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Clotting in severe COVID-19 blamed on auto-antibodies against phospholipids and cardiolipin: reasons to use anticoagulants routinely in hospital patients.

2020-11-09
SARS-COV-2 EM photo courtesy NIAID

This paper, published on November 2, 2020 in Science magazine, describes autoantibodies found in 172 patients in hospital with severe COVID-19.

From the abstract:

Here, we 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. We 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. 

https://stm.sciencemag.org/content/early/2020/11/02/scitranslmed.abd3876

Thus, about half of patients with severe COVID-19 had at least short-term presence of auto-antibodies (antibodies that are aimed at normal parts of the patient’s own body) that promote blood clotting.

These auto-antibodies are the source of the widespread blood clots that form in severe virus disease: clots in veins and arteries that block blood flow to vital parts of the lungs, brain, kidneys, and other body regions.

Patients with severe infection are often killed or rendered permanently disabled by blood clots in the brain, lungs, and kidneys. Strokes (cerebrovascular accidents or CVA) appear suddenly in patients who are in the intensive care unit and cause permanent paralysis. Lung infarctions (due to blood clots in the pulmonary arteries) cause further lowering of blood oxygen levels in patients already suffering from pneumonia.

This explains why the patients with severe COVID-19 benefit from routine administration of anticoagulants (drugs that prevent blood clotting.) Cheap and effective anticoagulants are widely available: warfarin, coumadin, and the like. Newer anticoagulants are also readily available. Further study will probably reveal anticoagulant drugs that are more effective against auto-antibody-mediated blood clots.

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