There is no approved therapy for coronavirus disease 2019 [severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection], and the number of worldwide deaths on current standard therapy is staggering [1]. Current therapy is aimed at decreasing viral replication, supporting vital functions and addressing the most damaging consequences of the disease such as hyperinflammation (the so-called cytokine storm) and thrombosis. The latter two involve the use of anti-inflammatory therapies and heparin, respectively. We suggest that complement-blocking strategies such as eculizumab should be considered in severe cases not responding well to current therapy, including tocilizumab, in the context of clinical trials. Complement is thought to contribute to microangiopathies associated with infectious diseases [2].Recent histological data from COVID-19 patients are compatible with acute respiratory distress syndrome (ARDS) [3]. Additionally, vascular congestion and inflammatory cell infiltrates were present [4], as well as microvascular thrombi in multiple organs including kidneys in patients who died of COVID-19 and SARS [5,6]. Immunohistochemically, deposits of C5b-9, C4d and mannose-binding lectin-associated serine protease-2 have been found in the microvasculature of lungs and skin in patients with . Furthermore, COVID-19 shares some features with entities that are complement mediated, such as disseminated intravascular coagulation, thrombotic microangiopathy (TMA) and antiphospholipid antibody syndrome. These include increased lactate dehydrogenase (LDH) , platelet disease, hypertransaminasaemia, anaemia and extrapulmonary involvement, such as the
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