And this was known to be a problem a year ago and Merck kept pushing it forward despite its low efficacy and risk for driving mutation. Meanwhile Paxlovid is underprescribed despite its effectiveness.
And then I've heard from too many patients their doctor doesn't think they need it because they're not that sick, so it's not worth managing the drug interactions. Unfortunately, paxlovid needs to be started within five days of symptom onset, but most patients aren't going to be hospitalized within those first five days.
Given the lack of monoclonal antibodies, the potential mutagenic effect of molupiravir, and the less-than-steller impact of remdesivir... if I or someone I loved got covid, I'd be jumping on paxlovid since there aren't many other options right now.
Managing drug interactions for paxlovid isn't much more complicated than inputting meds into a web form and looking at the color of the box that pops up after. I think most providers can handle that if they know these tools exist and get past the reflex of "paxlovid has drug interactions, you don't want to take it."
Managing drug interactions is part of ordering medications, and if it's really taking that much time (i.e., the EHR isn't just doing all the work for you), then it'd result in a higher E&M code when it's billed out. Medication management, in some cases, can also be billed and reimbursed by the pharmacist.
So, totally agree that the US medical system is optimized for billing. I don't think those of us in the US should be ok with that, and I don't think it's an excuse in this case to not prescribe paxlovid to patients who want it and would qualify for it.
By whom?
Medical professionals are overwhelmed, so you can't hospitalize these patients to monitor their compliance. And this is, in the large, not a demographic you can trust for maximal patient compliance.
One's ability to "trust" a patient isn't a factor here, and is, frankly, pretty condescending. The patient and provider have aligned interests, it's just a matter of ensuring the provider is making sure the patient understands what's going on. The provider should be doing that in all of their encounters, so that's nothing specific to paxlovid.
I suspect you haven't worked with elderly patients.
I help a relative manage his care. I keep having to hide the DayQuil so he doesn't take it alongside his arthritis medication and overdose on acetamenophin. He "knows" he's not supposed to, but it doesn't click when the pills are in his hand and his nose is running (because he took it for decades prior to the arthritis prescription and deeply-ingrained habits are not easily replaced). He definitely tells the doctor he understands, and the doctor believes him, but it's not like the doctor is in any way responsible for verifying that information.
Drug interactions are way past the maximum complexity capacity of the median patient at high risk for death by COVID.
> but it's not like the doctor is in any way responsible for verifying that information.
Yeah, that's the exact point. Everybody does things that the doctor says they shouldn't, but that doesn't mean we withhold care as a result.
People stop antibiotics before the scripts are done. People smoke and drink too much, some even drink and drive. People don't take their blood pressure or cholesterol or even HIV meds as prescribed. Some people take half a pill because the pill they were prescribed is "too big" -- people are weird and do all kinds of things.
Paxlovid is no different. The provider can be checking drug interactions, making adjustments as needed and counseling the patient. That's their job. They can't babysit the patient all of the time. If it's clear the patient doesn't understand and can't care for themselves, then there are larger conversations to be had.
My point is that deciding not to prescribe a medication to a qualifying patient because it generally has too many drug interactions and patients can't be trusted with their health is not ok. Patients don't need to understand that ritonavir is a protease inhibitor that was incidentally found to inhibit cytochrome P450-3A4, which subsequently boosts the levels of many other medications. They just need to know to stop taking their cholesterol pill for the next week. That's all. Some, like your elderly relative, may not be able to follow that direction. But there are millions of high risk people who are able to do that, and shouldn't be denied care based on the assumption they're incompetent.
If you're going to construct a new strawman argument, don't make up quotes that I never wrote. I also have a lot of thoughts about how controlled substance laws create problems and harm patients. But I'll stick to the main point of this thread: paxlovid drug interactions are easily checked and managed for the majority of patients, and should not be a reason for providers to reflexively deny prescription requests for it.
According to the CDC, risk factors that make you at "high risk" include being over 50, having a mood disorder (including anxiety and depression), being obese or overweight, being physically inactive, being a current or former smoker, or having asthma: https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-care/...
Most Americans would check one of those boxes, even the healthy and young among us. And some of those (e.g., "physically inactive") are pretty ill-defined that you could argue even more fit in that category. Just saying you're anxious about covid outcomes should qualify you for paxlovid because anxiety is a risk factor.
Many of the infectious disease doctors I work with think that paxlovid should be offered to virtually everybody because it seems to decrease your viral load (this could decrease the chance of onward transmission), there may be a decrease in risk of long covid, it may shorten your symptom duration, and there aren't many other treatment options if you get sicker. So, short of being on one of the medications that's absolutely contraindicated, their opinion is generally if you want paxlovid you should get it.
So if your doctor is saying you don't need it or don't qualify, and you want to take it, I would find a different doctor or use a telemedicine provider.
Never have had that type of experience with any drug.
Infuriating that, in the midst of the opioid crisis, the government wouldn't even consider permitting safe and effective treatment.
This paper [2] is a review of deaths associated with ibogaine known to the authors. They contacted different clinics around the world known to use ibogaine. They found 19 deaths over an 18 year period. 14 of these deaths had post-mortem data and 12 of the 14 had clear comorbidities that likely substantially contributed (e.g. also using heroin and meth, or having severe heart problems already).
You can find a number of papers[3], here is one for example, where no side effects are reported for ibogaine - "In two Phase 1 studies using very low doses, single 20 mg doses of ibogaine were well tolerated (N = 21), with no effect on vital signs and no adverse effects". And, here is the conclusion of that paper, just for fun - "A single ibogaine treatment reduced opioid withdrawal symptoms and achieved opioid cessation or sustained reduced use in dependent individuals as measured over 12 months".
Even if those were valid side effects, you'd still have to put them in context - being an opiod addict is likely much riskier than taking a one time dose of ibogaine in a clinical setting with a doctor's supervision. Net - ibogaine treatment is negative side effect.
1 - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4837967/
2 - https://pubmed.ncbi.nlm.nih.gov/22268458/
3 - https://www.tandfonline.com/doi/full/10.1080/00952990.2017.1...
If you’re a high risk patient like an addict, when you end up in the ER for whatever, they’re just going to cut off whatever medication you’re on, keep you from dying, and kick you out as soon as they aren’t liable.
Still a big improvement, but it makes me wonder whether a longer course of Paxlovid might have cleared the symptoms more completely. I have read that there have been suggestions that the five day course still leaves a significant amount of virus in the body and that lengthening it has been considered, but the FDA has not done anything about it.
The immune system often reacts to viral fragments leftover from replication or destruction. Some viruses are (hypothesized to be?) adapted to this, e.g. delaying sneezing and coughing (or at least the deliberate exacerbation of it) until viral load and viral shedding can be higher. Viral fragments can linger much longer than the primary infection, and in the case of COVID-19 are hypothesized to be responsible for or at least part of the process of some long-COVID symptoms.
Yes, agreed. But I have also read that studies of patients who took the 5-day course of Paxlovid showed that there were still significant numbers of "unassembled" viruses--i.e., the only reason they had not become full COVID viruses that could infect other cells was that Paxlovid was blocking the last stage of virus assembly--remaining at the end of the 5-day course, and once the Paxlovid stops, those unassembled viruses can now assemble themselves and cause further infection. This has been hypothesized to account not only for lingering symptoms but for recurrence of more severe symptoms in a significant number of patients.
That's wild, and apparently has only seen relatively recent confirmation as an evolved phenomenon according to this 2019 Quanta Magazine article: https://www.quantamagazine.org/viruses-can-scatter-their-gen...
What I was describing is a consequence of the way Paxlovid works: it doesn't "kill" the virus or get your immune system to kill it, it just stops the last step of virus assembly inside cells by inhibiting the enzyme, protease, that catalyzes that step. So while you are taking Paxlovid the virus can still go through all the stages of getting inside cells (the normal way, not the different way described in the Quanta article--each virus particle just infects one cell and does all of its replication there), replicating its RNA there, and expressing all of the proteins that form a complete virus particle along with the RNA; it just can't do the very last step, assembling all of those pieces into more complete virus particles, while the protease inhibitor from Paxlovid is present. But once you stop Paxlovid, the protease inhibitor goes away and all of those virus pieces can now assemble (each set of pieces inside a single cell) to become full virus particles that can infect more cells.
The worst side effect was the blood pressure. My eyes almost popped out of their sockets!
You may have recovered quickly regardless.
I never took paxlovid and my covid symptoms lasted 2 days and i recovered quickly.
N = 1 experiences arent convincing data.
Well, quite.
Of the four confirmed Covid cases we've had in our immediate family in the last 12 months, three of us took nothing stronger than standard painkillers and didn't even need to speak to a doctor; my OH spoke to our doctor and was given an inhaler to help with the cough.
https://www.empr.com/home/news/drugs-in-the-pipeline/mixed-r...
So, it's not a strong enough or consistent enough difference between treatment and placebo to be certain that it isn't just chance. (this could happen if for example if out of our 1000 data points, 2 people on placebo were hospitalised but only 1 on the treatment was hospitalised. That'd be "a 50% reduction in risk", but not be statistically significant since it could easily have just been random chance when we're talking about such a small difference).
Probably needs an even larger sample population to really nail down whether it's real or not. Seems suggestive that all the various reported tests showed (inconclusive) benefits when you'd expect an actually-ineffective treatment to show results varying randomly in both "effective" and "not-effective" directions, though that could certainly be positive reporting bias, especially since it's being run and reported by a company with a financial stake in the results.
But since we know the strains have changed over time it seems the most reasonable explanation as to why efficacy has dropped off.
Then the secondary analysis of another 1163 patients failed to show a difference AND the delta between the two arms was smaller than the first analysis.
Its trending towards no difference between arms.
And symptom relief has a huge subjective aspect to it since it based on a patient questionnaire.
If it shows no difference in hospitalization or death but some small effect on symptoms it has little value as a treatment. It going to end up like Tamiflu.
And i just checked clinicaltrials.gov, Pfizer terminated the trial.
This study just isn't powered well enough to say for sure whether Paxlovid provides a hospitalization/death benefit or not for the standard risk group. It also doesn't really provide any good information about whether newer variants cause Paxlovid to work better or worse.
https://www.scientificamerican.com/article/what-is-paxlovid-...
[0] https://www.npr.org/sections/health-shots/2016/09/28/4956945... [1] https://thehill.com/blogs/congress-blog/politics/452654-for-...