Once upon a time not that long ago, ‘teething’ was a leading cause of death in infants and children. Often associated with fits, convulsions, nervous disorders, and diarrhea, teething caused the death of at least one-tenth of all children in New Zealand in the 1700’s, and in England in 1880, 2,133 infants under the age of one year were registered to have died of teething.

“The tendency in the past to attribute serious disease to teething was so prevalent that in 1842 teething was the registered cause of death in 4.8% of all infants who died in London under the age of 1 year and 7.3% of those between the ages of 1 to 3 years according to the Registrar General’s report.”

Because teething was so dangerous, and parents didn’t want their children to suffer, an array of medical procedures, cordials and powders were used liberally to ease the pain and suffering of infants and children. Gums were often lanced, or cut with a lancet in a criss cross pattern to facilitate the eruption of teeth. Keeping the bowels “open” and loose by administering diuretics and purgatives of mercury or arsenic containing products was a common treatment for all kinds of ailments from teething to colds as well as other infectious diseases with equally high mortality rates at the time, such as scarlet fever, tuberculosis, chickenpox, and measles.

Calomel, once considered a miracle drug whose main ingredients were the toxic heavy metal mercury chloride, was used to treat almost every disease, including teething. Unknown at the time, the consumption of mercury chloride can cause burning of the mouth and pharynx, abdominal pain, vomiting, bloody diarrhea, weak pulse, shallow breathing, paleness, exhaustion, tremors, collapse, acute renal failure, and eventual death–ironically the side effects of “teething.”

Other common medicines used during this time for teething included: Steedman’s Teething Powder which was 42% Calomel; Dalby’s Carminative, which contained opium, castor oil, wine, and a poisonous root asafoetida (can cause convulsions and seizures); Godfrey’s Cordial, also known as Mother’s Friend, which contained the opiate laudanum in a sweet syrup, used as a sedative for fussy babies; and of course, Mrs. Winslow’s Soothing Syrup, which contained 65 mg of morphine per ounce, as well as alcohol. Just a few drops of the syrup was enough to kill an infant. In the mid-1800s, more than 1.5 million bottles of Mrs. Winslow’s Soothing Syrup was sold each year.

What is really going on right now?

I don’t pretend to know what’s going on. But there are a lot of people who are told by nurses that they “tried everything and nothing worked.” What is the everything? And is some of it causing more problems?

Ashley Everly made a video to capture what many families are experiencing:

@ashleyeverly.tox We did everything we could. #whatdidyoudo #sos ♬ original sound – ashleyeverly

When a person dies of COVID-19, most of them are no longer testing positive for the virus. Many people are dying of secondary bacterial infections, like they did during the Spanish Flu epidemic. It only takes a few days on the ventilator before a person acquires ventilator-associated pneumonia. Or they are dying of kidney failure, which is a known side effect of Remdesivir, or multiple organ failure, a known side effect of mechanical ventilation. Before the pandemic, ventilators killed half of the people in ICU’s who required their use. We knew this going in.

What really happens in hospitals has mostly been behind closed hospital doors, where even loved ones are not allowed to even visit or witness. Nurses have blown the whistle but change is slow.

Here is a nurse whistleblower:

Here is a wife who got her husband out of the ICU and saved his life. This is her story:

Our First Hand ICU Story – What is ACTUALLY Killing People In The Hospital

Remdesivir was found to be deadly, so why are we using it now?

A randomized, controlled trial of Ebola virus disease therapeutics from 2019 found that Remdesivir as a therapeutic increased the mortality of Ebola with respect to other therapeutics.

Over 53% percent of those treated with Remdesivir died, compared to 49% for triple monoclonal antibody ZMapp, 35% for single monoclonal antibody MAb114, and 33% for triple monoclonal antibody REGN-EB3.

Remdesivir failed with Ebola, and it’s failing with COVID-19.

A July 2021 paper cuts to the heart of the matter:

For both COVID-19 and Ebola, significant discordance between the robust preclinical data and remdesivir’s lackluster clinical performance have left many puzzled. Here, we critically evaluate the assumptions of the models underlying remdesivir’s promising preclinical data and show that such assumptions overpredict efficacy and minimize toxicity of remdesivir in humans. Had the limitations of in vitro drug efficacy testing and species differences in drug metabolism been considered, the underwhelming clinical performance of remdesivir for both COVID-19 and Ebola would have been fully anticipated.

WHO does not recommend Remdesivir

In November 2020, the World Health Organization recommended against the use of Remdesivir, regardless of disease severity. The $3000 per treatment Gilead Sciences drug is the only treatment for COVID-19 approved by the FDA.

The WHO sought mortality data of four re-purposed antiviral drugs in hospitalized COVID-19 patients, and based on 405 hospitals in 30 countries, 11,266 adults, the conclusions were:

These Remdesivir, Hydroxychloroquine, Lopinavir and Interferon regimens appeared to have little or no effect on hospitalized COVID-19, as indicated by overall mortality, initiation of ventilation and duration of hospital stay. The mortality findings contain most of the randomized evidence on Remdesivir and Interferon, and are consistent with meta-analyses of mortality in all major trials.

Remdesivir had no effect: it wasn’t found to increase death, it wasn’t found to decrease death over controls, which are described as other drug or “standard of care.”

Remdesivir can cause kidney failure

In April 2021, a pharmacovigilance retrospective study “Remdesivir and Acute Renal Failure: A Potential Safety Signal From Disproportionality Analysis of the WHO Safety Database, “ of World Health Organization’s VigiBase found a statistically significant disproportionality signal related to “acute renal failure” and “remdesivir” with 138 observed cases instead of the 9 expected.

The reporting odds ratio was of Acute Renal Failure with remdesivir was 20-fold what would be expected.

In May 2021, another pharmacovigilance analysis of spontaneous suspected adverse drug reactions reported to the World Health Organization’s VigiBase found based on postmarketing real-life data from >5000 COVID-19 patients, that kidney disorders, including acute kidney injury (AKI), which is potentially fatal, is a fatal drug reaction of Remsdesivir.

Compared with the use of chloroquine, hydroxychloroquine, dexamethasone, sarilumab, or tocilizumab, the use of remdesivir was associated with an increased reporting of kidney disorders (reporting odds ratio, 7.2; 95% confidence interval, 5.7–9.0)

Many studies find no benefit of Remdesivir

A September 2021 retrospective multicentre study reviewed the medical records of 3372 patients discharged between 1 March 2020 and 30 March 2021, with laboratory confirmed COVID-19 in the Mount Sinai Health System and treated with steroids. They evaluated the effect of remdesivir on the outcomes using propensity score analyses.

Results:

In-hospital mortality was similar between those with and without remdesivir (21.4% versus 21.6%, respectively, P = 0.96). Remdesivir was not significantly associated with in-hospital mortality regardless of endotracheal intubation or COVID-19 antibody status. 

However, there was a signal that remdesivir was associated with a reduced risk of [acute kidney injury] AKI in the propensity matched analysis (17.5% versus 23.4%, respectively, P = 0.001).

*Secondary outcomes were acute kidney injury (AKI) and liver injury. AKI was defined according to kidney disease improving global outcomes (KDIGOs) criteria stratified by creatinine level: Stage 1, 1.5–1.9 times baseline or 0.3 mg/dL increase; Stage 2, 2.0–2.9 times baseline; Stage 3, 3 times or creatinine >4.0 mg/dL.

There are many differences between the groups. Explore the groups here.

Typically, a person with an elevated creatinine would be withdrawn from Remdesivir, such as this case report of a 68-year-old man with COVID-19 and Acute Kidney Injury, so I don’t know what to make of that finding.

Other studies purport benefit need to be scrutinized

Study 1

Take this study for instance: “Impact of remdesivir according to the pre-admission symptom duration in patients with COVID-19,” which concludes:

Remdesivir was associated with 62% reduced odds of death versus standard-of-care and its survival benefit increased with shorter duration of symptoms.

It’s a retrospective analysis of patients admitted for over 48 hours to the hospital for a confirmed or suspected SARS-CoV-2 infection from Feb. 2020 to Feb. 2021 with a primary outcome of mortality at 30 days.

Out of 2607 total patients, the global mortality rate was 10.7%.

Deaths that occurred within the first 48 hours were included in the analysis (weird).

Exclusion criteria for remdesivir

This particular Spanish hospital had a remsdesivir clinical trial that some of these patients were part of from July 2020, and exclusion criteria for the clinical trial included:

requirement of supplemental high-flow oxygen, mechanical ventilation, vasoactive drugs, extracorporeal membrane oxygenation or fulfilling the criteria for multiorgan failure at the moment of prescription. Contraindications included AST and ALT ≥5 times the normal range values, glomerular filtration <30 mL/min, haemodialysis or peritoneal dialysis. 

Ok, so in order for a patient to be prescribed remdesivir at this hospital (in this study) they couldn’t be on a ventilator.

Then it says:

Exceptionally, some patients not fulfilling these criteria received remdesivir because the physician in charge considered it necessary due to comorbidity, severity or other criteria. The duration of remdesivir treatment in our institutional protocol was 5 days.

Contrasts with US protocol

In the US, remdesivir is given to patients for 10 days according to its EUA Remdesivir Fact Sheet, and given routinely to patients requiring high-flow oxygen, mechanical ventilation, and people on vasoactive drugs.

Death vs. Survival

In the study:

2328 people were alive at 30 days

of which, 419 had received Remdesivir (18%)

279 people were dead at 30 days

of which, 19 had received Remdesivir (6.8%)

 

That’s it. Because 18% of the people who survived to 30 days had received Remdesivir, vs. only 6.8% of those died received the drug, the study deduces that Remdesivir is the sole cause of the the difference in survival.

• Never mind 1909 people survived and didn’t get Remdesivir.
• Never mind more of the surviving group had received corticosteroids (wouldn’t we conclude that corticosteroids are associated with a reduced mortality?) or what about invasive mechanical ventilation?
• Only 9.2% of those who survived had ventilation compared to 17.9% of those who died. So is mechanical ventilation the cause of those deaths?
• The study included deaths within 48 hours of admission, which may include people who died before they were able to be started on Remdesivir.
• Not giving us an age adjusted mortality? The people who died were twice as likely to be over 66 years old. Could that have something to do with their increased mortality?
• They were 4x more likely to have chronic renal failure (which is an exclusion criteria for Remsdesivir!!)
• Twice as likely to have a solid organ transplant, twice as likely to have a neoplasm, a malignancy, chronic heart disease, hypertension.

 

Could this be why they died? Could this be why those who survived, survived? Because they were less likely to have those comorbidities??

But, for whatever reason the study concludes Remdesivir is the reason for the reduction in mortality.

Study 2

Here’s another: “Remdesivir and Mortality in Patients with COVID-19″ published August 2021.

The retrospective cohort study (following a group of people whom you allocated different drugs to) compared people who received Remdesivir to people who got “best supportive care.” Hospitalized between 2/28/20 and 5/28/20 with lab confirmed infections. Primary outcome was overall survival.

1,138 patients enrolled

• 286 received Remdesivir
• 852 given best supportive care, 400 of whom also received HCQ.

Compared to best supportive care, the Remdesivir group had 54% reduction in death in the univariate model, and 40% in the risk-adjusted model. In the sub-group of persons with baseline use of low-flow oxygen, the reduction was 37%.

Most patients were treated for a 5 day duration.

Inclusion/ exclusion criteria: Lab confirmed SARS-CoV-2.

Exclusions:

• If they received Remdesivir and HCQ simultaneously, or other investigational drug;
• multisystem organ failure
• severe renal dysfunction
• severe hepatitis
• pregnancy

To Repeat: Multisystem organ failure and renal dysfunction prior to death were EXCLUDED from the statistical analysis.

Remdesivir is purported to cause multisystem organ failure and renal dysfunction.

Results:

• 11% of those treated with Remdesivir died (excluding multisystem organ failure and renal dysfunction).
• 24% of those who received HCQ died.
• 26% of those who received best supportive care died.

 

Honestly, if the people with organ or kidney failure weren’t excluded, we may have a more transparent picture. Until then, this Remdesivir manufacturer Gilead-funded study is problematic.

SOURCES:

WHO Solidarity Trial

Remdesivir Fact Sheet

Impact of remdesivir according to the pre-admission symptom duration in patients with COVID-19

Kidney disorders as serious adverse drug reactions of remdesivir in coronavirus disease 2019: a retrospective case–noncase study

Remdesivir and Mortality in Patients with COVID-19

Remdesivir and Acute Renal Failure: A Potential Safety Signal From Disproportionality Analysis of the WHO Safety Database

Case 17-2020: A 68-Year-Old Man with Covid-19 and Acute Kidney Injury

Why Remdesivir Failed: Preclinical Assumptions Overestimate the Clinical Efficacy of Remdesivir for COVID-19 and Ebola

A Randomized, Controlled Trial of Ebola Virus Disease Therapeutics