BackgroundMany studies reported high prevalence of antiphospholipid antibodies (aPL) in patients with COVID-19 raising questions about its true prevalence and its clinical impact on the disease course.MethodsWe conducted a meta-analysis and a systematic review to examine the prevalence of aPL and its clinical impact in patients with COVID-19.Results21 studies with a total of 1159 patients were included in our meta-analysis. Among patients hospitalised with COVID-19, the pooled prevalence rate of one or more aPL (IgM or IgG or IgA of anticardiolipin (aCL) or anti-ß2 glycoprotein (anti-ß2 GPI) or antiphosphatidylserine/prothrombin, or lupus anticoagulant (LA)) was 46.8% (95% CI 36.1% to 57.8%). The most frequent type of aPL found was LA, with pooled prevalence rate of 50.7% (95% CI 34.8% to 66.5%). Critically ill patients with COVID-19 had significantly higher prevalence of aCL (IgM or IgG) (28.8% vs 7.10%, p<0.0001) and anti-ß2 GPI (IgM or IgG) (12.0% vs 5.8%, p<0.0001) as compared with non-critically ill patients. However, there was no association between aPL positivity and mean levels of C reactive protein (mean difference was 32 (95% CI −15 to 79), p=0.18), D-dimer (mean difference was 34 (95% CI −194 to 273), p=0.77), mortality (1.46 (95% CI 0.29 to 7.29), p=0.65), invasive ventilation (1.22 (95% CI 0.51 to 2.91), p=0.65) and venous thromboembolism (1.38 (95% CI 0.57 to 3.37), p=0.48).ConclusionsaPLs were detected in nearly half of patients with COVID-19, and higher prevalence of aPL was found in severe disease. However, there was no association between aPL positivity and disease outcomes including thrombosis, invasive ventilation and mortality. However, further studies are required to identify the clinical and pathological role of aPL in COVID-19.

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The coronavirus disease 19 (COVID-19) is a highly transmittable viral infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 utilizes metallocarboxyl peptidase angiotensin receptor (ACE) 2 to gain entry into human cells. Activation of several proteases facilitates the interaction of viral spike proteins (S1) and ACE2 receptor. This leads to cleavage of host ACE2 receptors. ACE2 activity counterbalances the angiotensin II effect, its loss may lead to elevated angiotensin II levels with modulation of platelet function, size and activity. COVID-19 disease encompasses a spectrum of systemic involvement far beyond respiratory failure alone. Several features of this disease, including the etiology of acute kidney injury (AKI) and the hypercoagulable state, remain poorly understood. Here, we show that there is a high incidence of AKI (81%) in the critically ill adults with COVID-19 in the setting of elevated D-dimer, elevated ferritin, C reactive protein (CRP) and lactate dehydrogenase (LDH) levels. Strikingly, there were unique features of platelets in these patients, including larger, more granular platelets and a higher mean platelet volume (MPV). There was a significant correlation between measured D-dimer levels and MVP; but a negative correlation between MPV and glomerular filtration rates (GFR) in critically ill cohort. Our data suggest that activated platelets may play a role in renal failure and possibly hypercoagulability status in COVID19 patients.

Background Pneumothorax has been increasingly observed among patients with coronavirus disease-2019 (COVID-19) pneumonia, specifically in those patients who develop acute respiratory distress syndrome (ARDS). In this study, we sought to determine the incidence and potential risk factors of pneumothorax in critically ill adults with COVID-19. Method This retrospective cohort study included adult patients with laboratory-confirmed SARS-CoV-2 infection admitted to one of the adult intensive care units of a tertiary, academic teaching hospital from May 2020 through May 2021. Results Among 334 COVID-19 cases requiring ICU admission, the incidence of pneumothorax was 10% (33 patients). Patients who experienced pneumothorax more frequently required vasopressor support (28/33 [84%] vs. 191/301 [63%] P = 0.04), were more likely to be proned (25/33 [75%] vs. 111/301 [36%], P<0.001), and the presence of pneumothorax was associated with prolonged duration of mechanical ventilation; 21 (1–97) versus 7 (1–79) days, p<0.001 as well as prolonged hospital length of stay (29 [9–133] vs. 15 [1–90] days, P<0.001), but mortality was not significantly different between groups. Importantly, when we performed a Cox proportional hazard ratio (HR) model of multivariate parameters, we found that administration of tocilizumab significantly increased the risk of developing pneumothorax (HR = 10.7; CI [3.6–32], P<0.001). Conclusion Among 334 critically ill patients with COVID-19, the incidence of pneumothorax was 10%. Presence of pneumothorax was associated with prolonged duration of mechanical ventilation and length of hospital stay. Strikingly, receipt of tocilizumab was associated with an increased risk of developing pneumothorax.