Biden’s ‘Test to Treat’ COVID Plan: Good Sound Bite, Bad Policy
It ignores the risk of hazardous drug-drug interactions with the Pfizer pill.
As someone who has closely followed and written extensively about the development of COVID-19 vaccines and drug treatments since the beginning of the pandemic, one pronouncement in President Joe Biden’s State of the Union speech raised red flags: “We’re also ready with antiviral treatments. If you get COVID-19, the Pfizer pill reduces your chances of ending up in the hospital by 90% … And we’re launching the ‘Test to Treat’ initiative so people can get tested at a pharmacy, and if they’re positive, receive antiviral pills on the spot at no cost.”
Highly effective antiviral pills, given out in a timely way – and free. Good sound bite, but bad idea – which Biden’s medical advisers should have warned him about.
The “Pfizer pill,” Paxlovid, consists of two kinds of tablets – drugs called nirmatrelvir and ritonavir. The first of these is the actual antiviral agent, while the second inhibits an enzyme that degrades the first, thereby increasing the concentration of nirmatrelvir in the blood. The problem is that ritonavir has problematic interactions with a huge number of commonly prescribed drugs, especially in the patient population most in need of COVID-19 treatment: Paxlovid is available under an Emergency Use Authorization for adults with a positive COVID-19 test “who are at high risk for progression to severe COVID-19, including hospitalization or death” – in other words, the elderly and others with one or more comorbidities.
The FDA’s Paxlovid fact sheet lists six pages of “Established and Other Potentially Significant Drug Interactions.” And while patients could probably do without or reduce the dose of their statin or anti-gout medicine during the five-day course of Paxlovid, that’s not the case for many other drugs on the drug interactions list. They include blood thinners and drugs that prevent cardiac arrhythmias, seizures, and psychotic behavior. A physician offered this pertinent comment on my Wall Street Journal commentary on this subject:
As an internist I have found safe prescribing of Paxlovid to be challenging. Those with comorbid conditions in greatest need of Paxlovid typically will be on chronic medications with high-risk interactions. The process of reconciling copious dangerous interactions and weighing the risks of holding or changing maintenance medications should not be shortchanged for convenience.
That perfectly captures the conundrum and gets us back to Biden’s Test to Treat initiative. Picture the patient at the pharmacy with a positive COVID-19 test. Has he brought a complete list of his medications? Who’s going to decide whether the probability of dangerous drug-drug interactions outweighs the potential benefit of Paxlovid?
Even the pharmacist isn’t likely to be capable of making that judgement. Pharmacists do make binary decisions about drug-drug interactions – they consult a database, and if there is a potential problem, the drug isn’t dispensed; otherwise, the patient gets the drug – but they’re ill-equipped to decide whether, for example, the patient can do without his blood thinner or seizure medication, or how to adjust the dose, for five days.
Test to Treat is half-baked. That’s unfortunate, because it needn’t have been so. A thoughtful and important announcement would have been that the National Institutes of Health was in the process of determining how nirmatrelvir could be administered alone. In the absence of ritonavir (thereby eliminating the drug interaction problems), to maintain therapeutic blood levels it would need to be given more frequently – say, every six hours, instead of twice a day. That would be an easy experiment to do, requiring only the measurement of blood levels of nirmatrelvir after different dosage schedules, in order to find one that would achieve appropriate levels.
Test to Treat is popular among American voters, with 71% approval, according to a recent Morning Consult/Politico poll. It could be an important tool, suppressing not only Omicron but also surges of future SARS-Cov-2 variants of concern, and possibly reducing the frequency of “long COVID,” but it needs to be further fleshed out to make it practical. That should have been done prior to a triumphal public announcement by the president.
Henry I. Miller, a physician and molecular biologist, is a senior fellow at the Pacific Research Institute. He is the co-discoverer of a critical enzyme in the influenza virus and was the founding director of the FDA’s Office of Biotechnology.