From here in Austria, neither Chris’ link, nor the alternative one in the comments is working. I get the message, that it has been removed for violating YouTube’s Terms of Service.
I hope he put it on vimeo or another platform . Im sure it will disappear off Facebook now to bc they work together to suppress news
Jesus. What are we becoming?
There was no mention of TWSNBN either, they were about Ivermectin.
This is some scary shit.
Here’s one that’s still up with similar info:
https://www.newswise.com/coronavirus/flccc-alliance-calls-on-national-health-authorities-to-immediately-review-medical-evidence-showing-the-efficacy-of-ivermectin-for-the-prevention-of-covid-19-and-as-an-early-outpatient-treatment
Let’s call it “Mectiniver” from now on.
I think it was just the last video that was deleted by Youtube.
In my mind it is Youtube that is violating our cultural guidelines. Free speech, free inquiry, questioning.
They seem to be against all of these things, which means they are purveyors of the Great Reset which, it should be noted, is based on compliance, conformity and informational power asymmetry.
Not surprising, but disappointing.
These ‘world improvers’ seem to lack any sense of history. Long periods of stasis and decline and/or sometimes collapse of civilizations were preceded by similar demands for obedience to a system of belief.
I haven’t even got the energy to submit an appeal. To even do so suggests I’ve already lost something. Something that needs to be appealed. Instead I hold my head high knowing that my work has saved and/or improved many lives.
I am 100% certain that studying the data is nothing to be ashamed of, or that requires appeal.
But Youtube thinks otherwise. To put a face to all this, here’s the Karen, er Susan, in charge of things.
I’m sure there are plenty of fine people working at Youtube. It wasn’t “Youtube” the amorphous blob that did this to me, or to countless other free-speech explorers, but this person.
I like to remember that all of this comes down to individuals, not corporations. The former reminds us of who really holds the power, the latter is disempowering because corporations are legal fictions, as it were, that have lawyers and crony judges and and entire ecosystem of defenders and protectors.
This study becomes more compelling because of the censorship. Please spread the data as best you can.
https://ivmmeta.com/
Maybe we could try blocking healthcare workers and doctors from ever leaving their state and mandating that they work for $15/hour. If they decide they no longer want to be a doctor or nurse we incarcerate their family members and if they still resist we shoot them.
Since we want to go with a Cuban model. Getting a captive workforce might be all we need.
You are being incredibly unfair. New York was the epicenter and I know a whole lot of people who came here from out of town and within the state to help out at the hospitals. They verify that a flood of cases occurred and many people died. We have lost friends/colleagues/family to this thing since March. I personally know dozens of people who were afflicted and became very ill. The doctors and nurses generally don’t give a damn about hospital profits when they are doing compressions on a Covid patient. When they lose one they mourn, they don’t count money for the hospital. They lived in hotels to avoid killing their families with the virus. No one can explain why we got hit so hard here but it is so apparent that MANY people outside of the NY metro area don’t have a clue about what we went through. Count your blessings that you don’t.
As much as I am not a fan of Jason Kenney, at least he has the balls to speak out against the Great Reset BS. Of course he will always say anything opposite to what (traitor) Trudeau espouses…
https://youtu.be/48CYo90gWU4
https://canadianpatriot.org/2020/12/05/alberta-premier-kenney-rejects-the-great-reset/
Here’s to hoping more ‘managers’ reject this ‘satanic’ plan (thank you ao), which is obviously the chaos part of this Fourth Turning we are enduring.
Das why she mad boss n stompin hup er oofs.
she donnnnnnnnn like da banana one
she wan da happle one
Milady and Runner -well dem love da banana paste but na Susan.
Chris please consider that banning your video as a badge of honor. Your message hit the bullseye and made the incompetent and immoral look bad.
People love to watch banned video’s after all we want to know what “they don’t want us to see”! They are exciting to share and have a risque’ quality about them. I would actually put “banned” on the thumbnail and upload to bitchute, brighteon and other sites. Making something off limits only heightens the interest and desire.
Hey, I have yummy chocolate chip cookies made from a secret recipe and they are fresh out of the oven, they are mouth watering and smell delicious- but you can’t have one. See, you didn’t want that cookie until I told you - you can’t have one. People will be interested in a video they are told they can’t see.
Play this one up Chris, a rebel, a boat rocker, a man with a cause, people love that! Go get-em - your a maverick!
AKGrannyWGrit
Can someone explain to me the best way to post content and/or videos to bypass the censors?
I have joined Parler to get what info I can…Is Vimeo a better alternative to YouTube?
https://www.corbettreport.com/goodbye-youtube-party-video/
*tried to post a moment ago but the spam filter did not allow. Not sure what triggered it but alt media folks who have been banned on CensorTube are posting on Bitchute.
Since Youtube’s (screwtube) censorship has become extreme, and some of my favorite sites have been banned I now frequent bitchute and brighteon. Brandnewtube.com is a new site too. They are not as user friendly or powerful as screwtube’s but I can search and find what I am looking for.
I really like Vernon Coleman on Brandnewtube.com. “An old man in a chair”. He is a retired, British doctor. You might enjoy him.
https://brandnewtube.com/v/uiRIm9
AKGrannyWGrit
I think - my guess - Chris’s video got banned by the “enthusiasm” of our recent new poster, Michael Stratil, Ph.D. Social Psychology, who seemed bent out of shape that Chris hadn’t done his research on the subject matter at hand, and had the effrontery to say something negative about the popular (in some places) Dr. Anthony Fauci.
https://peakprosperity.com/forum-topic/your-video-on-ivermectin-fauci/
Fauci, if you recall, is the same guy who led the fantastic research effort to get those treatments to the American public in record time.
Oh wait. No treatments. Wrong guy, sorry.
Fauci was the “wear a mask, hunker down, and wait for the barely-tested vaccine, which won’t protect you, but it will reduce symptoms.” I call him Mr 1918, because that’s his approach. Straight out of 1918.
Apparently, Mr Social Psychology didn’t approve of too much Fauci truth. My guess is, he is the “minder” who complained to YouTube about the Chris violating some sort of guideline. And of course YouTube was happy to help out a fellow traveler and suppress any criticism of the incredibly productive Anthony Fauci - the man who brought us all those treatments.
Oh wait. Sorry, wrong guy again. No treatments. After 9 months … bupkis.
We’d do better living in Turkey. Or Egypt. Or Argentina.
Apparently pointing this out violates YouTube’s community guidelines.
“Ivermectin inhibits the replication of SARS-CoV-2 in vitro”
https://www.sciencedirect.com/science/article/pii/S0166354220302011
I have made a torrent of Chris’ “banned” youtube update from Dec 4, 2020
https://kennycloud.ca/index.php/s/QpZ8DzCM7PBBF6K
This is the first time Ive made a torrent so please help me find out if it worked
I sent Chris’ latest (now banned) video to a retired surgeon who then sent it to a large Dr. group in Texas and below was their response about ivermectin (it’s at the very bottom so I will post it here.) - ●Ivermectin – Ivermectin has also been proposed as a potential therapy based on in vitro activity against SARS-CoV-2, but the drug levels used in vitro far exceed those achieved in vivo with safe drug doses [128]; various clinical trials of ivermectin are underway. Bottom line, they wouldn’t look at the studies in Chris’ video, sad.
COVID-19-SPECIFIC THERAPY
Specific treatments under evaluation
Dexamethasone and other glucocorticoids — We recommend dexamethasone for severely ill patients with COVID-19 who are on supplemental oxygen or ventilatory support. We use dexamethasone at a dose of 6 mg daily for 10 days or until discharge, whichever is shorter. If dexamethasone is not available, it is reasonable to use other glucocorticoids at equivalent doses (eg, total daily doses of hydrocortisone 150 mg, methylprednisolone 32 mg, or prednisone 40 mg), although data supporting use of these alternatives are more limited than those for dexamethasone. In contrast, we recommend that dexamethasone (or other glucocorticoids) not be used for either prevention or treatment of mild to moderate COVID-19 (patients not on oxygen). These recommendations are largely consistent with those of other expert and governmental groups [4,31-34]. (See 'Severe (including critical) disease'below.)
Patients receiving glucocorticoids should be monitored for adverse effects. In severely ill patients, these include hyperglycemia and an increased risk of infections (including bacterial, fungal, and Strongyloides infections); the rates of these infections in patients with COVID-19 are uncertain. Nevertheless, pre-emptive treatment of Strongyloides prior to glucocorticoid administration is reasonable for patients from endemic areas (ie, tropical and subtropical regions). This is discussed elsewhere (see "Strongyloidiasis", section on 'Preventive treatment'). Major side effects of glucocorticoids are also discussed in detail elsewhere. (See "Major side effects of systemic glucocorticoids".) Data from randomized trials overall support the role of glucocorticoids for severe COVID-19. In a meta-analysis of seven trials that included 1703 critically ill patients with COVID-19, glucocorticoids reduced 28-day mortality compared with standard care or placebo (32 versus 40 percent, odds ratio [OR] 0.66, 95% CI 0.53-0.82) and were not associated with an increased risk of severe adverse events [35]. In another systematic review and network meta-analysis of randomized trials that evaluated interventions for COVID-19 and were available through mid-August 2020, glucocorticoids were the only intervention for which there was at least moderate certainty in a mortality reduction (OR 0.87, 95% CI 0.77-0.98) or risk of mechanical ventilation (OR 0.74, 95% CI 0.58-0.92) compared with standard care [36]. The majority of the efficacy data on glucocorticoids in these meta-analyses comes from a large, randomized open-label trial in the United Kingdom in which oral or intravenous dexamethasonereduced 28-day mortality among hospitalized patients compared with usual care alone [37]. This trial included patients with confirmed or suspected COVID-19 who had no specific indications or contraindications to dexamethasone; 2104 and 4321 patients were randomly assigned to receive dexamethasone or usual care, respectively, and the proportions of baseline comorbidities and need for oxygen or ventilatory support were comparable between the two groups. Reductions in 28-day mortality with dexamethasone in the overall trial population and in prespecified subgroups were as follows: ●Overall – 17 percent relative reduction (22.9 versus 25.7 percent, rate ratio [RR] 0.83, 95% CI 0.75-0.93). ●Patients on invasive mechanical ventilation or extracorporeal membrane oxygenation (ECMO) at baseline – 36 percent relative reduction (29.3 versus 41.4 percent, RR 0.64, 95% CI 0.51-0.81). Age-adjusted analysis suggested a 12.3 percent absolute mortality reduction. ●Patients on noninvasive oxygen therapy (including noninvasive ventilation) at baseline – 18 percent relative reduction (23.3 versus 26.2 percent, RR 0.82, 95% CI 0.72-0.94). Age-adjusted analysis suggested a 4.1 percent absolute mortality reduction. In contrast, a benefit was not seen among patients who did not require either oxygen or ventilatory support; there was a nonstatistically significant trend towards higher mortality (17.8 versus 14 percent, RR 1.19, 95% CI 0.91-1.55). Results were similar when analysis was restricted to the patients with laboratory-confirmed COVID-19 (89 percent of the total population). This was a preliminary report, and some uncertainties remain. The baseline mortality rate in this report was higher than that from some other trials, and the absolute mortality benefit in other settings may not be as high as in this trial. Adverse effects (including secondary infections) were not reported. Patients on noninvasive oxygen therapy comprise a heterogeneous group, and additional details are needed to determine if there are subsets of patients in this group who would most benefit. Thus, overall confidence in the finding of a mortality benefit is low for patients with COVID-19 who need oxygen supplementation and moderate for those who are on mechanical ventilation (in part, given the effect size). Additional details from the trial may help increase confidence in the results. Data on the efficacy of other glucocorticoids are limited to smaller trials, several of which were stopped early because of the findings of the trial above [38-40]. Individual trials of hydrocortisone in critically ill patients failed to demonstrate a clear benefit [38,39]; in a meta-analysis that included three trials evaluating hydrocortisone, there was a nonstatistically significant trend toward reduced 28-day mortality compared with usual care or placebo (OR 0.69, 95% CI 0.43-1.12) [35]. Trials evaluating methylprednisone have not demonstrated a clear benefit. In a randomized trial from Brazil that included 393 patients with suspected or confirmed severe COVID-19 (77 percent of whom were on oxygen or ventilatory support), there was no difference in 28-day mortality rates with methylprednisolone compared with placebo (37 versus 38 percent) [41]. It is uncertain whether the apparent difference in results compared with the larger dexamethasonetrial is related to the glucocorticoid formulation and dose, other differences between the trial populations, or issues related to statistical power. Glucocorticoids may also have a role in the management of refractory shock in critically ill patients with COVID-19. These issues are discussed elsewhere. (See "Coronavirus disease 2019 (COVID-19): Critical care and airway management issues", section on 'Corticosteroids for COVID-19'.)Remdesivir — Remdesivir is a novel nucleotide analogue that has in vitro activity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [42]. If available, we suggest remdesivir for hospitalized patients with severe COVID-19 because data suggest it reduces time to recovery, which we regard as a clinical benefit. Among patients with severe disease, we prioritize remdesivir for those requiring low-flow supplemental oxygen because it may also reduce mortality in this population. However, the optimal role of remdesivir remains uncertain, and some guidelines panels (including the World Health Organization) suggest not using it in hospitalized patients because there is no clear evidence that it improves patient-important outcomes for hospitalized patients (eg, mortality, need for mechanical ventilation) [34,43]. Other guidelines panels, including the Infectious Diseases Society of America and the National Institutes of Health, suggest using remdesivir in hospitalized patients who require supplemental oxygen [4,32]. (See 'Severe (including critical) disease' below.)
In the United States, the Food and Drug Administration (FDA) approved remdesivir for hospitalized children ≥12 years and adults with COVID-19, regardless of disease severity [44]. The suggested adult dose is 200 mg intravenously on day 1 followed by 100 mg daily for 5 days total (with extension to 10 days if there is no clinical improvement and in patients on mechanical ventilation or ECMO). If a patient is otherwise ready for discharge prior to completion of the course, remdesivir can be discontinued. The pharmacokinetics of remdesivir in the setting of renal impairment are uncertain, and it is prepared in a cyclodextrin vehicle that accumulates in renal impairment and may be toxic; thus, remdesivir is not recommended in patients with an estimated glomerular filtration rate (eGFR) <30 mL/min per 1.73 m2 unless the potential benefit outweighs the potential risk. Given the short duration of therapy and the low concentration of the cyclodextrin vehicle, the risks in patients with renal impairment may be relatively low [45]. Liver enzymes should be checked before and during remdesivir administration; alanine aminotransferase elevations >10 times the upper limit of normal should prompt consideration of remdesivir discontinuation. Remdesivir should not be used with hydroxychloroquine or chloroquine because of potential drug interactions. The FDA has also issued an emergency use authorization (EUA) for the Janus kinase inhibitor baricitinib to be used in combination with remdesivir in patients with COVID-19 who require oxygen or ventilatory support [46]. However, we await additional data on the effect of baricitinib before using it with remdesivir in such patients. There is greater evidence of a benefit with dexamethasone in this population, and the safety and efficacy of using baricitinib with a glucocorticoid in patients with COVID-19 are unknown. (See 'Others' below.) Remdesivir has been evaluated for both severe and non-severe COVID-19 in hospitalized patients: ●Severe COVID-19 – Overall, data from randomized trials do not demonstrate a clear, major clinical benefit with remdesivir among hospitalized patients [47-51]. In a meta-analysis of four trials that included over 7000 patients with COVID-19, remdesivir did not reduce mortality (OR 0.9, 95% CI 0.7-1.12) or need for mechanical ventilation (OR 0.90, 95% CI 0.76-1.03) compared with standard of care or placebo [43]. This analysis, however, grouped patients with COVID-19 of all severities together, and based on results from one included placebo-controlled trial, there may be a mortality benefit for select patients with severe disease who only require low-flow supplemental oxygen. Results from that trial also indicate that remdesivir reduced time to recovery from severe COVID-19; in a smaller second trial that was stopped early for poor enrollment, there was also a trend toward reduced time to recovery with remdesivir, but it was not statistically significant. Data from these trials are detailed below: •In an interim report of the WHO-sponsored, multinational SOLIDARITY trial of patients hospitalized with COVID-19, there was no difference in overall 28-day mortality between the 2750 patients randomly assigned to open-label remdesivir and the 2708 patients assigned to standard care (RR 0.95, 95% CI 0.81-1.11) [49]. In an accompanying meta-analysis that included data from SOLIDARITY and the trials discussed below, there appeared to be a trend toward lower mortality with remdesivir among those who were not on mechanical ventilation at baseline, but this did not reach statistical significance (RR 0.8, 95% CI 0.63-1.01). There was no mortality benefit among those on ventilation at baseline (RR 1.16, 95% CI 0.85-1.60). •ACTT-1, a multinational, randomized, placebo-controlled trial of remdesivir(given for up to 10 days or until death or discharge) included 1062 patients with confirmed COVID-19 and evidence of lung involvement; 85 percent had severe disease and 27 percent were receiving invasive mechanical ventilation or ECMO at baseline [47]. Remdesivir resulted in a faster time to recovery, defined as discharge from the hospital or continued hospitalization without need for supplemental oxygen or ongoing medical care (median 10 versus 15 days with placebo; rate ratio for recovery 1.29, 95% CI 1.12-1.49). Remdesivir reduced time to recovery whether patients were randomized within or after 10 days of symptom onset. However, in subgroup analysis, the reduced time to recovery was only statistically significant among patients who were on low-flow oxygen at baseline. Among the subset of patients on mechanical ventilation or ECMO at baseline, the time to recovery was similar with remdesivir and placebo (rate ratio for recovery 0.98, 95% CI 0.70-1.36), although it is possible that follow-up was too short to detect a difference. Overall, there was a trend towards lower 29-day mortality that was not statistically significant (11.4 versus 15.2 percent with placebo, hazard ratio [HR] 0.73, 95% CI 0.52-1.03). Among the subset of patients who were on oxygen supplementation but did not require high-flow oxygen or ventilatory support (either noninvasive or invasive), there was a statistically significant mortality benefit at that time point (4.0 versus 12.7 percent, HR 0.30, 95% CI 0.14-0.64). •In contrast, in a double-blind randomized trial in China of 237 patients with severe COVID-19 (hypoxia and radiographically confirmed pneumonia), time to clinical improvement was not statistically different with remdesivir compared with placebo for 10 days (median 21 versus 23 days; HR for improvement 1.23 [95% CI 0.87-1.75]) [48]. Clinical improvement was defined as discharge from the hospital or a two-point improvement on a six-point clinical score that ranges from death to mechanical ventilation to lower levels of oxygen support to discharge. This study only included one patient who was on mechanical ventilation at baseline. Mortality at 28 days was also similar with remdesivir or placebo (14 versus 13 percent); there was also no difference in time to viral clearance. Among patients who had received treatment within 10 days of symptom onset, there were trends towards lower mortality and more rapid clinical improvement with remdesivir, but these differences were not statistically significant. Several limitations reduce confidence in the finding of no effect; concomitant therapies (lopinavir-ritonavir, interferon alpha-2b, and/or corticosteroids) were used by most study participants, patients in the remdesivir group had a higher proportion of comorbidities (hypertension, diabetes mellitus, and coronary heart disease), and the study was stopped early for poor enrollment (the target enrollment pre-determined to demonstrate effect was 435 patients). Although these trials evaluated 10 days of remdesivir, 5 days of therapy may result in similar outcomes in patients who do not need mechanical ventilation or ECMO. In an industry-sponsored, open-label randomized trial among nearly 400 patients who were hypoxic on room air or receiving noninvasive oxygen supplementation, the rates of clinical improvement and discharge by day 14 were numerically higher when remdesivir was given for 5 days (65 and 60 percent, respectively) versus 10 days (54 and 52 percent, respectively) [52]. However, patients in the 10-day group had higher rates of invasive or noninvasive ventilation and high-flow oxygen receipt at the time of remdesivir initiation, and on adjusted analysis, the differences in outcomes were not statistically significant. Mortality rates at day 14 were 8 and 11 percent with 5 and 10 days of treatment, respectively, and varied by geographic location. In a propensity analysis of a subset of participants in this trial, the adjusted clinical improvement rate was higher and the adjusted mortality rate was lower than those in a cohort of patients who had severe COVID-19 but did not receive remdesivir [53]. However, this comparison of patients from two separate studies should be interpreted with caution because of potential confounders in patient characteristics and management approaches that cannot be fully accounted for by the propensity analysis. ●Nonsevere COVID-19 – Among hospitalized patients with nonsevere disease, remdesivirmay have a modest benefit, but the clinical significance of the benefit is uncertain. In an open-label randomized trial, 584 patients with moderate severity COVID-19 (pulmonary infiltrates on imaging but oxygen saturation >94 percent on room air) were assigned to receive remdesivir for up to 5 days, remdesivir for up to 10 days, or standard of care [54]. By day 11, the five-day remdesivir group had better clinical status according to a seven-point scale compared with standard of care (odds ratio 1.65, 95% CI 1.09 to 2.48). There was not a statistically significant difference at day 11 in clinical status between the 10-day remdesivir group and the standard of care group. Although discharge rates by day 14 were higher with remdesivir (76 percent in each of the remdesivir groups versus 67 percent with standard of care), these differences were not statistically significant. Interpretation of this trial is limited by the open-label design and an imbalance in co-therapies. In ACTT-1, the large trial described above, remdesivir (given for up to 10 days) did not appear to reduce time to recovery among the 119 patients with mild-moderate disease (ie, no hypoxia or tachypnea; five versus six days, recovery rate ratio 1.29, 95% CI 0.91-1.83), although the number of patients in that subgroup was underpowered to show a significant effect [47]. Reported side effects include nausea, vomiting, and transaminase elevations. In one trial, the most common adverse events were anemia, acute kidney injury, fever, hyperglycemia, and transaminase elevations; the rates of these were overall similar between remdesivir and placebo [47]. However, in another trial, remdesivir was stopped early because of adverse events (including gastrointestinal symptoms, aminotransferase or bilirubin elevations, and worsened cardiopulmonary status) more frequent than with placebo (12 percent versus 5 percent) [48].Convalescent plasma and other antibody-based therapies
●Convalescent plasma – Convalescent plasma obtained from individuals who have recovered from COVID-19 can provide passive antibody-based immunity. Neutralizing antibodies are thought to be the main active component; other immune mediators in plasma may also contribute. Convalescent plasma that contains high neutralizing antibody titers is hypothesized to have clinical benefit when given early in the course of disease, and it may be of particular interest for individuals with deficits in antibody production (eg, those receiving anti-CD20 therapies) [55]. However, the available evidence does not support a clear role for convalescent plasma in patients with severe disease. In the United States, convalescent plasma is available for hospitalized patients with COVID-19 through emergency use authorization [56]; nevertheless, because of the lack of evident benefit, we suggest not using convalescent plasma in hospitalized patients outside clinical trials. It is also being evaluated in outpatient populations and as post-exposure prophylaxis. (See 'Severe (including critical) disease' below and "Coronavirus disease 2019 (COVID-19): Convalescent plasma and hyperimmune globulin".) Randomized trials have not demonstrated a clear clinical benefit of convalescent plasma [57-60]. As an example, a placebo-controlled trial from Argentina that included 333 patients with severe COVID-19 found no differences in clinical status at 30 days (adjusted odds ratio 0.92, 95% CI 0.59-1.42) or in 30-day mortality (10.96 versus 11.43 percent, risk difference -0.46 percent, 95% CI -7.8-6.8) between convalescent plasma (with a median total antibody titer of 1:3200) and placebo [60]. The median time from symptom onset to enrollment was eight days, and 46 percent of the 218 patients who underwent baseline antibody testing had no detectable levels at enrollment. In an open-label trial from China, 103 patients with severe or life-threatening COVID-19 were randomly assigned to receive standard treatment with or without convalescent plasma [58]. Only plasma with a high titer of binding antibody was administered. Although convalescent plasma improved the rate of nasopharyngeal viral RNA clearance at 72 hours compared with standard treatment alone, there were no statistically significant differences in the overall rates of clinical improvement by 28 days. Among the subset of patients who had severe but not life-threatening disease, the rate of clinical improvement was greater with convalescent plasma (91 versus 68 percent, HR 2.15, 95% CI 1.07-4.32). There were trends toward lower mortality with convalescent plasma, but these were not statistically significant. The trial was stopped early for poor enrollment, which may have limited the ability to detect a statistically significant difference in clinical outcomes in the overall group. Additionally, convalescent plasma was administered quite late in the course of illness; the median time from symptom onset to randomization was 30 days. In another open-label trial from India that included 464 patients with hypoxia but no oxygen requirement, convalescent plasma did not reduce mortality or progression to severe disease compared with standard of care [59]. However, plasma was not pre-screened for neutralizing titers, and on post-hoc testing, the median titer in the donated plasma was only 1:40, which was lower than the median baseline titer among the trial participants. Use of convalescent plasma for severe COVID-19 has also been reported in observational studies, several of which suggest that administration of convalescent plasma with higher antibody titers and earlier in presentation are associated with a greater clinical effect [57,61-65]. As an example, in an unpublished report of over 35,000 patients who had or were at risk for severe COVID-19 and received convalescent plasma, plasma transfusion within three days of diagnosis was associated with lower unadjusted mortality rates compared with transfusion four or more days after diagnosis (8.7 versus 11.9 percent at day 7 and 21.6 and 26.7 percent at day 30) [64]. However, both overall mortality rate and time to plasma transfusion decreased over the course of the study; during the last month of the study, the difference between unadjusted seven-day mortality rates for transfusion within and after three days was smaller, at 6.1 versus 7.4 percent. An adjusted analysis estimated a 0.65 relative risk (95% CI 0.47-0.92) of mortality at day 7 with high versus low antibody titer plasma units, but this was based on a smaller number of patients, and there were several differences in baseline clinical severity between the two groups. These and other potential confounding factors highlight the limitations of these observational data; additionally, the lack of peer review to date warrants further caution when interpreting the results. Some smaller observational studies have not suggested a mortality benefit with convalescent plasma [66]. The value of screening donor and plasma for sufficiently high neutralizing titers was highlighted in a small study in which none of 12 donated plasma specimens had a neutralizing titer >1:160 despite detectable binding antibodies, and none of the recipients had increases in neutralizing titers after transfusion [67]. However, routine testing for neutralizing activity may not be widely available. (See "Coronavirus disease 2019 (COVID-19): Convalescent plasma and hyperimmune globulin", section on 'Antibody measurements'.) Convalescent plasma has generally been well tolerated [68]. Preparation, administration, and adverse effects of convalescent plasma are discussed in detail elsewhere. (See "Coronavirus disease 2019 (COVID-19): Convalescent plasma and hyperimmune globulin".) ●Monoclonal antibodies – Trials of monoclonal antibodies that have been developed to neutralize SARS-CoV-2 by targeting the SARS-CoV-2 spike protein and preventing viral cell entry are also underway. Hospitalized patients should only receive monoclonal antibodies as part of a clinical trial [4]. Evaluation of monoclonal antibodies in outpatients with mild to moderate COVID-19 is discussed in detail elsewhere. (See "Coronavirus disease 2019 (COVID-19): Outpatient evaluation and management in adults".) In the United States, the FDA is also facilitating the evaluation of hyperimmune globulin for patients with COVID-19 [69].IL-6 pathway inhibitors — Markedly elevated inflammatory markers (eg, D-dimer, ferritin) and elevated pro-inflammatory cytokines (including interleukin [IL]-6) are associated with critical and fatal COVID-19, and blocking the inflammatory pathway has been hypothesized to prevent disease progression [70]. Several agents that target the IL-6 pathway have been evaluated in randomized trials for treatment of COVID-19; these include the IL-6 receptor blockers tocilizumab and sarilumab and the direct IL-6 inhibitor siltuximab.
However, results from randomized trials, some of which have only been reported in press release form, do not indicate a mortality benefit or other clear clinical benefit of these agents [71-76]. As an example, one double-blind, randomized trial of 243 patients with severe COVID-19 who were not intubated but had evidence of a pro-inflammatory state (with elevations in C-reactive protein [CRP], ferritin, D-dimer, or lactate dehydrogenase) did not detect a difference in the rate of intubation or death with a single dose of tocilizumab compared with placebo (10.6 versus 12.5 percent, HR 0.83, 95% CI 0.38-1.81) [74]. Although there were more subjects older than 65 years in the tocilizumab arm, the HR was not statistically significant after adjustment for age and other clinical features. Tocilizumab also did not reduce the risk of disease progression (eg, worsening oxygen requirements). In another trial that included 131 hospitalized patients with COVID-19 who were not on ventilatory support, open-label tocilizumab did not reduce 28-day mortality compared with usual care, even though it did reduce progression to non-invasive or invasive ventilation or death at 14 days [75]. Additional trials of tocilizumab and other IL-6 pathway inhibitors, each in combination with other interventions, are ongoing. Results of these randomized trials contrast with those from observational studies, most of which identified an association between tocilizumab and decreased risks of intubation and/or death [77,78]. This discrepancy highlights the challenges in interpreting observational data because of the impact of unmeasured confounders. Use of IL-6 pathway inhibitors may be associated with an increased risk of secondary infections [79,80], although this was not observed in several randomized trials [74-76]. (See "Secondary immunodeficiency induced by biologic therapies", section on 'Tocilizumab'.)Hydroxychloroquine/chloroquine — We suggest not using hydroxychloroquine or chloroquine in hospitalized patients given the lack of clear benefit and potential for toxicity. In June 2020, the US FDA revoked its emergency use authorization for these agents in patients with severe COVID-19, noting that the known and potential benefits no longer outweighed the known and potential risks [81].
Both chloroquine and hydroxychloroquine may inhibit SARS-CoV-2 in vitro [82]. However, accumulating data from controlled trials suggest that they do not provide a clinical benefit for patients with COVID-19 [83-88]. In a randomized, blinded, placebo-controlled trial of 479 hospitalized patients with COVID-19, hydroxychloroquine did not improve 14-day clinical status or 28-day mortality (10.4 versus 10.6 percent; adjusted OR 1.07, 95% CI 0.54-2.09) compared with placebo; the trial was terminated early because of this lack of benefit [88]. Other large, open-label trials comparing various potential therapies with standard of care also terminated the hydroxychloroquine arms after failing to detect a mortality benefit or reduction in hospital stay [49,83]. In another open-label trial of hospitalized patients who required no or only low-flow oxygen supplementation (≤4 L/min), hydroxychloroquine (with or without azithromycin) did not improve clinical status at 15-day follow-up compared with standard of care [87]. Observational data are somewhat mixed and have methodologic limitations, but overall also suggest no benefit with hydroxychloroquine or chloroquine [89-94]. Studies have highlighted the potential toxicity of hydroxychloroquine or chloroquine [93,95]. One trial comparing two doses of chloroquine for COVID-19 was stopped early because of a higher mortality rate in the high-dose group [95]. QTc prolongation, arrhythmias, and other adverse effects associated with hydroxychloroquine and chloroquine are discussed in detail elsewhere. (See "Coronavirus disease 2019 (COVID-19): Arrhythmias and conduction system disease", section on 'Patients receiving QT-prolonging treatments' and "Antimalarial drugs in the treatment of rheumatic disease", section on 'Adverse effects' and "Methemoglobinemia", section on 'Dapsone and some antimalarials'.) The evidence on the combination of hydroxychloroquine and azithromycin is discussed elsewhere. (See 'Others' below.)Others — Many other agents with known or putative antiviral or immunomodulating effects have been proposed for use in patients with COVID-19 [96-98], and some are in preclinical or clinical evaluation. Use of these agents for COVID-19 should be limited to clinical trials; their efficacy has not been proven, and extensive off-label use may result in excess toxicity and critical shortages of drugs for proven indications. A registry of international clinical trials can be found at covid-trials.org, as well as on the WHO websiteand at clinicaltrials.gov. Some examples of agents under clinical evaluation are detailed here:
●Favipiravir – Favipiravir is an RNA polymerase inhibitor that is available in some Asian countries for treatment of influenza, is available in India for treatment of mild COVID-19, and is being evaluated in clinical trials for treatment of COVID-19 in the United States and elsewhere. Favipiravir may hasten SARS-CoV-2 RNA clearance, although data are limited. In a randomized, open-label trial from Russia that included hospitalized patients who were on room air or receiving supplemental oxygen through mask or nasal cannula, the rate of viral RNA clearance from upper respiratory tract specimens at day 5 was higher with favipiravir compared with standard of care, which included hydroxychloroquine or chloroquine (clearance rates of 62 versus 36 percent) [99]. In a non-randomized study from China of patients with non-severe disease (including oxygen saturation >93 percent), use of favipiravir was associated with faster rates of viral clearance (median time to clearance 4 versus 11 days) and more frequent radiographic improvement (in 91 versus 62 percent by day 14) compared with lopinavir-ritonavir [100]. However, since other therapies (eg, immunomodulatory agents) were administered in these studies, the results should be interpreted with caution given potential confounders. ●Baricitinib – Baricitinib is a Janus kinase inhibitor used for treatment of rheumatoid arthritis. In addition to immunomodulatory effects, it is thought to have potential antiviral effects through interference in viral entry. In the United States, the FDA issued an EUA for baricitinib (4 mg orally once daily for up to 14 days) to be used in combination with remdesivir in patients with COVID-19 who require oxygen or ventilatory support [46]. Adding baricitinib to remdesivir appears to modestly improve the time to recovery, but effects on other endpoints are uncertain and interactions with glucocorticoid use are unknown. We await additional data on the effect of baricitinib before using it with remdesivir in such patients. In an unpublished randomized trial of 1033 hospitalized adults with COVID-19, baricitinibplus remdesivir reduced time to recovery (defined as hospital discharge or continued hospitalization without need for oxygen or medical care) compared with placebo plus remdesivir (7 versus 8 days, hazard ratio [HR] 1.15, 95% CI 1.0-1.31) [46]. There was also a trend towards lower 29-day mortality with the addition of baricitinib to remdesivir (4.7 versus 7.1 percent), but this was not statistically significant. In an observational study that included 83 patients with COVID-19 who received baricitinib and 83 propensity score-matched controls, baricitinib use was associated with a lower rate of death or mechanical ventilation, but potential confounders reduce confidence in these findings [101]. In these studies, there was no apparent increase in the rate of adverse effects, including infection rates and venous thromboembolism, with baricitinib. ●Interferons – Interferons modulate immune responses and may have antiviral effects. Interferon beta, specifically, has been reported to inhibit SARS-CoV-2 replication in vitro [102]. Defects in production of type 1 interferons (which include interferon beta), as well as autoantibodies that neutralize type 1 interferons, have been identified in patients with severe COVID-19 [103,104]. (See "Toll-like receptors: Roles in disease and therapy", section on 'Severe COVID-19'.) Some trials, detailed below, have suggested a clinical benefit with interferon beta for patients with COVID-19, although methodologic limitations reduce confidence in the findings [105,106]. Furthermore, interim results of a large multinational trial of patients hospitalized with COVID-19 showed no difference in 28-day mortality with subcutaneous or intravenous interferon beta compared with standard of care (2703 patients in each group; RR 1.16, 95% CI 0.96-1.39) [49]. In one open-label trial from Hong Kong, 127 adults hospitalized with primarily nonsevere COVID-19 were randomly assigned 2:1 to a combination intervention (subcutaneous interferon beta, oral ribavirin, plus lopinavir-ritonavir if symptom onset was within 7 days or ribavirin plus lopinavir-ritonavir if symptom onset was between 7 to 14 days) versus control (lopinavir-ritonavir alone) [105]. Patients in the intervention group had more rapid times to a negative SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) test on a nasopharyngeal swab (median 7 versus 12 days), clinical improvement (median 4 versus 8 days), and hospital discharge (median 9 versus 15 days); in a subgroup analysis, the differences were only observed among patients with symptom onset within 7 days who thus received interferon beta as part of the intervention. Adverse effects were similar between the intervention and control groups. No hemolysis was detected with ribavirin (400 mg orally twice daily). In another open-label randomized trial from Iran that included 81 hospitalized patients, the addition of subcutaneous interferon beta to local standard of care (hydroxychloroquine plus either lopinavir-ritonavir or atazanavir-ritonavir) did not reduce the time to clinical recovery but was associated with a lower 28-day mortality and higher likelihood of hospital discharge compared with local standard of care alone [106]. However, there were multiple confounders in this trial; these included concurrent use of other interventions (including corticosteroids and intravenous immune globulin), early drop out following randomization (including four deaths in the interferon arm that were not included in the analysis), and inclusion of patients without laboratory confirmed COVID-19. Inhaled interferon beta, an investigational formulation of the drug delivered by nebulizer, is also being evaluated. In a randomized trial of 101 patients hospitalized with COVID-19, inhaled interferon beta increased the likelihood of recovery by day 15 compared with placebo (OR 3.19, 95% CI 1.24-8.24); a reduction in the likelihood of severe disease or death was not statistically significant [107]. There are also several pilot trials evaluating the use of interferon lambda for COVID-19. ●Other immunomodulatory agents – Because of the observation that some patients have a clinical presentation that resembles cytokine release syndrome and the association between severe disease and a number of pro-inflammatory markers, interrupting the inflammatory cascade has been proposed as a potential therapeutic target for severe COVID-19. In addition to IL-6 pathway inhibitors (see 'IL-6 pathway inhibitors' above), immunomodulatory agents from various classes, including IL-1 inhibitors [108-111], other cytokine inhibitors [112], kinase inhibitors [113-116], complement inhibitors [117], bradykinin pathway inhibitors [118], and recombinant hematopoietic colony-stimulating factors [119] are being evaluated. Their use has been described mainly in case series and other observational studies. As an example, in a retrospective study of patients with COVID-19, ARDS requiring non-invasive ventilation, and markedly elevated CRP or ferritin, receipt of high-dose anakinra in 29 patients (in addition to hydroxychloroquineand lopinavir-ritonavir) was associated with a lower 21-day mortality rate compared with a historical cohort of 16 patients who received only hydroxychloroquine and lopinavir-ritonavir (10 versus 44 percent); however, the historical group was older, and the likelihood of other, unmeasured confounders makes the findings difficult to interpret [108]. Results of well-powered randomized trials are necessary to determine the effect of these agents. ●Azithromycin (with or without hydroxychloroquine) – We do not use azithromycin, either alone or in combination with hydroxychloroquine, for treating COVID-19. Studies have compared the combination of azithromycin and hydroxychloroquine with usual care or with hydroxychloroquine alone, and most have not suggested an associated clinical benefit [87,89,92,120-122]. Furthermore, both azithromycin and hydroxychloroquine are associated with QTc prolongation, and combined use may potentiate this adverse effect [92]. (See "Coronavirus disease 2019 (COVID-19): Arrhythmias and conduction system disease", section on 'Patients receiving QT-prolonging treatments'.) ●Lopinavir-ritonavir – We suggest not using lopinavir-ritonavir for treatment of COVID-19 in hospitalized patients. Several clinical trials have failed to demonstrate efficacy [8,49,123,124]. As an example, in an open-label randomized trial of patients hospitalized with COVID-19, lopinavir-ritonavir for up to 10 days (n = 1616) did not reduce 28-day mortality (23 versus 22 percent) or need for mechanical ventilation (10 versus 9 percent) compared with usual care (n = 3424) [124]. It also did not improve 28-day hospital discharge rates. Whether lopinavir-ritonavir has a role in outpatients with nonsevere disease is uncertain; we suggest it only be used in outpatients in the context of a clinical trial. Although it has in vitro activity against SARS-CoV [125], lopinavir-ritonavir is highly protein-bound and does not appear to achieve plasma levels close to the EC50 [126,127]. ●Ivermectin – Ivermectin has also been proposed as a potential therapy based on in vitro activity against SARS-CoV-2, but the drug levels used in vitro far exceed those achieved in vivo with safe drug doses [128]; various clinical trials of ivermectin are underway. Other agents that have been proposed for COVID-19 therapy include the HCV antivirals sofosbuvirplus daclatasvir [129-131], the selective serotonin receptor blocker fluvoxamine [132], famotidine[133,134], colchicine [135], vitamin D [136], and zinc [137]. Clinical data thus far are insufficient to support a role for these agents, and, as above, their use for COVID-19 should be limited to clinical trials.
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