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To address this allegation: this is neither interacts with the rebuttal nor does it address my motivations. I clarified many times that this hyperbolic phrasing was for common purpose rather than mentioning "my hypothesis" time and time again. Either way, my point still stands. https://twitter.com/alexandrosM/status/1463943011700658189 …pic.twitter.com/JMOkUlwBzT
That point being that only a small number of deaths need be attributable to Strongyloides in order for a substantial proportion of the mortality benefit.
I'm not interested in playing mind-reading games with @alexandrosM. So instead I'll just address the rest of his points:
Using the numbers provided here, if 20 patients had a Strongyloides infection, only 2 (10%) of those patients would need to have died from it to explain the majority of the deaths (only 3 patients died), and even if only 1 patient (5%) died from worms, that explains 33% of deathspic.twitter.com/coO2IfNLZ5
A few other things to add: Strongyloides doesn't only disseminate in response to steroids. You don't need to get admitted to the ICU to disseminate. COVID-19 is associated with eosinopenia (cells responsible for fighting parasitic worms) even without steroids.
This intuition pump also isn't compelling for skepticism. Firstly, we don't need to speculate if corticosteroids were given in trials from endemic regions. It happend. Ravikirti gave steroids to ALL patients in the control group (stated in their own publication).pic.twitter.com/qKdf7fHFRB
Lopez-medina included patients on steroids, who started steroids since the onset of symptoms (again, stated in their own publication), you don't need to take my word that this was happening. The authors of trials themselves say it was happening in their own publications!
What about I-TECH? It's not published, but I emailed the principle investigator who confirmed that steroids were indeed given, and all 10 deaths in the control group received steroids.
What about Mahmud? Of the high prevalence trials not reporting steroid usage, Mahmud did not respond to my email. I'll note that methylprednisolone was published as the standard of care for all patients progressing to severe COVID in his country at the time of his trial.
What if they gave Ivermectin to the patients before steroids? If that happened, they would need either exclude them from the endpoint of death or mention this in a separate analysis (this is standard in RCTs where patients in the control group get the treatment intervention).
I'll also add that excluding Mahmud doesn't actually change the conclusions here:pic.twitter.com/2RPcABdDNE
I'll also note that excluding TOGETHER doesn't change the conclusions either. Excluding TOGETHER and Mahmud doesn't change the conclusions either.pic.twitter.com/jucNrs92KR
What about viral positivity? As I noted before, the viral positivity trials do appear to be the textbook example of funnel plot asymmetry, but I was mistaken to think that Strongyloides couldn't explain viral positivity in part either.pic.twitter.com/Aw6MlICKkt
The general idea here is that Th2 loaded patients have decreased risk of decompensation because they have less risk of a cytokine storm associated with Th1 immune responses. So they do better clinically, but clear the virus slower.
So patients with parasites generally do clinically better with COVID, but would be expected to clear the virus at a slower rate. But of course, with strongyloides ... if a patient develops eosinopenia in response to COVID (or steroids) all bets may be off...
Now, this is more speculative. I'm not sure if it explains viral positivity or not, but I was mistaken to claim Strongyloides could not explain it.
Overall, I see Strongyloides hypothesis as an explanation of the majority of the IVM mortality benefit as unproven, but quite plausible.
If character attacks by @alexandrosM and the remainder of his analysis exhausts the skepticism, I find little reason to change my credence
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