TY - JOUR T1 - Antiphospholipid antibodies and COVID-19 thrombotic vasculopathy: one swallow does not make a summer JF - Annals of the Rheumatic Diseases JO - Ann Rheum Dis SP - 1105 LP - 1107 DO - 10.1136/annrheumdis-2021-220520 VL - 80 IS - 9 AU - Pier Luigi Meroni AU - Maria Orietta Borghi Y1 - 2021/09/01 UR - http://ard.bmj.com/content/80/9/1105.abstract N2 - The high morbidity and mortality of COVID-19 have been associated with the thrombotic microangiopathy described in the patients in addition to the increased prevalence of thrombosis affecting medium/large arterial and venous vessels.1 2 Initial reports demonstrating prolonged activated partial thromboplastin times (aPTT) and positivity for antiphospholipid antibody (aPL) assays raised the issue of whether common pathogenic mechanisms were shared by the antiphospholipid antibody syndrome (APS) and COVID-19.3 4 In particular, the systemic thrombotic microangiopathy and the increased circulating levels of proinflammatory cytokines underlined the similarity between catastrophic APS (CAPS) and COVID-19.5 6 The similarities between APS/CAPS and COVID-19 are even more complex and intriguing as summarised in table 1. A proinflammatory environment that includes the activation of the complement system has been reported in all these conditions, although at different degrees. The involvement of several cell types playing a role in the coagulation cascade, such as platelets, monocytes and neutrophils, has been described which is closely associated with the proinflammatory and prothrombotic phenotypes.7 8 In particular, an endothelial perturbation is generally thought to be a common denominator in these diseases and several authors described it with the term ‘endothelitis’ in the COVID-19.9–11 View this table:In this windowIn a new windowTable 1 Pathogenic pathways reported in APS, CAPS and COVID-19Both proinflammatory cytokine (eg, interleukin-6) and complement activation products (ie, C5a and C5b9) were thought to play a role in mediating the endothelitis together with a direct effect of SARS-CoV-2 on the endothelium.10–12 However, the SARS-CoV-2 endothelial tropism is still a matter of debate despite the presence of the entry molecule (ie, ACE2) on the endothelial surfaces.13 So, it is not surprising that additional potential mediators of endothelial perturbation have been suggested. In particular, aPL came into the limelight because of their well-known … ER -