by Oui
Fri Mar 12th, 2021 at 09:36:35 AM EST
From the earliest studies, this has been reported. Developing vaccines which induces immunization to the SARS CoV-2 virus may very likely cause such an effect receiving a jab by a minimal number of healthy persons. Having a genetic risk of blood clots in the family, Leyden V blood factor, I'm well aware of the risk and will be critical to the vaccine I will receive. No Russian roulette on not having a choice but just get in line and STFU.
Scott Morrison says AstraZeneca vaccine is safe for Australians after reports of blood clots | The Guardian |
Let Pharma and politicians speak ... it's a lot about business and opening the economy ...
Coronavirus blood-clot mystery intensifies | Nature - May 8, 2020 |
Purple rashes, swollen legs, clogged catheters and sudden death -- blood clots, large and small, are a frequent complication of COVID-19, and researchers are just beginning to untangle why. For weeks, reports have poured in of the disease's effects throughout the body, many of which are caused by clots. "This is like a storm of blood clots," says Behnood Bikdeli, a fourth-year cardiology fellow at Columbia University in New York City. Anyone with a severe illness is at risk of developing clots, but hospitalized patients with COVID-19 seem to be more susceptible.
Studies from the Netherlands and France suggest that clots arise in 20-30% of critically ill COVID-19 patients.
SARS-CoV-2 and coagulation disorders in different organs | Life Sciences |
In this review, we focused on COVID-19 coupled with the coagulopathy contributes to severe outcome inclusive of comorbidities such as venous thromboembolism, stroke, diabetes, lung, heart attack, AKI, and liver injury. Initially, the COVID-19 patient associated coagulation disorders show an elevated level of the D-dimer, fibrinogen, and less lymphocyte count such as lymphopenia. COVID-19 associated with the Kawasaki disease has acute vasculitis in childhood which further affects the vessels found all over the body.
COVID-19 linked with the thrombotic microangiopathy triggers the multiple vasculitis along with the arterioles thrombosis, medium, large venous and arterial vessels mediates the disseminated intravascular coagulation (DIC). SARS-Co-V-2 patients have reduced primary platelet production, increased destruction of the platelet, decreased circulating platelet leads to the condition of increased thrombocytopenia which contributes to the coagulation disorder.
Massive inflammatory response, the cytokine storm | John Hopkins |
COVID-19 and Blood Clots | Harvard - Nov. 9, 2020 |
Patients hospitalized with severe COVID-19 infections who have high levels of the blood clotting protein Factor V are at elevated risk for serious injury from blood clots such as deep vein thrombosis or pulmonary embolism, according to a new study by Harvard Medical School investigators at Massachusetts General Hospital.
On the other hand, critically ill patients with COVID-19 and low levels of factor V appear to be at increased risk for death from a form of coagulopathy that resembles disseminated intravascular coagulation (DIC)--a devastating, often fatal abnormality in which blood clots form in small vessels throughout the body, leading to exhaustion of clotting factors and proteins that control coagulation.
Their findings, based on studies of patients with COVID-19 in Mass General intensive care units, point to disturbances in factor V activity as both a potential cause of blood clotting disorders with COVID-19 and potential methods for identifying at-risk patients with the goal of selecting the proper anticoagulation therapy.
Can Autoimmune Antibodies Explain Blood Clots in COVID-19?
Our blood vessels normally strike a balance between producing clotting and anti-clotting factors. This balance keeps us ready to seal up vessels after injury, but otherwise to keep our blood flowing at just the right consistency so that neutrophils and platelets don’t stick and form clots at the wrong time. But previous studies have suggested that SARS-CoV-2 can tip the balance toward promoting clot formation, raising questions about which factors also get activated to further drive this dangerous imbalance.
To learn more, a team of physician-scientists, led by Yogendra Kanthi, a newly recruited Lasker Scholar at NIH’s National Heart, Lung, and Blood Institute and his University of Michigan colleague Jason S. Knight, looked to various types of aPL autoantibodies. These autoantibodies are a major focus in the Knight Lab’s studies of an acquired autoimmune clotting condition called antiphospholipid syndrome. In people with this syndrome, aPL autoantibodies attack phospholipids on the surface of cells including those that line blood vessels, leading to increased clotting. This syndrome is more common in people with other autoimmune or rheumatic conditions, such as lupus.
It’s also known that viral infections, including COVID-19, produce a transient increase in aPL antibodies. The researchers wondered whether those usually short-lived aPL antibodies in COVID-19 could trigger a condition similar to antiphospholipid syndrome.
