The official numbers say you are only about 4% likely to have a rebound after paxlovid. But anecdotally, it seems much higher. So i thought I’d poll this group, and see what our collective anecdotes say.
0 voters
I didn’t vote that way, since the choices are all 1st person, but both my parents (96 and 90) had Covid recently, took Paxlovid, and both had rebound. But it really didn’t impact them much, just a few more days of feeling under the weather.
I have not had Covid, but my wife did 7 weeks ago, got Paxlovid immediately, tested negative and then rebounded kind of hard.
DH and I both had Covid in late August (I was nearly as sick as he was, and I’m vaccinated, while he isn’t). Neither of us gave much thought to Paxlovid, TBH. DH elected to tough it out, a friend of mine suggested it to me, but I take atorvastatin (Lipitor). Having had a TIA in April, I decided that staying on the statin was higher priority than asking my doctor for Paxlovid. Apparently, it doesn’t play nicely with statins.
Only one in my group of five took Paxlovid while recovering from COVID, and no rebound. (She’s almost 80 with a slew of health complications, hence her taking it in the first place. She recovered in 24 hours. No issues. Her son (also caretaker), 47, who caught it first, did not take Paxlovid and had three days of severe flu-like symptoms, but also recovered fine.)
I had covid and recovered rather quickly without Paxlovid. My wife got sick a few days later, took Paxlovid and rebounded hard. We are both fully boosted.
But the OP’s poll doesn’t include people who rebounded without Paxlovid. Anecdotes are a lousy way to collect data unless one is trying to reach a pre-conceived conclusion.
I have covid now and have to decide about Paxlovid by tomorrow. I am leaning against.
Well, the poll is in the first person to reduce bias. And i note that no one has voted “rebound”, yet.
And anecdotally, i suppose my mother died of a covid rebound before paxlovid hit the market. Although her initial symptoms never returned, it was really secondary symptoms that killed her. (Covid attacked her brain, and i think that’s what killed her, not the lungs.)
Anecdotes are less reliable than formal studies, but also produce data much faster. Most meaningful “after-market” studies are inspired by anecdotes. In the middle ages, anecdotes inspired cities to quarantine against plague when scientists were saying “that’s just superstition”. A lot of anecdotes are a red flag. Anecdotally, i know an awful lot of people who rebounded after paxlovid, whose untreated family members did better.
My issue with Paxlovid is the number of interactions and contraindications.
We had a script filled for my 84 year old mother when she had Covid in June, but after reading the patient info we had her speak with her GP first. He advised her against it, largely due to her kidney disease.
I took Paxlovid and rebounded. The entire course of my illness mirrored Joe Biden’s…or rather his mine. I was two days ahead.
I didn’t take it because I’m on blood thinners, and by the time I got my telesession with a doctor I was pretty much recovered.
My wife did take it and didn’t rebound. However she recovered more slowly than I did.
I just erased a 600 word rant about my MAGA-loving doctor brother, and the horseshit advice he’s been giving our elderly mom, but buried in there was some commentary about a recent meta-study on paxlovid rebound. So, we’ll at least leave the study part, which suggest weak or no indication of a difference between antiviral rebound and regular rebound.
I mean, I’m always glad to go back to the rant, but that’s a different thread, I suppose.
(Background)
Mrs. Cretin and I were infected simultaneously* last mid-November. I’m 73, she’s 77. During Day Two of symptoms we got Paxlovid shots. Symptoms eased up after several days, had several days feeling pretty normal, then had a rebound that lasted another couple of days. Infection to end of Pax rebound: two weeks.
I’m now nearly back to normal, but Mrs. C has long Covid (the only symptom being fatigue, but it’s a bitch). Considering our ages we’re VERY damn glad we got the Pax shots.
I’d like to apologize for my earlier rant. One of the painful emotions resulting from our infection is anger, I apparently needed to vent. Sorry it went in all your particular directions.
No need to apologize, IMHO. May your (justified) rant serve as a reminder to others.
Yeah, it seems like rebound might be a feature of the virus itself rather than the Paxlovid, and we just tend to notice it more when the Paxlovid is involved.
I’d also say that people who take Paxlovid are way more likely to retest in five days than those who don’t, so they are more likely to call their course a rebound rather than just a protracted course with a brief lull in symptoms.
Anyway, yeah, I had the classic rebound case on Paxlovid. The rebound was worse than the first round, and I narrowly avoided getting admitted to the hospital.
100% of my friends who had rebound took paxlovid. (some took paxlovid without rebound). Almost all my friends test when they start to feel better to decide when to hang out with friends again, so I don’t think there’s a lot of bias in “who tests” among my observed sample.
Why yes, I do know where to buy boxes of 25 high-quality tests cheap. (A German company. Shipping is expensive, but the tests are really cheap per unit. They sell boxes of one test, too, but the boxes of 25 take up MUCH less space in your cupboard. And you are buying at least 50 tests for the shipping to be worth it.)
There is a bias in that people at higher risk in general are more likely to take paxlovid, and people at higher risk are also more likely to rebound. But recent studies have shown more rebound among paxlovid patients, it’s not just my friends.
from the CDC article linked in this post:
Some observational studies demonstrated a higher frequency of rebound among treated persons (10%–14%) (11 ,14 ,22 ) than reported by the randomized controlled trial, EPIC-HR (8 ,10 ) (Supplementary Table, https://stacks.cdc.gov/view/cdc/137156). Viral rebound might occur in persons on antiviral treatment because they are at high risk for severe disease and might have host factors, such as immunosuppression, that contribute to the natural variability in viral dynamics (21 ). Risk factors for rebound appear to be similar to risk for severe disease, but further studies are needed to understand whether persons with certain characteristics or underlying medical conditions are predisposed to experiencing rebound. Another important consideration is that persons receiving antiviral treatment might be at higher risk for experiencing rebound given the viral suppression related to use of treatment early in the disease course and resumption of viral replication after completion of treatment because of delayed viral clearance. This elevated risk could be due to early discontinuation of antiviral treatment or the need for longer courses of treatment among certain persons, such as those who are immunocompromised (14 ). Two ongoing clinical trials of nirmatrelvir/ritonavir will further characterize the frequency of rebound after different durations of nirmatrelvir/ritonavir treatment among immunocompromised subjects¶¶ and the potential benefit of nirmatrelvir/ritonavir retreatment among subjects with posttreatment rebound.***
To summarize:
Some observational studies show higher rebound rates among those who took antivirals. This might be due to their being at higher risk to begin with (older, more immune compromised, etc.) but the early viral suppression might also contribute. It’s possible that this is because the standard course of treatment isn’t long enough, and there is a study underway to investigate the impact of different courses of treatment with antivirals.
I’m rooting on that study, by the way, as I suspect a longer course of treatment would be better.
Just to add other parts of the conclusions, for those interested:
Four retrospective cohort studies found similar frequencies of viral rebound among persons who did and did not receive COVID-19 antiviral treatment (10,12,15 – 16). Three studies found higher frequencies of rebound among treated persons: the first study examined persons with chronic lymphocytic leukemia (14); the second examined treated persons who were older (median age = 57 years versus 39 years; p<0.001), received more COVID-19 vaccine doses (4 versus 3; p<0.001), and had higher rates of immunosuppression (32% versus 9%; p<0.001) than did untreated persons (11); and the third used propensity score matching to ensure the treated and untreated groups were well matched, but had limited follow-up time (13).
A large retrospective, observational study found similar rates of rebound and no statistically significant differences among patients treated with nirmatrelvir/ritonavir (6.6%; 95% CI = 4.1%–10.5%), molnupiravir (4.8%; 95% CI = 3.3%–6.9%) and those who received no treatment (4.5%; 95% CI = 3.9%–5.2%) (Table 2) (15). Persons with immunocompromising conditions had higher odds of viral rebound regardless of treatment status: nirmatrelvir/ritonavir (odds ratio [OR] = 7.37; 95% CI = 2.56–21.26), molnupiravir (OR = 3.05; 95% CI = 1.28–7.25), and no treatment (OR = 2.21; 95% CI = 1.50–3.27). Among patients receiving nirmatrelvir/ritonavir, the odds of virologic rebound were higher among those aged 18–65 years compared with those aged >65 years (OR = 3.09; 95% CI = 1.00–9.53), those with high comorbidity prevalence (score >6 on the Charlson Comorbidity Index [OR = 6.02; 95% CI = 2.09–17.38]), and those concomitantly taking corticosteroids (OR = 7.51; 95% CI = 1.67–33.82), whereas the odds