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Source: COVID-19 Latest  Nov 03, 2020  3 years, 5 months, 2 weeks, 21 hours, 27 minutes ago

COVID-19 Latest: University Of Michigan And NIH Study Identifies Autoimmune Antibodies As New Cause Of COVID-19 Blood Clots

COVID-19 Latest: University Of Michigan And NIH Study Identifies Autoimmune Antibodies As New Cause Of COVID-19 Blood Clots
Source: COVID-19 Latest  Nov 03, 2020  3 years, 5 months, 2 weeks, 21 hours, 27 minutes ago
COVID-19 Latest:  A new study by researchers from University of Michigan, U.S. NIH-Bethesda and Shanghai Jiao Tong University School of Medicine-China have surprisingly discovered that the culprit that is causing blood clots in most  severe COVID-19 infections is an autoimmune antibody that's circulating in the blood, attacking the cells and triggering clots in arteries, veins, and microscopic vessels. Blood clots can cause life-threatening events like strokes and in COVID-19, these microscopic clots may restrict blood flow in the lungs, impairing oxygen exchange.


 
Besides COVID-19 disease, these clot-causing antibodies are typically seen in patients who have the autoimmune disease called antiphospholipid syndrome.
 
Antiphospholipid syndrome is an acquired and potentially life-threatening thrombophilia in which patients develop pathogenic autoantibodies targeting phospholipids and phospholipid-binding proteins (aPL antibodies).
 
These aPL antibodies were recently detected in patients with COVID-19. In this study, the researchers measured eight types of aPL antibodies in serum samples from 172 patients hospitalized with COVID-19. These aPL antibodies included anticardiolipin IgG, IgM and IgA; anti-β2 glycoprotein I IgG, IgM, and IgA; and anti-phosphatidylserine/ prothrombin (aPS/PT) IgG and IgM. The study team detected aPS/PT IgG in 24% of serum samples, anticardiolipin IgM in 23% of samples, and aPS/PT IgM in 18% of samples. Antiphospholipid autoantibodies were present in 52% of serum samples using the manufacturer’s threshold and in 30% using a more stringent cutoff (≥40 ELISA-specific units). Higher titers of aPL antibodies were associated with neutrophil hyperactivity including the release of neutrophil extracellular traps (NETs), higher platelet counts, more severe respiratory disease, and lower clinical estimated glomerular filtration rate.
 
Similar to IgG from patients with antiphospholipid syndrome, IgG fractions isolated from COVID-19 patients promoted NET release from neutrophils isolated from healthy individuals. Furthermore, injection of IgG purified from COVID-19 patient serum into mice accelerated venous thrombosis in two mouse models.
 
These study findings suggest that half of patients hospitalized with COVID-19 become at least transiently positive for aPL antibodies and that these autoantibodies are potentially pathogenic.
 
The study findings were published in the peer reviewed journal: Science Translational Medicine https://stm.sciencemag.org/content/early/2020/11/02/scitranslmed.abd3876
 
The connection between autoantibodies and COVID-19 was unexpected, says co-corresponding author Dr Yogen Kanthi, M.D., an assistant professor at the University of Michigan Medicine Frankel Cardiovascular Center and a Lasker Investigator at the National Institutes of Health's National Heart, Lung, and Blood Institute.
 
Dr Kanthi told Thailand Medical News, "In patients with COVID-19, we continue to see a relentless, self-amplifying cycle of inflammation and clotting in the body. Now we are learning that autoantibodies could be a culprit in this loop of clotting and inflammation that makes people who were already struggling even sicker."
 
The study team says that studies of COVID-19 have shown some of the worst clotting ever seen.
 
Dr Jason Knight, M.D., Ph.D., a rheumatologist at Michigan Medicine who has been studying antiphospholipid syndrome antibodies in the general population for years and is the co-corresponding author of the study commented, "Half of the patients hospitalized with COVID-19 were positive for at least one of the autoantibodies, which was quite a surprise.”
 
Dr Knight, also an associate professor of internal med