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Could severe COVID-19 be considered a complementopathy?
  1. Katerina Chatzidionysiou,
  2. Elisabet Svenungsson and
  3. Francesca Faustini
  1. Rheumatology Unit, Karolinska University Hospital, Karolinska Institutet Department of Medicine Solna, Stockholm, Sweden
  1. Correspondence to Dr Katerina Chatzidionysiou; Aikaterini.Chatzidionysiou{at}ki.se

https://doi.org/10.1136/lupus-2020-000415

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    COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Acute respiratory distress syndrome (ARDS), observed in most critically ill cases with SARS-CoV-2, is a life-threatening inflammatory lung injury.1 It necessitates hospitalisation, oxygen supplementation and in some cases mechanical ventilation, and is associated with high mortality rates, reaching around 40%.2

    It is the effects of an over-reacting immune system, rather than the viral load, which are believed to cause ARDS. A cytokine storm characterised by proinflammatory cytokines, such as interleukin (IL)-1 and IL-6, together with hypercoagulability is seen in a majority of hospitalised patients. Elevated D-dimer, lactate dehydrogenase and fibrinogen and clinical thromboembolic manifestations, such as pulmonary emboli, are common features of severe COVID-19. Zhang et al 3 recently reported significant coagulopathy with multiple infarctions accompanied by prothrombotic antiphospholipid antibodies in three cases of COVID-19. Endothelial damage, …

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