an anti-malarial that was regularly administered to soldiers, some of whom sued the military for debilitating side effects. Service members reported insomnia, anxiety, dizziness, vertigo, and paranoia—symptoms concerning enough that the military largely ended its use of the drug in 2009. In 2013, the FDA placed a “black box warning”—its strongest advisory—on use of the mefloquine…..
What are the implications of all this in terms of the treatment of COVID-19?
There’s adequate and ample theoretical evidence to suggest the potential efficacy of these drugs against COVID-19, but whether that actually translates to effective use in practice is still far from proven. It’s certainly worth exploring, particularly in the context of this current emergency, but as with all experimental drugs, that exploration should be done in a fully transparent and ethical manner with the risks well disclosed to all parties, including the participants. I’m not convinced that that is being done.
The argument for quinolines seems to be that they might have anti-viral qualities, which were explored during SARS and Zika outbreaks. Why does this drug have the potential to be effective against a virus?
There is reasonably strong evidence dating back well over a decade that drugs of this class, chloroquine in particular—and we would expect HCQ to have similar effects—have quite potent anti-viral activity against SARS-like viruses in the lab. There has been fairly strong anecdotal evidence of clinical effectiveness in the few months experience that we’ve had with this virus. Unlike other drugs posed as treatment for COVID-19, HCQ is extremely inexpensive, it is ubiquitous, it’s easy to produce at scale, it’s off-patent, and it’s thought to have a well-understood adverse effect profile. And it’s thought—erroneously in my opinion—to be well tolerated by all. All of those factors would seem to make it the ideal candidate to prioritize for widespread clinical investigation. So it’s not at all surprising that it’s touted as a wonder drug, a magic bullet. And it’s not that unreasonable—with the exception of the risk of adverse effects that I’ve described, and additionally with the risk of cardiac and ocular adverse effects.
The drug is not safe in the sense that this drug would never be—under ordinary circumstances—approved by the FDA for sale to the public as an over-the-counter drug. I do think that in our zeal to find a potential solution to the COVID pandemic, these risks are being understated. The drug is not completely benign, even though it is well tolerated by the vast majority of patients prescribed it for rheumatological disorders at relatively high doses. That doesn’t mean that everyone can take the drug and be free from serious, lasting, and adverse effects.”
“We would expect”? I would expect my consistent construction lines to run the same old part over and over again with no issues. Never happens that way. I would get my ass up out of my desk chair, walk through the plant to the line to see what was wrong and ask for their assistance in solving the issue – “Gemba.”
If you read what she has said, it is working successfully in southern France. I have no reason to disbelieve her. Why would see risk her reputation. It was used successfully on a neighbor’s 70 year old father as a first line of defense at the University of Michigan. You do want to prevent the virus from getting into the cells. It is being used at the University of Colorado (my NP daughter is there). It was (and still is) being used at Montefiore Hospital in NY. Of course, there are risks to this. Offer something else which is “readily” available which will work before the virus invades the cells, requiring ventilation, and the patient dies anyways? Every time I have to get Rituxan, I am faced with the potential of TLS syndrome, infections, kidney issues, and bowel/stomach issues . . . all of which can kill me. The first infusion was about 5 hours to see if I would have a reaction. It still may get me.
Trump should have kept his mouth shut because it is all about Trump now and no one is objectively looking at the source of this information by going there to see if what they are saying is really true. Go and see, look at their data, review the medical records, talk to some of the patients.
It seems to me that treating HCQ and Remdesivir is a comparison of chalk and cheese. HCQ is not recommended for severe infections and Remdesivir is. HCQ might stop an infection from becoming severe, Remdesivir might allow you to recover where nothing else will. Seems to me they have different purposes and that if we are going to relax controls then it is more likely that Remdesivir will help us, because the window of effectiveness for HCQ is more limited. Fewer people dying is a prerequisite for relaxing controls. (But having fewer cases and testing contacts more intensively is also a prerequisite.) Only a few countries have reduced the number of cases so much that they really can change the control regime – e.g. Austria, Australia, New Zealand, South Korea.
I guess know one else has read about the results published by the VA hospital?
Welcome to Angry Bear. It is not unusual for first time comments to go to moderation as the system weeds out first time comments, commenters, spam, and advertising. You are set.
I read the results. The important factors to the VA attempt at a trial was the clientele used were older vets like I am and hydroxychloroquine was the only drug administered. From what I have read Hydroxychloroquine is a gateway drug which allows entry to the cell of other drugs such as azidothymidine, azithromycin, zinc, etc. which will inhibit the virus. Hydroxychloroquine by itself will not work. In this thread, there are comments by Rick Horocholyn (provided links explaining how hydroxychloroquine works) and also Fabrice Allais (who discusses the success rate for hydroxychloroquine in southern France when the drug is administered with an inhibiter (which also allows the body to kill the COVID virus). It has to be administered early on in the infection also.
It is not the ultimate drug for COVID. Just another tool in the doc’s old black bag.
My neighbors father’s experience with hydroxychloroquine + zinc was exactly dealt with in such a manner. I hope that helps you understand?