Do these two vaccines (J&J and AstraZeneca) have tPA as an adjuvant?
I could see a scenario in which an over-activated fibrinolytic system could steadily consume platelets leaving a patient thrombocytopenic.
I’m also wondering if recent (possibly asymptomatic) infection with SARS-Cov-2 might be at play? I’m not very familiar with the vascular effects of this virus but I could also see how compromised vessel walls could also consume platelets and simultaneously activate the body’s coagulation system.
As a platelet donor, I selectively notice stuff about thromobocytopenia (and thrombocytes in general). It isn't that uncommon for clotting syndromes to be associated with thrombocytopenia, in at least some cases because suddenly forming a lot of clots removes many platelets from circulation (literally). Note also that COVID-19 seems to be associated with thromobocytopenia in some cases, e. g. https://pubmed.ncbi.nlm.nih.gov/32178975/
You wrote, "All have been between the ages of 18 and 48. Even early in 2020, before many treatment modalities were available, patients in this age range were seen to have a case-fatality rate from COVID-19 that is substantially less than 1%, ranging from about 0.2% in the youngest bracket in this range to 0.4% in the oldest bracket. These risks will be lower now." Contrariwise, the variants like B.1.1.7 seem to be more dangerous for younger patients than the originally-detected strain.
As a critical thinking person, it's interesting watching myself think about this matter. I find myself looking for ways to explain away the J&J/AZ clotting phenomenon, because I really, really want it to not be real. It takes real mental effort to acknowledge one's own bias and force oneself to follow the evidence.
Hi John,
Do these two vaccines (J&J and AstraZeneca) have tPA as an adjuvant?
I could see a scenario in which an over-activated fibrinolytic system could steadily consume platelets leaving a patient thrombocytopenic.
I’m also wondering if recent (possibly asymptomatic) infection with SARS-Cov-2 might be at play? I’m not very familiar with the vascular effects of this virus but I could also see how compromised vessel walls could also consume platelets and simultaneously activate the body’s coagulation system.
Hi, John,
As a platelet donor, I selectively notice stuff about thromobocytopenia (and thrombocytes in general). It isn't that uncommon for clotting syndromes to be associated with thrombocytopenia, in at least some cases because suddenly forming a lot of clots removes many platelets from circulation (literally). Note also that COVID-19 seems to be associated with thromobocytopenia in some cases, e. g. https://pubmed.ncbi.nlm.nih.gov/32178975/
You wrote, "All have been between the ages of 18 and 48. Even early in 2020, before many treatment modalities were available, patients in this age range were seen to have a case-fatality rate from COVID-19 that is substantially less than 1%, ranging from about 0.2% in the youngest bracket in this range to 0.4% in the oldest bracket. These risks will be lower now." Contrariwise, the variants like B.1.1.7 seem to be more dangerous for younger patients than the originally-detected strain.
As a critical thinking person, it's interesting watching myself think about this matter. I find myself looking for ways to explain away the J&J/AZ clotting phenomenon, because I really, really want it to not be real. It takes real mental effort to acknowledge one's own bias and force oneself to follow the evidence.