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Methylprednisolone, the main ingredient in the MATH+ protocol, is not a "natural, non-pharmaceutical" cure. It's a synthetic (designer) drug. It's rather invasive as an immunosuppressor but it does do the trick (of dampening the cytokine storm). There are other less invasive options though, such as preventing the cytokine storm altogether with early treatment (outpatient, before they get to the hospital) with HCQ + Azithromycin + zinc + copper + vitC+D3 (+ melatonin, optional).
But it's pretty decent as part of a hospital protocol (but then again, if these patients have never been given HCQ, it's advisable to try that first to see if that's enough, in the outpatient setting it's almost always enough with the combination of substances earlier mentioned). Methylprednisolone is a way to take the treatment to the next level (in terms of taking more drastic measures to prevent further damage from the cytokine storm, should be determined on a patient by patient basis, not a rigorous protocol that people feel the need to follow to the letter, regardless of patient specifics, or whether or not the patient has already had HCQ + quality care, including those substances I mentioned).
Note: Early termination of ascorbic acid and corticosteroids will likely result in a rebound effect with clinical deterioration (see Figure 3).
Scientific Rational for MATH+ Treatment Protocol
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), Infectious Diseases Association of America (IDSA) 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.[31,80] 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. [81-84] 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 use of HFNC, with frequent patient repositioning (proning) and the acceptance of “permissive hypoxemia”. However, this approach entails close patient observation.
Patients in whom the cytokine storm is not “dampened” will progress into the “H phenotype” characterized by poor lung compliance, severe oxygenation failure and PEEP recruitability (see Figure 7). Progression to this phase is exacerbated by ventilator induced lung injury (VILI). The histologic pattern of the “H Phenotype” is characterized by an acute fibrinous and organizing pneumonia (AFOP), with extensive intra-alveolar fibrin deposition called fibrin “balls” with absent hyaline membranes. Corticosteroids seem to be of little benefit in established AFOP. High dose methylprednisolone should be attempted in the “early phase” of AFOP, however many patients will progress to irreversible pulmonary fibrosis with prolonged ventilator dependency and ultimately death. [85,86]
(the term 'HCQ's effectiveness' is referring to using HCQ in the right way, Dr. Ban-style, so this includes vitamin C + D3 + Azithromycin with a possible escalation with corticosteroids like prednisone and its derivatives like "methylprednisolone", an immunosuppressor, if needed or warranted, patient specific, if we're talking about "dampening the storm", quoting the EVMS; it also includes 'avoiding intubation at all cost' as the EVMS puts it only to then include intubation into their protocols that have HCQ as an optional and go straight to the more invasive immunosuppressors that open up their patients to those nasty hospital bacteria, regardless of whether or not HCQ + quality care, Dr. Ban-style was tried first to avoid such drastic risky measures that can cause nasty bacterial infections especially in the hospital and especially if you go to intubation eventually anyway. C'mon man!!! What is wrong with these people?! Does nobody get it?)
... this approach has FAILED and has led to the death of tens of thousands of patients.
... In addition to their antimalarial and antiviral effects, their anti-inflammatory properties have been demonstrated in the treatment of autoimmune diseases such as rheumatoid arthritis and lupus erythematosus. Chloroquine and hydroxychloroquine can inhibit major histocompatibility complex class II expression, antigen presentation and immune activation (reducing CD154 expression by T cells) via Toll-like receptor signalling and cGAS stimulation of interferon genes . Thus, chloroquine and hydroxychloroquine can reduce the production of various pro-inflammatory cytokines, such as IL-1, IL-6, interferon-α and tumour necrosis factor, which are involved in the cytokine storm .
Immunomodulatory agents that directly target the key cytokines involved in COVID-19 may also help alleviate hyperinflammation symptoms in severe cases . [whereislogic: he can leave out the "may", it should be obvious that it helps] Elevated levels of the inflammatory indicator IL-6 in the blood have been reported to be predictive of a fatal outcome in patients with COVID-19 . ...
11. Schrezenmeier E, Dörner T. Mechanisms of action of hydroxychloroquine and chloroquine: implications for rheumatology. Nat Rev Rheumatol. 2020 Feb 7 doi: 10.1038/s41584-020-0372-x. [CrossRef] [Google Scholar]
12. Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ. COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet. 2020;395:1033–1034. [PMC free article] [PubMed] [Google Scholar]
13. Ruan Q, Yang K, Wang W, Jiang L, Song J. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med. 2020 Mar 3 doi: 10.1007/s00134-020-05991-x. [CrossRef] [Google Scholar]
Author: Ming Zhao
a. Department of Pharmacy, Beijing Hospital, National Centre of Gerontology, Beijing, P.R. China
b. Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, P.R. China
No funding is always a good sign. Just an honest guy doing his research properly, the right way. Note, this is called a "literature review", then he uses his common sense to draw rational conclusions based on the data already available. Here, I'll do the same based on the information highlighted above (just the first sentence, the rest is responding to what you said):
HCQ works great even at the latest stages of the disease during the cytokine storm. High dose vitamin C works pretty good at this stage as well, but not as effective at dampening the storm. ...
originally posted by: whereislogic
...Dr. Ban already explained in what situations corticosteroids (like dexamethasone, prednisone or methylprednisolone; all immuno-suppressors) are warranted or needed as an escalation of care on March 25 (see after 3:29 in that video where he literally names the first 2). Corticosteroids are the focal point of the MATH+ protocol and the Covid-19 protocol of the Eastern Virginia Medical School (EVMS).
originally posted by: Phage
a reply to: Violater1
He'll say that it's all anecdotal and should be studied for 10 months before trials.
Why would he say that? This is a controlled trial, part of a project which has been running since March.
A total of 2104 patients were randomised to receive dexamethasone 6 mg once per day (either by mouth or by intravenous injection) for ten days and were compared with 4321 patients randomised to usual care alone. Among the patients who received usual care alone, 28-day mortality was highest in those who required ventilation (41%), intermediate in those patients who required oxygen only (25%), and lowest among those who did not require any respiratory intervention (13%).
...to receive dexamethasone 6 mg (equivalent to 32 mg methylprednisolone) once per day (either by mouth or by intravenous injection) for ten days... It should be noted that we would consider the non-titratable ‘fixed” dose of dexamethasone used in the RECOVERY-DEXAMETHASONE study to be very low. Furthermore, as indicated above, we consider methylprednisolone to be the corticosteroid of choice for the treatment of COVID-19 pulmonary disease.
[going back a little to compare the quantities mentioned above as "very low" with the quantities in the MATH+ protocol that the EVMS uses]
Essential Treatment (dampening the STORM); MATH +
1.Methylprednisolone 80 mg loading dose then 40 mg q 12 hourly for at least 7 days and until transferred out of ICU. In patients with an increasing CRP or worsening clinical status increase the dose to 80 mg q 12 hourly, then titrate down as appropriate. [48-54]
16. Salvage Treatments
High dose corticosteroids; 120 -250 mg methylprednisolone q 6-8 hourly
17.Treatment of Macrophage Activation Syndrome (MAS)
“High dose corticosteroids.” Methylprednisolone 120 mg q 6-8 hourly for at least 3 days, ...