COVID - where are we now?
Somehow I’ve been writing this newsletter for 6 months already. I can’t believe it. I started this to process my COVID experience, ended up enjoying it more than I expected, and have continued writing longer than I initially anticipated.
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Since the impetus to write was COVID, I figured that at the 6 month mark, it was the right time to take stock of what we’ve learned about this disease.
What we’ve learned about testing
We started out with tests that were unreliable and took too long to come back. It’s hard to believe how long we were asking the same question: “Why does our testing still suck so much?”
But things are getting better as we’re learning more.
Testing is important for two major reasons:
Individual impact - Identifying people who have COVID
Public health impact - Identifying outbreaks so that we can reduce spread
On an individual level, testing still isn’t available quite as easily as it should be, and the results aren’t perfect in terms of accuracy, but for the most part, it’s adequate for people who have symptoms of disease.
On a public health level, we’re not where we need to be. The key for testing is fast, low cost, rapidly deployed testing to identify outbreaks and contain them.
While the rapid testing isn’t as accurate as the nasopharyngeal swab we use on sick people, testing a lot is of enormous public health utility.
Widely available rapid testing of people without symptoms is a vital part of the way forward to get back to school, work, and our regular way of life.
What we’ve learned about treatment
In short: we’ve learned a ton about how to treat these patients.
First, avoiding a ventilator makes sense if you can. Not all cases can - patients with COVID induced ARDS (acute respiratory distress syndrome) certainly require a ventilator, and often for a long period of time. But for those folks with more mild respiratory disease, holding off on intubation avoids a lot of the associated risks - prolonged immobilization, heavy doses of multiple medications for sedation, and infection risk from medical lines and tubes.
Second, the list of medications that work is short: dexamethasone (or other steroids) and remdesivir.
Dexamethasone is a game changer for the sickest patients. Remdesivir probably helps a bit on the margins for folks with mild disease but it isn’t a panacea.
Hydroxychloroquine appears to be useless.
Convalescent plasma has no proof of effectiveness despite widespread use.
The other things that have been discussed - tocilizumab, colchicine, zinc, azithromycin, etc - either have no data or unimpressive data to suppor their use.
But better supportive care and the addition of steroids have caused death rates to go down.
What we’ve learned about antibody testing
No much to report here. Antibody testing is both unreliable - testing negative doesn’t mean you haven’t had COVID - and not particularly useful - testing positive doesn’t mean much about immunity, especially long term.
I wouldn’t waste my money on this test.
If you’ve had testing confirmed COVID, you probably have some immunity, but how much and for how long remains unclear.
What we’ve learned about the heart
Just like with any viral infection, COVID can impact the heart.
The scary research that’s been presented on athletes is sort of meaningless.
But there is a suggestion that there may be long term cardiovascular impact after COVID infection, at least for a subset of the population. It’s too early to draw conclusions, but there are some really smart people who are worried about this.
The story of COVID and the heart is still to be written.
What we’ve learned about a vaccine
I’ve been incredibly concerned about the rush to approve a vaccine as well as the adverse event signal that we’ve seen from early trial data.
But perhaps an even bigger concern is that the ongoing vaccine trials may not be even asking the right questions.
Eric Topol and Peter Doshi raise vital questions about the design of these trials in their NY Times Op-Ed:
Knowing how a clinical trial defines its primary endpoint — the measure used to determine a vaccine’s efficacy — is critical to understanding the knowledge it is built to discover. In the Moderna and Pfizer trials, even a mild case of Covid-19 — for instance, a cough plus a positive lab test — would qualify and muddy the results. AstraZeneca is slightly more stringent but would still count mild symptoms like a cough plus fever as a case. Only moderate or severe cases should be counted.
There are several reasons this is a problem.
The two most concerning major questions here:
If a vaccine only reduces mild cases but doesn’t prevent deaths or reduce severe cases, what is the point?
How certain are we about extrapolating the results from a clinical trial enrolling 30,000 or 40,000 patients to a vaccine that may be distributed to hundreds of millions?
There’s a leap of faith that we will need to take in any vaccine before mass distribution, and so far we’ve seen a lot to be concerned about.
I’ll give Dr. Topol and Dr. Doshi the last word here:
The trials need to focus on the right clinical outcome — whether the vaccines protect against moderate and severe forms of Covid-19 — and be fully completed. It is not too late for the companies to do this, and the Food and Drug Administration, which reviewed the protocols, could still suggest modifications.
These are some of the most important clinical trials in history, affecting a vast majority of the planet’s population. It’s hard to imagine how much higher the stakes can be to get this right. Cutting corners should not be an option.
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