Abstract
Infection with SARS-COV-2 leads to a number of pathologies in the hematopoetic system that have significant impact on clinical symptoms and mortality. There are 3 stages of infection: (1) early upper respiratory tract infection with fever and lymphopenia (2) pulmonary phase and (3) hyperinflammatory phase with the clinical signs of organ failure such as ARDS/shock. Hyperinflammation, which is triggered by activation of T cells and monocytes/macrophages, is essential for organ pathologies. Interferon IFN-ɣ, tumor necrosis factor (TNF)-α, IL-10 and interleukin-6 (IL-6) play important roles as mediators of inflammation. In analogy to the cytokine release syndrome (CRS) after CAR-T cell therapy, the therapeutic activity of the IL-6 receptor antibody tocilizumab is investigated in clinical studies.
The coagulation system is activated during the inflammatory phase of COVID infection, most likely on the pathophysiological basis of immune thrombosis. Clinically, there is a significantly increased incidence of venous (especially pulmonary artery embolism), but also arterial thromboembolism (TE). In laboratory chemistry, the D-dimer, fibrinogen but also vWF and FVIII are significantly increased. Guidelines for the prophylaxis and therapy of COVID-associated coagulopathy have been developed. Analogous to other viral infections, there are approaches to passive immunization using convalescent plasma. Its administration has shown promising activity in first uncontrolled case series and is currently being examined in clinical studies worldwide for its therapeutic activity.
Die Infektion mit SARS-CoV-2 führt zu einer Reihe von Pathologien im hämatopoetischen System, die die klinische Symptomatik und die Mortalität erheblich beeinflussen. Auch kommt es durch die Aktivierung des Gerinnungssystems zu einer deutlich erhöhten Inzidenz an Thromboembolien. Der Beitrag stellt Pathomechanismen, relevante diagnostische Parameter und den aktuellen Stand zur passiven Immunisierung durch Rekonvaleszentenplasma vor.
Schlüsselwörter
Hyperinflammation - CRS - Tocilizumab - Rekonvaleszentenplasma - Thromboembolie
Key words
hyperinflammation - CRS - tocilizumab - convalescent plasma - thrombembolism
