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I likely wouldn't bother.

There's literally no known method through which this should work. That means they're literally grasping at theories... they are suggesting it's impact as an anti-inflammatory is avoiding a cytokine storm, they're thinking because it's mildly basic it's inhibiting endosome uptake of the viral particles in the cell (ps, if that's the theory, then there's probably other problems, because that's an important function)

What I'm getting at, is that without a clear pathway of function, something we actually understand, then it's VERY difficult to give the study the benefit of the doubt. They need to show clear, statistically significant effects for me to accept their handwaving "maybe it works like this, but we're not sure".

I was just assuming that at that level of flawless superhero like goldilocks perfection you'd need complete silence and all the concentration you can bring to bear..... but, I was wrong. You wake up, look in the mirror and pull a Fonzie. My bad! Woah!

Are you referencing the anti-inflammatory effects I mentioned?

Or are there other immune suppressing effects of this stuff? I'm just going off the in vitro study, so there's possibly other things I haven't read.

It is one of those classic combine a little bit of truth and knowledge with a whole lot of bunk, and try to sound smart to push an agenda.

And it's no different than a facebook post.

Meh... I'm not riled. People are going to believe what they want. In the end the science will show up.

I did have a couple favorite lines though.

I disregarded the whole thing as garbage but what are you going to do? And I think you may be right, gene cant have bought this crap.

Ventilators are damaging and can be counterproductive at some point. You never want to use one unless absolutely necessary. Its that truth combined with the other drivel he is trying to tie together.

The whole thing was bunk even if the drugs do end up working. And as long as one trivial thread in that steaming pile of nonsense randomly proves true the guy is a genius in his own mind. There is a lot of this garbage out there. You can't stop it and some will believe it. It's futile to try to change that.

It's not presented as a study or medical advice, it was a discussion of the way Covid-19 prevents oxygen uptake and why Hydroxychloroquine may counter that problem. Nothing more nothing less, however, just like the author, you just cannot get past the politics.

Don't forget to update your living wills to preclude the use of Hydroxychloroquine.

The role of oxidative stress during malaria infection is still unclear. Some authors suggest a protective role, whereas others claim a relation to the physiopathology of the disease [21]. However, recent studies suggest that the generation of reactive oxygen and nitrogen species (ROS and RNS) associated with oxidative stress, plays a crucial role in the development of systemic complications caused by malaria. Malaria infection induces the generation of hydroxyl radicals (OH•) in the liver, which most probably is the main reason for the induction of oxidative stress and apoptosis [22]. Additionally, Atamna et al. [23] observed that erythrocytes infected with P. falciparum produced OH• radicals and H2O2 about twice as much compared to normal erythrocytes.

A potential source of free radical production in this disease is the host’s hemoglobin molecule, since the parasite uses this molecule as a source of amino acids for its own nutrition during the erythrocytic stage of the disease, resulting in the liberation of large amounts of circulating heme. By having Fe2+-associated groups, these heme groups are able to induce intravascular oxidative stress, causing changes in erythrocytes and endothelial cells and facilitating the internalization of the parasite in tissues such as the liver and brain [14].

A free radical species, which appears to be involved in this disease is nitric oxide (NO) [7–12,24,25]. However, its role is still controversial. Some researchers claim that cerebral malaria is probably an unfortunate consequence of high amounts of NO production to promote the death of the parasites [26,27] while others support the idea that cerebral malaria results from a low bioavailability of this compound [28].

Additionally, host-parasite interactions are quite complex and promote constant changes in the delicate balance between pro-oxidant and antioxidant molecules since the host and parasite are capable of producing both. Nevertheless, even anti-malarial drug therapy constitutes a source of oxidation, as many drugs such as chloroquine, primaquine and derivatives of artemisinin are inducers of free radical production [29–31].

This review endeavors to present the oxidative stress mechanisms in malaria as well as discuss the potential benefits of antioxidant supplementation therapy as an adjunct to anti-malarial treatment.

We have recently reported that two drugs, remdesivir (GS-5734) and chloroquine (CQ) phosphate, efficiently inhibited SARS-CoV-2 infection in vitro1. Remdesivir is a nucleoside analog prodrug developed by Gilead Sciences (USA). A recent case report showed that treatment with remdesivir improved the clinical condition of the first patient infected by SARS-CoV-2 in the United States2, and a phase III clinical trial of remdesivir against SARS-CoV-2 was launched in Wuhan on February 4, 2020. However, as an experimental drug, remdesivir is not expected to be largely available for treating a very large number of patients in a timely manner. Therefore, of the two potential drugs, CQ appears to be the drug of choice for large-scale use due to its availability, proven safety record, and a relatively low cost. In light of the preliminary clinical data, CQ has been added to the list of trial drugs in the Guidelines for the Diagnosis and Treatment of COVID-19 (sixth edition) published by National Health Commission of the People’s Republic of China.

In the desperate search to find effective treatments for coronavirus disease 2019 (COVID-19), 2 generic drugs, used largely by rheumatologists and dermatologists to treat immune-mediated diseases, have entered the spotlight. The antimalarials hydroxychloroquine (HCQ) and chloroquine (CQ) have demonstrated antiviral activity against severe acute respiratory syndrome–coronavirus 2 (SARS–CoV-2) in vitro and in small, poorly controlled or uncontrolled clinical studies (1–3). Normally, such research would be deemed hypothesis-generating at best. A tweet by President Trump on 21 March 2020 claiming that the combination of HCQ and azithromycin “ha[s] a real chance to be one of the biggest game changers in the history of medicine” accelerated a worldwide run on the drugs, with pharmacies reporting shortages within 24 hours. Here, we try to provide guidance regarding clinical decision making both for patients with COVID-19 and those with immune-mediated conditions, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), and strategies to mitigate further harm to these patients.


Data to support the use of HCQ and CQ for COVID-19 are limited and inconclusive. The drugs have some in vitro activity against several viruses, including coronaviruses and influenza, but previous randomized trials in patients with influenza have been negative (4, 5). In COVID-19, one small nonrandomized study from France (3) (discussed elsewhere in Annals of Internal Medicine [6]) demonstrated benefit but had serious methodological flaws, and a follow-up study still lacked a control group. Yet, another very small, randomized study from China in patients with mild to moderate COVID-19 found no difference in recovery rates (7). Sadly, reports of adverse events have increased, with several countries reporting poisonings and at least 1 death reported in a patient who drank fish tank cleaner because of its CQ content. Antimalarial drugs can cause ventricular arrhythmias, QT prolongation, and other cardiac toxicity, which may pose particular risk to critically ill persons. Given these serious potential adverse effects, the hasty and inappropriate interpretation of the literature by public leaders has potential to do serious harm. At this time of crisis, it is our ethical obligation as physicians and researchers to organize and refer patients to expedited, well-performed randomized trials that can clarify if, when, and for whom antimalarial medications are helpful in COVID-19. As of this writing, 10 such trials are under way, and information should be forthcoming within weeks.


Whereas the evidence supporting the use of antimalarial medications for COVID-19 is equivocal, the evidence for the use of these drugs to treat immune-mediated diseases is not. For example, HCQ is a cornerstone of therapy for SLE. Hydroxychloroquine can effectively treat disease manifestations, such as joint pain and rashes; reduce thrombotic events; and prolong survival. Of note, landmark clinical trials have demonstrated that the withdrawal of HCQ can lead to flares of disease, including life-threatening manifestations, such as lupus nephritis (8). The current shortages of HCQ have therefore alarmed rheumatologists and patients. Offices across the country report fielding calls from concerned patients who are having difficulty obtaining their medication.


Given the likelihood that shortages will continue in the near term, we propose that manufacturers, clinicians, pharmacies, health systems, and governmental health agencies continue to coordinate an aggressive response to ensure that antimalarial drug use is appropriately managed during the COVID-19 pandemic. First, it is important to prioritize available supply for clinical trials evaluating important questions, such as dosing, prophylaxis, and treatment in COVID-19. Second, treatment interruptions for those with SLE and other rheumatic diseases must be prevented, because lapses in therapy can result in disease flares and strain already stretched health care resources. Third, stakeholders should work together to see whether dispensation of remaining supply to patients with COVID-19 makes sense as evidence rapidly changes. Fourth, clear messages that reflect the proper interpretations of available data must be disseminated with high frequency to counteract misinformation, including misleading statements or articles with “clickbait” material.
Finally, safeguards should be put into place to discourage overutilization by health professionals who are depleting supply by prescribing antimalarials for preexposure prophylaxis. Hoarding by health professionals for themselves and their friends or family is already occurring, but state governments and pharmacy boards have started to institute strict utilization policies to prevent further HCQ overutilization. Meanwhile, multiple manufacturers have already made critical commitments to initiate or increase production of HCQ.


What advice should clinicians give to patients with SLE or RA who have difficulty securing HCQ? The pharmacokinetics of HCQ are an important consideration in answering this question. With long-term use of HCQ, peak plasma levels occur 3 to 4 hours after each dose, with a terminal half-life of 40 to 50 days (9). The long half-life means that brief gaps in therapy, on the order of 1 to 2 weeks, are less concerning. However, longer treatment lapses put patients at risk for disease exacerbations, given studies showing that lower plasma concentrations of HCQ correlate with more SLE disease activity (10). In addition, in a well-designed clinical trial, a higher incidence of SLE flares was seen as soon as 2 weeks after the drug was stopped (8).


Patients may also wonder whether rationing their supply by halving their current dose is a good approach. Studies show significant heterogeneity in plasma concentrations of HCQ, even when standard doses of approximately 5 mg/kg are used (9). Therefore, some patients may do better than others with this approach.


The looming public health crisis for people with rheumatic diseases who will be unable to obtain HCQ is the result of a perfect storm of fear and dissemination of overpromised data. However, there is still time to mitigate the damage. Physicians should educate themselves about the strength of available data regarding HCQ and CQ in treating COVID-19. They should avoid misuse of HCQ and CQ for the prophylaxis of COVID-19, because there are absolutely no data to support this. Public figures should refrain from promoting unproven therapies to the public, and instead provide clear messages around the uncertainties we face in testing and using experimental treatments during the current pandemic, including the risk for serious adverse events. Well-done, randomized clinical trials should be performed urgently to test potential therapies, including HCQ. In the meantime, physicians should remember that first, we must do no harm to the patients with rheumatic disease for whom high-quality evidence shows that HCQ improves health.

I wouldn't take a drug based on what a president says. But as a last second hail mary? I'd hate to ignore it simply because 4 out of 5 Presidents say it's purely anecdotal.

Medical community.....I think not. I get all my medical info from the Interwebs. Same thing for constitutional law advice.

Funny thing is, if you listen to the first time Trump mentioned this drug, it seemed to be an attempt to instill some hope against this pandemic.
But the media attacked him for it.
And Trump, being Trump, fought back by driving it home.

I blame him, but we need to understand how this began.

Not really unless others are now responsible for our own actions.... and that is a very generous understanding for him, one you likely would offer to no other and doesn't change the facts or the potential danger from those actions