COVID-19 and ischemic stroke: Should we systematically look for lupus anticoagulant and antiphospholipid antibodies?

Aubignat, M.; Godefroy, Olivier

doi:10.1016/j.neurol.2020.05.001

Cited by 19 publications

(22 citation statements)

References 15 publications

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“…Lupus anticoagulant is the most commonly found marker of antiphospholipid syndrome in patients with severe forms of SARS-CoV-2 infection. But the presence of anti-cardiolipin and anti-β2-glycoprotein I antibodies also constitute a significant thrombotic risk factor, even if the patients infected with this virus do not have a history of anti-phospholipid syndrome 53 .…”

Section: The Role Of Laboratory In Highlighting Hypercoagulabilitymentioning

confidence: 99%

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Coagulation disorders in SARS-CoV-2 infection

Mihăilă¹,

Mihaila²

2020

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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A better understanding of the pathogenetic mechanisms triggered by SARS-CoV-2 infection may contribute to a more effective management of patients with COVID-19. Coagulation dysfunction is a key pathogenetic element of this disease as well as a challenge for practitioners. Marked inflammatory process found in severe forms of COVID-19, the complement activation, the cytokine storm, and disruption of the renin-angiotensin-aldosterone system are involved in the onset of thrombotic microangiopathy and large vessel coagulopathy. Virus-induced procoagulant activity occurs at the systemic level. Intravascular microthrombi disrupt vascularization in various tissues and organs, contributing to the occurrence of multiorgan failure and explain the higher morbidity and all-cause mortality of patients. It is estimated that almost 20% of patients with COVID-19 have significant coagulation disorders, and about a quarter of those hospitalized in intensive care units are prone to develop thrombosis events under prophylactic anticoagulant treatment. Some of patients who have been immunized after healing from the SARS-CoV-2 infection have a hypercoagulable state and are prone to develop thrombosis. Hypercoagulability is supported by thrombelastographic analysis: patients have an acceleration of the propagation phase of blood clot formation and higher clot strength. Markers of coagulation dysfunction in SARS-CoV2 are: decreased platelet count, increased INR, presence of fibrin degradation products, and especially higher plasma levels of D-dimers, which predict unfavorable outcome in these patients. Age, pre-existing diseases and associated risk factors, together with careful monitoring of clinical evolution and laboratory parameters allow the choice of the best personalized prophylactic or curative anticoagulant treatment.

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Section: The Role Of Laboratory In Highlighting Hypercoagulabilitymentioning

confidence: 99%

“…Lupus anticoagulant and anti-phospholipid antibodies may be transiently positive in acute infections, with no clinical signs, and do not require anticoagulant treatment. But, their presence in COVID-19 patients is an indication for full intensity prophylactic anticoagulant treatment 53,64 .…”

Section: The Need For High-prophylactic Anticoagulant Dosesmentioning

confidence: 99%

Coagulation disorders in SARS-CoV-2 infection

Mihăilă¹,

Mihaila²

2020

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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“…Anticoagulation treatment, particularly low molecular weight heparin, has been recommended due to benefits in reducing mortality and anti-inflammatory properties in patients with sepsis-induced coagulopathy scores ≥4 and D-dimers > 6-fold of upper limit of normal (3.0 μg/ml) [2,8,9]. However, full anti-coagulation is not routinely recommended [2,10]. Of note, our patient was fully anticoagulated prior to development of her stroke.…”

mentioning

confidence: 90%

Stroke as a delayed manifestation of multi-organ thromboembolic disease in COVID-19 infection

Liu

Khawaja

Majjhoo

2020

Journal of the Neurological Sciences

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Stroke as a delayed manifestation of multi-organ thromboembolic disease in COVID-19 infection Dear Editor, Here, we report a patient with COVID-19 with delayed onset multivessel cerebral infarcts and systemic pro-thrombotic state and coagulopathy manifesting as acute limb ischemia and pulmonary embolism to highlight the importance of vigilant monitoring for neurologic impairment and coagulopathy in patients with severe cases of COVID-19 infection. In December 2019, a cluster of pneumonia cases emerged in Wuhan, Hubei Province; later identified as a novel severe acute respiratory syndrome coronavirus (SARS-CoV-2), also known as coronavirus disease 2019 (COVID-19). The virus has spread globally with subsequent designation as a pandemic by the World Health Organization. Clinical manifestations encompass numerous systems, including pulmonary, renal, gastrointestinal, hepatic, but more recently, neurologic, cardiovascular, and hematologic domains [1]. Guidelines for the management of the neurologic and hematologic complications of COVID-19 are under development. A 72-year-old woman with a past medical history significant for hypertension, diabetes, chronic renal failure, and gout presented with 3 weeks of progressive cough, general myalgia, and shortness of breath. On presentation, she was hypoxic and tachypneic with evidence of wheezing with abnormal lung sounds, but normal neurological examination. Laboratory tests showed leukocytosis, acute kidney injury, transaminitis, and rhabdomyolysis. Elevated C-reactive protein and ferritin were detected. Chest X-ray revealed bilateral patchy airspace opacities, consistent with multifocal pneumonia. The patient was initiated on vancomycin, cefepime and azithromycin. She was confirmed to have a positive COVID-19 PCR-based test, consistent with infection. Hydroxychloroquine could not be started due to a quinine allergy and prolonged QTc interval. On days 3 and 4 of admission, the patient developed acute hypoxic respiratory failure and septic shock, requiring intubation and vasopressor support. The patient's condition continued to decline with persistent bilateral pneumonia, worsening renal failure with uremia, acidosis and hyperkalemia requiring dialysis and lymphopenia. The patient had a repeat COVID-19 test with positive result. A head CT without contrast did not reveal acute pathology. On day 7, the patient was noted to have bilateral light blue or purple skin mottling of both feet with palpable left dorsalis pedis pulse (Fig. 1a and b). The patient did not have a baseline coagulation profile on admission, but, on day 7, a prolonged prothrombin time (PT) and elevated INR were noted (PT 13.5 s (normal: 9.4-11.7); INR 1.32 s (normal: 0.90-1.13)), along with a normal activated partial thromboplastin time (aPTT) of 28.5 s (normal: 23.1-33.1), and platelets (146,000/mm 3 , normal: 150-450,000/mm 3) prior to transitioning from subcutaneous heparin prophylaxis to intravenous heparin infusion due to concerns of COVID-19 related microvascular disease. No antiplatelet or therapeutic a...

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“…96 Despite anticoagulation, a high number of patients with ARDS secondary to COVID-19 developed potentially life-threatening thrombotic complications. 94,[97][98][99] It has been suggested that higher anticoagulation targets may be necessary in severe COVID-19 infection and that antiphospholipid antibodies may help identify patients at a higher risk of thrombosis, who should be fully anticoagulated. 100 This is challenged by studies undermining the reliability of APL antibody testing, as markers of proinflammatory state, such as CRP and Fibrinogen, may lead to false positive or negative APL antibody results.…”

Section: Anti-phospholipid Syndrome and Covid-19mentioning

confidence: 99%

Clinical management of Lupus patients during the COVID-19 pandemic

Mason

Rose

Edwards

2020

Lupus

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Severe acute respiratory syndrome coronavirus (SARS-CoV-2), the virus causing Coronavirus disease 2019 (COVID-19), has had a huge impact on health services with a high mortality associated with complications including pneumonia and acute respiratory distress syndrome. Historical evidence suggests that Lupus patients have a higher incidence of several viral infections. This is likely due to a combination of immune dysfunction, immunosuppressive therapy and excess co-morbidities. In this context there has been concern that Lupus patients may be at a higher risk of developing COVID-19 and suffering a severe disease course. As a result, many Lupus patients have been advised to ‘shield’ by isolating from social contact in the hope that this will reduce the likelihood of infection. Early clinical data does not appear to show that the incidence of COVID-19 is higher in Lupus patients. Reassuringly, the clinical course of COVID-19 in Lupus does not generally seem to be more severe than in the general population. There has been huge interest in repurposing existing drugs as potential treatments, including several used to treat Lupus. Of these, corticosteroids and hydroxychloroquine are the most well researched so far. The current evidence suggests that the corticosteroid dexamethasone improves outcome for the sickest COVID-19 patients requiring respiratory support. Initial reports suggested that hydroxychloroquine could have a positive impact on the course of COVID-19, however larger prospective studies have not supported this. Janus kinase inhibitors, currently being investigated for efficacy in lupus, have been shown to have anti-viral effects in vitro and inhibiting the JAK-STAT pathway may dampen down the host hyper-inflammatory response. Several trials are ongoing to assess the outcome of the use of JAK inhibitors in COVID-19 positive patients. For most patients continuing with their existing therapies to prevent a lupus flare or adverse events associated with sudden corticosteroid withdrawal is important whilst an Individualised risk assessment remains vital.

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COVID-19 and ischemic stroke: Should we systematically look for lupus anticoagulant and antiphospholipid antibodies?

Cited by 19 publications

References 15 publications

Coagulation disorders in SARS-CoV-2 infection

Coagulation disorders in SARS-CoV-2 infection

Stroke as a delayed manifestation of multi-organ thromboembolic disease in COVID-19 infection

Clinical management of Lupus patients during the COVID-19 pandemic

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