Doctors in Brazil reported that they were able to help people with COVID-19 pneumonia—quite significantly, possibly even sparing some from death—by giving a drug called tofacitinib. (Yes, it's a terrible name. This class of immune-modulating drug typically ends in "ib," short for inhibitor, which doesn't roll off the tongue. You may be more familiar with this one as a treatment for rheumatoid arthritis, sold under the brand name Xeljanz. Which is ... no better.)
Using drugs like tofacitinib to help treat people with COVID-19 has been widely speculated about, as a plausible idea, but not yet used or studied widely. That may change in the wake of the current findings. Out of 289 hospitalized patients, those who receive tofacitinib had only an 18 percent chance of dying or going into respiratory failure. I say only because among people who got the placebo, that rate was 29 percent.
Both numbers are too high for comfort, but a difference like that would be meaningful to anyone in that hospital bed.
I'm also drawn to the study because this class of drug can be made cheaply, and given orally, and so could be used in lower-income countries where ICUs and vaccines are few or nonexistent.
And it would make sense if this sort of drug, known as a JAK inhibitor, helped some people with COVID-19. These drugs inhibit a specific inflammatory pathway that's part of the infamous "cytokine storm"—immune-system overdrive—seen when people who suddenly spiral from feeling like they have a bad cold to gasping for air. Other JAK inhibitors have shown some signs of promise, apparently because of their role in blocking our bodies' production of cytokines, mitigating the unwanted surge.
The people in the Brazilian hospital also received other treatments, among various variables that make it difficult to say with confidence that tofacitinib will reliably mitigate the most devastating effects of the disease in other circumstances to the same degree that it appeared to here (or how safely, or who might be best served by taking it). But this is a heartening sign. If it bears out in further studies, JAK inhibitors could add to the growing toolbox of treatment options (steroids, remdesivir, tocilizumab) and help turn the tide in serious cases—help keep people alive who might otherwise have died in the ICU.
Still, for all the advances in treating COVID-19, none of this medicinal progress has fundamentally changed the nature of this disease. None of these drugs comes close to constituting a "cure." Even if an 18 percent chance of respiratory failure or death were one you'd be fine taking, there is much that these numbers don't capture. Being hospitalized, especially in an intensive care unit, is typically a harrowing, life-altering experience. Almost no one who is on the brink of death recovers to 100 percent of what they were before. And even if physiological metrics like lung and cardiac capacity come fully back, the psychological trauma can have lasting effects.
So as news of these treatment advances comes along, and as doctors are gradually able to save lives that would've been lost the year before, remember that we already have several medicines that bring your chances of any such experience down to nearly zero. They work before you even get sick, by training your own cells to fight off the virus without falling into cytokine storm. If everyone had access to these medicines—and chose to take them—we wouldn't need to think about how to pronounce tofacitinib at all.