The trending wild-ass guess on #COVID19 of the day is this paper by gastroenterologist Farid Jalali, joining a spate of papers that boil down to explaining how respiratory symptoms in #coronavirus are mere epiphenomena of something else. This time, thrombotic vasculopathy.

His suggestion, as far as I understand, is a combo of antithrombotic therapy for moderate to severe cases (hep, tPA, defibrotide) and ACEIs, NAC, NSAID avoidance and vit C (omg.) for early endothelial dysfunction. Okay, that sounds ok, but I'm not buying it just yet.

To an extent, he's acknowledging perhaps the weakest point of his argument himself: mortality is a strong correlate of certain risk factors, which just so happen to be also risk factors for hypercoagulation. They're correlates and co-causals, not necessarily causally related.

I am a lot more dubious about the coagulation explanation for ischaemic CNS insults (which we have relatively little evidence on as to their existence to begin with) and cardiac insults (which are well enough explained without coagulopathy).

I'm in particular concerned about his suggestion that glucocorticoids could worsen endothelial dysfunction and therefore ought to be avoided, because for the inflammatory component of ARDS, it seems to work relatively well.

So: this is darn interesting stuff, but I'm taking it with a nice heaping of salt. I'd like to see whether the evidence from incidental anticoagulation (e.g. hep to make ECMO work) supports any of his statements.

(I'd add that one of the things he asserts, discordant rise of D-dimer in the setting of normalising ferritin, CRP and IL-6 (w/ or w/o toci), is not something I've seen documented at a large scale anywhere.)