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Hydroxychloroquine (Plaquenil) and Chloroquine don't seem to stand out much in the survey in comparison to most other treatments.
originally posted by: puzzled2
a reply to: Phage
Then why do it why bring it to the discussion?
What was the purpose of your original post? To confuse spread misinformation?
originally posted by: puzzled2
a reply to: Phage
from you own source - differs from your fake news -
Almost twice as many doctors think that a cuppa Chinese tea works
Please indicate which medications you are currently using to treat COVID-19 patients In the hospital (moderate-severe symptoms, excluding ICU patients).
Hydroxychloroquine (Plaquenil) or Chloroquine
56%
Azithromycin or similar antibiotics
54%
Traditional Chinese Medicine
3%
Please indicate which medications you are currently using to treat COVID-19 patients in the ICU (critical symptoms).
Hydroxychloroquine (Plaquenil) or Chloroquine
45%
Which is why I ask you for a source to verify the BS.
originally posted by: infolurker
originally posted by: sligtlyskeptical
Published in March 2020. What is the % of use now after trial results were less than stellar?
The last "trials" have been bunk. Instead of providing it early they give it as a last resort once you are already hospitalized which pretty much defeats the purpose and it needs to be given with Zinc to achieve the anti-viral impact needed.
... first time he mentioned it on March 19 the writing was already on the wall concerning HCQ's effectiveness, no need for conveniently selective agnosticism and pretending it isn't clear yet, setting up Fauci's line of argumentation concerning gold standard clinical trials in order to delay, since these will never happen concerning HCQ, nobody wants such a clinical trial for HCQ, and it's not even required to observe and acknowledge the reality of the matter: that HCQ works highly effectively).
originally posted by: Phage
a reply to: Dr UAE
Without proper controls and blinding, there is no way to know if it was the treatment which was effective or some other factor.
so after more than almost two months since weve heard about this drug and the doctors who tried it and worked with them?
Clinical trials are underway. Properly conducted trials are not completed overnight.
www.clinicaltrials.gov...
www.clinicaltrials.gov...
clinicaltrials.gov...
www.nih.gov...
www.ncbi.nlm.nih.gov...
originally posted by: sligtlyskeptical
Published in March 2020. What is the % of use now after trial results were less than stellar?
originally posted by: whereislogic
...
Any of those continuing that high quality care once HCQ becomes less useful in the later stages of the disease, with treatments that are more specifically tailored to 'dampening the cytokine storm'? ... Any of them care at all if the HCQ treatment is optimized and tailored to the specific needs per patient like that (with proper follow-up and extensive monitoring of the patient all the way through from the earliest to the latest stages of the disease and not doing this)?
Scientific Rational for MATH+ Treatment Protocol
Three core pathologic processes lead to multi-organ failure and death in COVID-19:
1) Hyper-inflammation (“Cytokine storm”) – a dysregulated immune system whose cells infiltrate and damage multiple organs, namely the lungs, kidneys, and heart. It is now widely accepted that SARS-CoV-2 causes aberrant T lymphocyte and macrophage activation resulting in a “cytokine storm.”.
2) Hyper-coagulability (increased clotting) – the dysregulated immune system damages the endothelium and activates blood clotting, causing the formation of micro and macro blood clots. These blood clots impair blood flow.
3) Severe Hypoxemia(low blood oxygen levels) –lung inflammation caused by the cytokine storm, together with microthrombosis in the pulmonary circulation severely impairs oxygen absorption resulting in oxygenation failure.
The above pathologies are not novel, although the combined severity in COVID-19 disease is considerable. Our long-standing and more recent experiences show consistently successful treatment if traditional therapeutic principles of early and aggressive intervention is achieved, before the onset of advanced organ failure. It is our collective opinion that the historically high levels of morbidity and mortality from COVID-19 is due to a single factor: the widespread and inappropriate reluctance amongst intensivists to employ anti-inflammatory and anticoagulant treatments, including corticosteroid therapy early in the course of a patient’s hospitalization. It is essential to recognize that it is not the virus that is killing the patient, rather it is the patient’s overactive immune system. The flames of the “cytokine fire” are out of control and need to be extinguished. Providing supportive care (with ventilators that themselves stoke the fire) and waiting for the cytokine fire to burn itself out simply does not work... this approach has FAILED and has led to the death of tens of thousands of patients.
The systematic failure of critical care systems to adopt corticosteroid therapy resulted from the published recommendations against corticosteroids use by the World Health Organization (WHO), the Centers for Disease Control and Prevention (CDC), and the American Thoracic Society (ATS) amongst others. A very recent publication by the Society of Critical Care Medicine and authored one of the members of the Front Line COVID-19 Critical Care (FLCCC) group (UM), identified the errors made by these organizations in their analyses of corticosteroid studies based on the findings of the SARS and H1N1 pandemics. Their erroneous recommendation to avoid corticosteroids in the treatment of COVID-19 has led to the development of myriad organ failures which have overwhelmed critical care systems across the world.
Our treatment protocol targeting these key pathologies has achieved near uniform success, if begun within 6 hours of a COVID19 patient presenting with shortness of breath or needing ≥4L/min of oxygen. If such early initiation of treatment could be systematically achieved, the need for mechanical ventilators and ICU beds will decrease dramatically.
It is important to recognize that “COVID-19 pneumonia” does not cause ARDS. The initial phase of “oxygenation failure” is characterized by normal lung compliance, with poor recruitability and near normal lung water (as measured by transpulmonary thermodilution). This is the “L phenotype” as reported by Gattonini and colleagues. [57-60] Treating these patients with early intubation and the ARDNSnet treatment protocol will cause the disease you are trying to prevent i.e. ARDS. These patients tolerate hypoxia remarkable well, without an increase in blood lactate concentration nor a fall in central venous oxygen saturation. We therefore suggest the liberal us of HFNC, with frequent patient repositioning (proning) and the acceptance of “permissive hypoxemia”. However, this approach entails close patient observation.
...
Finally, it is important to acknowledge that there is no known therapeutic intervention that has unequivocally been proven to improve the outcome of COVID-19. This, however, does not mean we should adopt a nihilist approach and limit treatment to “supportive care”. Furthermore, it is likely that there will not be a single “magic bullet” to cure COVID-19. Rather, we should be using multiple drugs/interventions that have synergistic and overlapping biological effects that are safe, cheap and “readily” available. The impact of COVID-19 on middle- and low-income countries will be enormous; these countries will not be able to afford expensive designer molecules.
originally posted by: whereislogic
...
No? Because that's not what a clinical trial focuses on? Then why not have a look at the true potential of HCQ if optimized like that in actual case studies from Dr. Ban (which are without melatonin btw):
Don't expect too much from those works in progress you linked. Key point at 14:19.