Thank you. I have just reviewed some autopsy reports the primary finding is clotting in small vessels in the lungs a microangiopatic process for medical people. ( no not associated with zinc deficiency) We have a lot to learn but this may be why the IL inhibitors work. As to those who flame I don’t take them to heart other than to note the character of those who get nasty discussing things they know little about. May all here find the love out Savior lavished so richly on us this day
I am aware of microangiopathy in the elderly (dementia), those with hypertension and in diabetics, the very targets of this virus. The way it hurts the lungs is bad for them. I looked up Diabetic pulmonary microangiopathy and learned that it may not show as the diabetic has sufficient lung capacity. They call it clinically silent respiratory dysfunction. I don’t know what difference it makes as the diabetics all seem to know their risks with covid-19. Now I will pray for them with more urgency.
Remember Chris? He lived. They never put him on the vent, just plenty of O2. Also anti-virals (yes but not HCQ) and antibiotics (I think?)
https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.25839
That paper about recovery in a seriously ill patient being treated with erythropoietin kept me wondering about what might be happening with that.
I ran across this:
https://content.iospress.com/articles/advances-in-neuroimmune-biology/nib140076
“If high dose of recombinant human erythropoietin is used, it will stimulate platelet production, which is a transient effect. Expanded erythropoiesis exerts a negative impact on platelet production.”
Wouldn’t that be what you’d want in COVID-19 patients who need oxygen (more red blood cells) but are having clotting in the small vessels of the lungs (less platelets)? Would the EPO given to the COVID-19 patient who recovered be considered high dose?
I probably don’t know what I’m talking about but I thought I’d run the idea by an MD.