Lupus anticoagulant is frequent in patients with Covid-19: Response to Reply.

We have recently published in the Journal of Thrombosis and Haemostasis the presence of lupus anticoagulant (LAC) at high frequency in Covid-19 patients (1). Different authors had confirmed these results (2). Connell and colleagues had discussed, in the Journal, technical points concerning LAC as well as anti-phospholipids (aPL) auto-antibodies detection (3).

Acquired Thrombotic Thrombocytopenic Purpura After BNT162b2 COVID-19 Vaccine: Case Report and Literature Review.

Thrombotic thrombocytopenic purpura (TTP) is a thrombotic microangiopathy that is deadly if not treated promptly. The treatment of choice in patients presenting with TTP is plasma exchanges. However, immunosuppressive therapy and caplacizumab have significantly improved outcomes in TTP. This microangiopathy is classically divided into 2 entities: hereditary and acquired TTP (aTTP), caused by an autoantibody against ADAMTS 13. We present a case study of a patient wth TTP occurring after a second dose of the BNT162b2 (Pfizer-BioNTech) COVID-19 vaccine along with a review of the literature. A 55-year-old patient presented with gastrointestinal symptoms, anemia, and severe thrombocytopenia. The blood film revealed the presence of schistocytes. A diagnosis of aTTP was established because the patient had severe ADAMTS 13 deficiency and autoantibodies against ADAMTS 13 were positive. This episode occurred 10 days after the patient received the COVID-19 vaccine. The patient received plasma exchanges, prednisone, rituximab, and caplacizumab and achieved complete remission. Ten patients with aTTP induced by the COVID-19 vaccine have been reported in the literature. Most of these situations occurred after the second dose of COVID-19 vaccine, and 7 patients were noted to have received the BNT162b2 vaccine. Caplacizumab was used in 6 patients, and complete remission was achieved in 8 patients.

Macrophage Activation in COVID-19 Patients in Intensive Care Unit.

We report six cases of patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, admitted to intensive care unit (ICU), for whom bone marrow aspirate revealed hemophagocytosis. We compared their clinical presentation and laboratory findings to those that can be encountered during a hemophagocytic lymphohistiocytosis. These observations might evoke a macrophage activation mechanism different from the one encountered in the hemophagocytic lymphohistiocytosis (HLH).

Multiple Arterial Thrombosis in a 78-Year-Old Patient: Catastrophic Thrombotic Syndrome in COVID-19.

We describe a patient with coronavirus disease 2019 (COVID-19) and multiple concomitant thromboses occurring on the 9th day of hospital stay. Thromboses were found in distinct zones of the aorta, as well as in the renal, humeral, and pulmonary arteries. The extensive biological workup performed following this catastrophic thrombotic syndrome found no evidence for underlying prothrombotic disease. In light of current evidence regarding endothelium abnormalities related to COVID-19, this extreme case of catastrophic thrombotic syndrome suggests that COVID-19 can induce severe arterial thrombosis following intense endothelial activation.

Nous décrivons le cas d'un patient atteint de la maladie à coronavirus 2019 (COVID-19) et présentant de multiples thromboses concomitantes survenant au 9e jour d'hospitalisation. Les thromboses ont été identifiées dans des zones distinctes de l'aorte, ainsi que dans les artères rénales, humérales et pulmonaires. Un examen biologique approfondi effectué à la suite de ce syndrome thrombotique catastrophique n'a révélé aucun signe de maladie prothrombotique sous-jacente. À la lumière de ces éléments concernant les anomalies de l'endothélium liées à la COVID-19, ce cas extrême de syndrome thrombotique catastrophique suggère que la COVID-19 peut induire une thrombose artérielle sévère suite à une activation endothéliale intense.

Antiphospholipid antibodies in patients with coronavirus disease 2019 infection hospitalized in conventional unit.

Antiphospholipid (aPL) antibodies can arise transiently at times of viral diseases. The objective of this work was to evaluate the incidence of aPL antibodies in patients hospitalized in conventional unit for coronavirus disease 2019 (COVID-19) infection and confirmed venous thromboembolic events (VTE) associated with aPL antibodies. 41 patients infected with COVID-19 were tested for aPL antibodies. None had reported history of aPL syndrome. Arterial and venous duplex ultrasound of lower limbs was performed in all patients at Day 0 and Day 5. All patients had antithrombotic-prophylaxis upon admission using lower molecular weight heparin with Enoxaparin. Biological parameters were collected and analyzed. Nine patients (22%) developed VTE and seven (17%) were positive for aPL antibodies of which five had isolated positive lupus anticoagulant. The sixth patient was double aPL positive IgM anticardiolipin (147.8 U/ml) and anti-Beta2 Glyco protein 1 (97.3 U/ml) antibodies. The seventh was triple positive, IgM anticardiolipin 85.6 UI/ml, IgM anti-Beta2 Glyco protein 1 63.0 U/ml and positive lupus anticoagulant. Among the seven patients with aPL antibodies 2 (28.60%) had VTE. However, the incidence of VTE in patients negative for aPL antibodies was also significant as 20.6% (seven of 34). aPL antibodies were significantly associated with the transfer to ICUs of, P = 0.018. Not only the incidence of aPL antibodies was quite significant within our cohort, but also we observed 28.6% of VTE in aPL-positive patients. We strongly recommend routine testing for aPL antibodies in COVID-19 patients and systematic screening with duplex ultrasound search of vascular complications.