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We still do not know everything about COVID-19, but the current knowledge based on the clinical picture of patients indicates that comorbidities favor the severe course of coronavirus infection. New research is helping to shed light on why this is happening and has highlighted the role of the clotting mechanism in COVID-19.
Co-morbidities and the acute course of COVID-19
There are many risk factors that increase the likelihood of severe COVID-19 disease. Very often, comorbidities are mentioned here, from which a patient infected with the SARS-CoV-2 coronavirus suffers. These include chronic diseases, including diabetes, high blood pressure, heart disease, cerebrovascular disease, kidney disease, and chronic obstructive pulmonary disease (COPD).
Researchers are still trying to determine exactly what mechanisms cause these ailments to negatively affect the course of COVID-19. In a new study published in the journal Physiological Reviews, the authors note that haemorrhage and bleeding disorders are at the forefront of the ailments contributing to the death of COVID-19 patients.
Dr. Hong-Long Ji of the University of Texas Health Science Center in Tyler and other study co-authors believe that an overactivity of the anticoagulant system may cause a dysfunction of the coagulation system. This means excessive activity anticoagulant mechanisms may cause bleeding in patients infected with the coronavirus.
Too intense fight against blood clots is called hyperfibrinolysis. The process of fibrinolysis consists in breaking down blood clots – in its course it occurs to break down fibrin. In the publication, Dr. Hong-Long Ji and his team point out that patients with acute COVID-19 may have fibrin degradation products and have a reduced platelet count. Such results may indicate the occurrence of hyperfibrinolysis.
Also read: Degradation products of fibrinogen / fibrin
According to the researchers, multi-organ haemorrhage, as well as the association of fibrinolysis with patient mortality, prove that hyperfibrinolysis may explain the high mortality of patients with comorbidities.
Another issue supporting this thesis relates to plasminogenem (a protein in the blood) i plasmin (an enzyme that dissolves clots), high levels of which are found in coronavirus-infected patients who also suffer from diabetes, heart, lung or kidney disease. Too high levels of plasminogen and plasmin can cause hemorrhages.
D-dimer levels in COVID-19 patients
The authors of the study found in 97 percent. patients treated for COVID-19 high levels of d-dimers, a protein made when blood clots break down. In more severe cases of coronavirus infection the level of d-dimers was higherwhich was seen especially in patients with acute respiratory distress syndrome (ARDS). D-dimer levels gradually decreased in patients without ARDS or treated with COVID-19.
According to the researchers, the use of antiplasmin complexes to reduce hyperfibrinolysis could be a promising strategy that could improve clinical outcomes in people with comorbidities.
Have a question about the coronavirus? Send them to the following address: [email protected]. You will find a daily updated list of answers HERE: Coronavirus – frequently asked questions and answers.
Also read:
- Coronavirus dangerous for seniors. How should the elderly protect themselves against it?
- Why does the coronavirus kill some and run like a cold in others?
- How does the body fight the coronavirus?