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You’re choosing a narrow band of the population. Undoubtedly there are thousands of groups out there who, by way of genotype, phenotype or lifestyle, are at higher risk.

Teasing these all out is going to be the work of the next decade. It’s all in the last paragraph - (to paraphrase) ‘we’re having to learn in months what we’ve had hundreds of years to learn about other diseases’

When I was at Med school I naively thought ‘there will be no new pathophysiology’ - we knew all the continents and had mapped most of the interiors, in varying levels of detail. This is an entirely new continent. (So was vaping associated lung injury actually)

It’s fascinating



It's not that narrow among aforementioned populations though - 15% iirc.

Enough that (again, as a naïve layman) I'd have thought it would be noticed or considered when discussing clotting and DVT/PEs? And enough to have an counteracting impact on the opposite African/Caucasian divide that's actually being seen - not to say that they couldn't coexist, but that if so it'd make the latter even more dramatic.


From UpToDate:

In the general population without a personal history of VTE, a study involving 1690 unrelated individuals from Europe found a prevalence of FVL of approximately 4 percent, and a study involving 356 individuals from Canada found an incidence of approximately 5 percent [47,48]. In a series of 4047 men and women participating in the Physicians' Health Study and the Women's Health Study (both in the United States), the following frequencies for FVL heterozygosity were found [49]:

●Caucasians – 5.3 percent ●Hispanic Americans – 2.2 percent ●Native Americans – 1.2 percent ●African Americans – 1.2 percent ●Asian Americans – 0.45 percent

A higher prevalence of FVL (12 to 14 percent) has been reported in populations in parts of Greece, Sweden, and Lebanon

Compared to a more likely cause for thrombophilia in the patient population, ie inflammatory response, endothelial damage, up regulation of clotting factors; I think focusing on factor V Leiden (and I’m speaking just as a clinician, not as someone who has had to work with covid patients, we’ve had relatively SFA here in Australia thankfully) is a footnote. And any patient who is admitted is going to be on anticoagulants anyway, nullifying most of any procoagulant effect of FVL in hospitalised patients.

It might show up in the data, it might be a footnote, but treatment would be covered under normal VTE prophylaxis (and seems like many protocols are now stepping up fairly significantly the prophylaxis regime)


"This is an entirely new continent. (So was vaping associated lung injury actually)"

I haven't read anything about this yet. Link?


https://en.wikipedia.org/wiki/Vaping-associated_pulmonary_in...

Probably not inherent to vaping, but a nasty additive in some of the fluid.


It was from using vit-e oil as the base liquid, found exclusively in one individuals homemade THC carts (although others are suspected as having the same mistake). The media really dropped the ball on tht one.


You also kind of dropped the ball on providing a source.


Find it yourself, a single Google search will find that he's correct about the vitamin E


A deeper dive will find that it’s not conclusively proven yet, and I can’t find much evidence for the “one guy’s fuckup” assertion.




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