chango369 wrote:This was tough reading for sure....
In seven patients (four female), regardless of anticoagulation status, all autopsies demonstrated platelet-rich thrombi in the pulmonary, hepatic, renal, and cardiac microvasculature. Megakaryocytes were seen in higher than usual numbers in the lungs and heart. Two cases had thrombi in the large pulmonary arteries, where casts conformed to the anatomic location. Thrombi in the IVC were not found, but the deep leg veins were not dissected.
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Lancet: Megakaryocytes and platelet-fibrin thrombi characterize multi-organ thrombosis at autopsy in COVID-19: A case series
Another paper that discusses COVID-19's coagulopathy and identifies the following key points:
1. SARS-CoV-2 induces robust gene expression and functional changes in platelets.
2. Platelet hyperreactivity may contribute to COVID-19 pathophysiology through increased
platelet-platelet and platelet-leukocyte interactions
Available through link to PDf: Platelet Gene Expression and Function in COVID-19 Patients
Troubling for sure, but a good article.
Another one saying much the same thing...
ScienceDaily:
30 June 2020
COVID-19 causes 'hyperactivity' in blood-clotting cells
Could good-old acetylsalicylic acid (aspirin), long used as an anti-inflammatory and a coagulation inhibitor, have a role in treatment of Covid-19?
From the ScienceDaily article (link above):
(My bold)
...
Surprisingly, Campbell and his colleagues didn't detect evidence of the virus in the vast majority of platelets, suggesting that it could be promoting the genetic changes within these cells indirectly.
One possible mechanism is inflammation, according to Bhanu Kanth Manne, Ph.D., one of the study's lead authors and a research associate with the University of Utah Molecular Medicine Program (U2M2). In theory, inflammation caused by COVID-19 could affect megakaryocytes, the cells that produce platelets. As a result, critical genetic alterations are passed down from megakaryocytes to the platelets, which, in turn, make them hyperactive.
In test tube studies, the researchers found that pre-treating platelets from SARS-CoV-2 infected patients with aspirin did prevent this hyperactivity. These findings suggest aspirin may improve outcomes; however, this will need further study in clinical trials. For now, Campbell warns against using aspirin to treat COVID-19 unless recommended by your physician.
In the meantime, the researchers are beginning to look for other possible treatments.
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