key: cord-1018208-3ndolxsb
authors: Parodi, Aurora; Gasparini, Giulia; Cozzani, Emanuele
title: Could antiphospholipid antibodies contribute to coagulopathy in COVID-19?
date: 2020-06-04
journal: J Am Acad Dermatol
DOI: 10.1016/j.jaad.2020.06.003
sha: bc1c46e0ef4f51d3d66ea8dcb7ab5fe699b98b09
doc_id: 1018208
cord_uid: 3ndolxsb

nan

1 Could antiphospholipid antibodies contribute to coagulopathy in COVID-19? We read with great interest the article "A Dermatologic Manifestation of COVID-19: Transient Livedo Reticularis" 1 . COVID-19 patients may develop a thrombophilic state and extensive 23 microthromobsis was found at autoptic examination in numerous organs 2 . We agree with Manalo 24 et al. that it is very likely that this phenomenon doesn't spare the skin, where it plausibly 25 expresses itself through livedo reticularis and acral ischemia 1, 2 . Hypercoagulability in COVID-19 26 patients shouldn't be underestimated, since it may lead to death by determining in the worst-case 27 scenario pulmonary embolism or disseminated intravascular coagulation (DIC) 2 . The pathogenesis 28 underlying thrombophilia in COVID-19 patients is not clear yet. Notably, a recent report described 29 three cases of Chinese patients affected by COVID-19 with coagulopathy and antipospholipid 30 antibodies (aLP) 3 . Indeed, livedo reticularis and acral ischemia can be seen antiphospholipid 31 syndrome (APS). DIC as well may be substantially indistinguishable from the most severe form of 32 APS, namely catastrophic APS, in which a "thrombotic storm" affects simultaneously three or 33 more organs or systems, leading to multiorgan failure 4 . Zhang et al. caution that this might be a 34 fortuitus coincidence, since aLP may arise transiently in patients with critical illness and various 35 infections 3 . Moreover, the presence of these antibodies may rarely lead to thrombotic events that 36 are difficult to differentiate from other causes of multifocal thrombosis in critically patients, such 37 as disseminated intravascular coagulation, heparin-induced thrombocytopenia, and thrombotic 38 microangiopathy 3 . 39

Nonetheless, APS often arises after infectious triggers 4 . Viral induction of autoimmunity can be 40 explained by various phenomena, including epitope spreading, molecular mimicry, cryptic antigen, 41 and bystander activation 5 . Remarkably, over 1/3 of the immunogenic proteins in SARS-CoV-2 have 42 potentially problematic homology to proteins that are key to the human adaptive immune 43 3 system 5 . Moreover, SARS-CoV2 seems to induce organ injury through alternative mechanisms 44 beyond direct viral infection, including immunological injury 2 . 45

Could it be possible for aLP to play a role in inducing coagulopathy in COVID-19 patients? Is 46 coagulopathy in COVID-19 patients a manifestation of mild to very severe forms of APS? 47 This is could be a far-fetched hypothesis, but perhaps worth perusing to better understand the 48 pathological mechanisms underlying the very dangerous coagulopathy seen in COVID-19 patients. 49

Moreover, aPL testing is simple, rapid and easily accessible. Further studies are needed to 50 investigate the validity of this hypothesis and its possible clinical implications on anticoagulant 51 therapy management in COVID-19 patients. 52 53

A Dermatologic Manifestation of COVID-19: Transient 56

Clinical and Coagulation Characteristics of 7 Patients With Critical 59

Pneumonia and Acro-Ischemia

Coagulopathy and Antiphospholipid Antibodies in Patients with 62

Antiphospholipid syndrome -an update

Pathogenic Priming Likely Contributes to Serious and Critical Illness and 66

Mortality in COVID-19 via Autoimmunity