The first at-home coronavirus test is out, and it's useless

The FDA and a major laboratory testing company, LabCorp, just announced the first FDA-approved at-home test for COVID-19.

The problem is, it's almost useless. Here's why.

1. It's far too expensive, at $119 per test. Only wealthy people will be able to take advantage of this.
2. The kit itself (called the Pixel) is little more than a long Q-tip and saline solution. As the FDA describes it:

"LabCorp’s molecular test permits testing of a sample collected from the patient’s nose using a designated self-collection kit that contains nasal swabs and saline."

Your $119 pays for FedEx shipping both ways and for the actual test, which is done at LabCorp's facility.
3. It's far too slow. You have to apply for the kit, get it authorized by a physician, wait for the kit to arrive, ship it back, and only then will LabCorp run the test. You find out the results online. This sounds like it will take at least 5 days, probably a week. Much faster tests are available already for those who can drive to a testing site.
4. LabCorp doesn't have many of the kits available yet. Their own website, citing "limited quantities," says they will only sell the kits to healthcare workers and first responders for now.
5. For unexplained reasons, the company states that the kits aren't available at all in New York, New Jersey, Maryland, and Rhode Island. As everyone knows by now, New York has more cases than any other state in the country.

I was briefly excited when I saw this announcement. It turns out to describe a low-volume, overpriced test that will likely have little or no impact on the pandemic. We need millions of tests, freely available to everyone, not a small number of expensive tests only available to a few.

A possible treatment for COVID-19?

Amidst all of the unproven and ineffective treatments being promoted for coronavirus treatment, a new possibility has just emerged.

Scientists around the globe are devoting enormous resources to trying to develop new treatments for COVID-19, the pandemic that is sweeping across the world. So far, though, we don't have any effective therapies or vaccines.

That might be about to change. What's particularly exciting is that this new treatment uses a widely-available drug that has already been shown to be safe in humans.

In a new preprint, a team of my colleagues at Johns Hopkins University School of Medicine, led by Maximilian Konig, Bert Vogelstein, Joshua Vogelstein, Susan Athey, Shibin Zhou, and Chetan Bettegowda, describe the potential of prazosin to slow down and possibly prevent one of the worst effects of COVID-19: the cytokine storm.

[Some background: a cytokine storm is an extreme immune response of your own body. When coronavirus (SARS-CoV-2) enters the lungs, your immune system responds with virus-fighting cells that release small proteins called cytokines. In some cases, the immune system just keeps amplifying its response, sending more and more cytokines even though the infection might be under control. If it gets too bad, the cytokine storm itself may be fatal. Cytokine storms have been implicated in other viral diseases, including influenza and SARS.]

Let me start with a caveat: if prazosin works, it isn't a cure. However, it might prevent the need to go on a ventilator, which would be a huge benefit in a country (and a world) that has a severe shortage of ventilators right now. Even more important, it might save patients with severe COVID-19 from dying.

Several of the scientists involved in this new study have shown previously that drugs like prazosin (which are known technically as alpha-1AR antagonists) can prevent a cytokine storm–in mice. They realized that results in mice often fail to translate to humans, but in the current pandemic, how could they find time to do a new study?

They didn't: instead, they looked at a medical database and collected records from 13,125 men who had acute respiratory distress (ARD) from a variety of causes in the years 2007-2015. ARD is not the same as COVID-19, but it's similar; and if a cytokine storm occurs in ARD, patients are more likely to require a ventilator and/or die. Because prazosin is widely used by men (most commonly for enlarged prostates), they were able to compare the outcomes of men who had incidentally been taking prazosin to men who hadn't.

The results: men who had been taking prazosin had a 22% lower risk of either needing a ventilator or dying. That's not a huge effect, but it could be a game changer for our overwhelmed hospitals in the midst of this pandemic. Even a modest reduction in the number of patients needing ventilators–or dying–would be a huge win for public health. Also, the patients in this retrospective study weren't taking prazosin to treat their respiratory distress, and it's possible that higher doses might have a larger effect.

There are many more caveats here. First, the study I'm describing is a medRxiv preprint, meaning that it has not been peer-reviewed. In addition, the data are from a retrospective study of men who had a different disease, not COVID-19. So maybe prazosin won't work to prevent cytokine storms caused by the coronavirus.

But maybe it will. My colleagues shared their preprint with me because they are convinced that, if nothing else, their hypothesis needs to be examined by as many scientists and doctors as possible. They are starting their own clinical trial, but they hope that these preliminary findings "will inspire immediate clinical trials in countries now desperate for new ways to reduce hospital admissions, ventilator needs, sickness, and death."

Prazosin has been in medical use since 1974 and is widely available and inexpensive. It's one of the most promising treatments I've heard of, far more promising than hydroxychloroquine. Even if it only slightly reduces the need for ventilators, it may have a huge impact on this pandemic. We need to start investigating it right away.

(Note: I've made it a rule not to write columns about my own or my colleagues' scientific accomplishments. Many rules are being broken in this pandemic, and I decided the urgency of this potential treatment was more than sufficient to break my usual rule.)