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She can only support her model now by saying current data is wrong, because of "unreliable" tests, but that seems a judgement call based on my reading of the article.
But really, with over 90k fatalities in only about 10 weeks, her claim of mortality equal to or lower than seasonal flu just doesn't seem to pass a simple sniff test.
The likes of the Sunetra Gupta were responsible for the early strategy of the UK government and the disastrous results it produced. Great to have her voice in the public sphere (rather than just BoJo whisperer) but she doesn't get a free pass either (nor should anyone else). I am not exactly persuaded by her.
Norwegian-British cancer medicine to be tested on British COVID-19 patients
This likely has some commercial angle to it as well but might be promising ...
Hopes of finding a successful treatment have so far centered on the American drug remdesivir. In recent studies, patients receiving remdesivir recovered a little faster from COVID-19. But it is still unclear whether the drug has any effect on the mortality rate from the disease caused by the coronavirus.
Godfrey told the British newspaper that bemcentinib's effect on COVID-19 as seen in the laboratory completely overshadows the effect of other drugs. He says this is because the Norwegian-British drug works in a completely different way than other treatments, such as remdesivir.
The drug from BerGenBio is intended to prevent the body's immune system from being weakened in the face of the virus behind COVID-19. More specifically, it prevents the virus from lurking into the body by using a special protein made from the AXL gene.
Last week bemcentinib was selected by the UK Government as one of the most promising treatments for COVID-19.
Consequently, the drug from Bergen and Oxford will now be the first in a project to test several possible coronavirus remedies. The rapid testing is being done under a programme the British health authorities have called ACCORD (The Accelerating COVID-19 Research & Development Platform).
BerGenBio believes it is 80 per cent likely that their bemcentinib pill will help people who are sick with the coronavirus. The pill is now being tested on 120 British patients who have COVID-19.
The gist is to use a simple ($40) "pulse oximeter" that measures the level of oxygen in your blood, which should be 94% to 100%. In the early stages of COVID Pneumonia the oxygen saturation declines but the person does not feel short of breath as in 'normal' pneumonia so people think all is well.
By the time a person feels sick enough to go to the ER, their pulse/ox is in the 50% range and bam, on a ventilator they go, where far too many die. Attending to people on ventilators places stunning workloads on hospital staffs.
The doctor who wrote the article said if they can get you in before your pulse/ox gets down to that 50% level they can keep you off a ventilator and get you recovered and out of the hospital fairly fast.
Pulse oximeters may be bought at most drugstores or online all over the internet.
My reading is consistently 98% which is very good. Daily readings take less than a minute. I keep my pulse-ox on the desk next to my keyboard. If I detect a drop in my ox levels I'll be on the phone with my Doc asap.
Hope this helps. Please take care and stay well.
It's called happy hypoxia. The COVID infection attacks the lungs with little infection in the throat so they don't have the normal coughing and phlegm early in the pneumonia.
This just released study is damaging to the HCQ proponents - "...decreased in-hospital survival and an increased frequency of ventricular arrhythmias when used for treatment of COVID-19."
Hydroxychloroquine or chloroquine, often in combination with a second-generation macrolide, are being widely used for treatment of COVID-19, despite no conclusive evidence of their benefit. Although generally safe when used for approved indications such as autoimmune disease or malaria, the safety and benefit of these treatment regimens are poorly evaluated in COVID-19.
Methods
We did a multinational registry analysis of the use of hydroxychloroquine or chloroquine with or without a macrolide for treatment of COVID-19. The registry comprised data from 671 hospitals in six continents. We included patients hospitalised between Dec 20, 2019, and April 14, 2020, with a positive laboratory finding for SARS-CoV-2. Patients who received one of the treatments of interest within 48 h of diagnosis were included in one of four treatment groups (chloroquine alone, chloroquine with a macrolide, hydroxychloroquine alone, or hydroxychloroquine with a macrolide), and patients who received none of these treatments formed the control group. Patients for whom one of the treatments of interest was initiated more than 48 h after diagnosis or while they were on mechanical ventilation, as well as patients who received remdesivir, were excluded. The main outcomes of interest were in-hospital mortality and the occurrence of de-novo ventricular arrhythmias (non-sustained or sustained ventricular tachycardia or ventricular fibrillation).
Findings
96,032 patients (mean age 53·8 years, 46·3% women) with COVID-19 were hospitalised during the study period and met the inclusion criteria. Of these, 14 888 patients were in the treatment groups (1868 received chloroquine, 3783 received chloroquine with a macrolide, 3016 received hydroxychloroquine, and 6221 received hydroxychloroquine with a macrolide) and 81 144 patients were in the control group. 10 698 (11·1%) patients died in hospital. After controlling for multiple confounding factors (age, sex, race or ethnicity, body-mass index, underlying cardiovascular disease and its risk factors, diabetes, underlying lung disease, smoking, immunosuppressed condition, and baseline disease severity), when compared with mortality in the control group (9·3%), hydroxychloroquine (18·0%; hazard ratio 1·335, 95% CI 1·223–1·457), hydroxychloroquine with a macrolide (23·8%; 1·447, 1·368–1·531), chloroquine (16·4%; 1·365, 1·218–1·531), and chloroquine with a macrolide (22·2%; 1·368, 1·273–1·469) were each independently associated with an increased risk of in-hospital mortality. Compared with the control group (0·3%), hydroxychloroquine (6·1%; 2·369, 1·935–2·900), hydroxychloroquine with a macrolide (8·1%; 5·106, 4·106–5·983), chloroquine (4·3%; 3·561, 2·760–4·596), and chloroquine with a macrolide (6·5%; 4·011, 3·344–4·812) were independently associated with an increased risk of de-novo ventricular arrhythmia during hospitalisation.
Interpretation
We were unable to confirm a benefit of hydroxychloroquine or chloroquine, when used alone or with a macrolide, on in-hospital outcomes for COVID-19. Each of these drug regimens was associated with decreased in-hospital survival and an increased frequency of ventricular arrhythmias when used for treatment of COVID-19.
Covid19 is toowelladapted to humans to have a zoonotic origin ! All previous zoonotic events were one-way streets, i.e. the more the virus spread through humans, the replication creates errors such that the virus is less virulent. Covid19 has gone through at least 5.2M people, and no degradation ??
You'd think the chinese would be thoroughly investigating all the other wet markets, that have bats on sale, to see if there's reservoirs of possible covid19 still out there ! It's not like they don't have a massive incentive to show the world they aren't responsible.
Last edited by JG183; 05-22-2020 at 11:50 AM..
Reason: sp
Pulse oximeters may be bought at most drugstores or online all over the internet.
I've been shopping for one for the last 5 weeks, no luck. Online sellers will show it as in stock, then just prior to placing the order, it'll show a shipping date that's 6-8 weeks out.
Sweden is a puzzle, for sure. They are the fly in the ointment because, by rights, they should be MUCH worse than they are. Yet, daily deaths are falling. Yesterday, I back-envelope calculated a 40-50% infection rate for Sweden based on some government flunky claiming they were 20% infected around April 17th. That would have explained their falling death rate, as they peaked and headed down the herd immunity slope.
Well, the late-April serosurvey shows that was totally untrue. Taking this 7% data, comparing the death rate around April 28, and extrapolating, it looks like they're only 15% infected at present. That's certainly not enough to explain the falling death rate.
Unfortunately, the Sweedish data also force me to bump the fatality rate from my older 0.2% estimate to 0.28% to even get a ballpark match of the data. A 0.28% estimate for the healthy, wealthy, Swedes with great health care systems is seriously BAD NEWS for us fat Americans and our crap system.
However, more recent--and detailed--serosurvey data from Los Angeles yields a 0.14% fatality rate. Much earlier serosurvey studies from NYC gave a >0.5% death rate! Some of the original antibody assays from San Francisco also pegged the death rate around 0.14%
So, like I said, Sweden is a puzzle. They should be more infected. They shouldn't be dying so quickly. Maybe there is something to this dangerous Europe/East-Coast mutation vs. the supposedly-less-deadly original strain of China/West-Coast virus.
I mostly use American data to make guesstimates. I'll have to watch to see if the data continues to diverge between the East and West antibody studies. Since it looks like we're stumbling down the open up and infect everyone path, I'm beginning to feel better about living on the West Coast!
My guess on NYC is a few things:
- They totally botched nursing homes. (This is the danger of anointing Cuomo as some kind of 9/11-Giuliani-like hero) https://www.businessinsider.com/cuom...g-homes-2020-5
- High density = higher viral load exposure.
- many multigenerational, tight households. Often in poverty.
- African Americans may be more at risk not only due to prevalence of diabetes, but low Vit D
It's called happy hypoxia. The COVID infection attacks the lungs with little infection in the throat so they don't have the normal coughing and phlegm early in the pneumonia.
They may be happy but also possibly unaware of their own breathing function.
With falling oxygen saturation numbers respiration rate must increase significantly, which is something that should be noticed.
Good idea to have pulse oximeter on hand. Dropping below 90s would be time to seek assistance.
It's called happy hypoxia. The COVID infection attacks the lungs with little infection in the throat so they don't have the normal coughing and phlegm early in the pneumonia.
I thought that the mechanism to causes shortness of breath was different from pneumonia effect. That the CO2 is not building up with COVID, so the person doesn't experience that build-up/SOB feeling. Not that the virus doesn't infect the throat, but that it affects the vascular structures of the lungs.
She can only support her model now by saying current data is wrong, because of "unreliable" tests, but that seems a judgement call based on my reading of the article.
But really, with over 90k fatalities in only about 10 weeks, her claim of mortality equal to or lower than seasonal flu just doesn't seem to pass a simple sniff test.
On your latter point, why not?
It seems from an epidemiological standpoint, this was a virus whose spread characteristics are more perfectly designed to disproportionally affect places like nursing homes with “super spreader” events. That’s why we saw so many deaths so quickly in a short period.
That does not mean it is necessarily drastically more deadly than flu to any given person. It means their spread characteristics are different.
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