Covid-19 CasesTo rapidly communicate information on the global clinical effort against Covid-19, the Journal has initiated a series of case reports that offer important teaching points or novel findings. The case reports should be viewed as observations rather than as recommendations for evaluation or treatment. In the interest of timeliness, these reports are evaluated by in-house editors, with peer review reserved for key points as needed. Coagulopathy and Antiphospholipid Antibodies in Patients with Covid-19We describe a patient with Covid-19 and clinically significant coagulopathy, antiphospholipid antibodies, and multiple infarcts. He was one of three patients with these findings in an intensive care unit designated for patients with Covid-19. This unit, which was managed by a multidisciplinary team from Peking Union Medical College Hospital in the Sino-French New City Branch of Tongji Hospital in Wuhan, China, was set up on an emergency basis to accept the most critically ill patients during the outbreak of Covid-19. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection was confirmed in all the patients by reverse-transcriptase-polymerase-chain-reaction (RT-PCR) assay or serologic testing.A 69-year-old man with a history of hypertension, diabetes, and stroke presented with fever, cough, dyspnea, diarrhea, and headache. Covid-19 was diagnosed in the patient on January 25, 2020, on the basis of RT-PCR testing that detected SARS-CoV-2. The initial treatment was supportive; however, the illness subsequently progressed to hypoxemic respiratory failure warranting the initiation of invasive mechanical ventilation.

The role of clinical laboratory data in the differential diagnosis of the severe forms of COVID-19 has not been definitely established. The aim of this study was to look for the warning index in severe COVID-19 patients. We investigated 43 adult patients with COVID-19. The patients were classified into mild group (28 patients) and severe group (15 patients). A comparison of the hematological parameters between the mild and severe groups showed significant differences in interleukin-6 (IL-6), D-dimer (D-D), glucose, thrombin time, fibrinogen, and C-reactive protein (P < .05). The optimal threshold and area under the receiver operator characteristic curve (ROC) of IL-6 were 24.3 and 0.795 µg/L, respectively, while those of D-D were 0.28 and 0.750 µg/L, respectively. The area under the ROC curve of IL-6 combined with D-D was 0.840. The specificity of predicting the severity of COVID-19 during IL-6 and D-D tandem testing was up to 93.3%, while the sensitivity of IL-6 and D-D by parallel test in the severe COVID-19 was 96.4%. IL-6 and D-D were closely related to the occurrence of severe COVID-19 in the adult patients, and their combined detection had the highest specificity and sensitivity for early prediction of the severity of COVID-19 patients, which has important clinical value. K E Y W O R D S D-dimer, diagnostic utility, IL-6, the severe COVID-19

Objective Coagulopathy is one of the characteristics observed in critically ill patients with coronavirus disease 2019 (COVID‐19). Antiphospholipid antibodies (aPLs) contribute to coagulopathy, though their role in COVID‐19 remains unclear. This study was undertaken to determine the prevalence and characteristics of aPLs in patients with COVID‐19. Methods Sera collected from 66 COVID‐19 patients who were critically ill and 13 COVID‐19 patients who were not critically ill were tested by chemiluminescence immunoassay for anticardiolipin antibodies (aCLs), anti–β2‐glycoprotein I (anti‐β2GPI) (IgG, IgM, and IgA), and IgG anti‐β2GPI–domain 1 (anti‐β2GPI–D1) and IgM and IgG anti–phosphatidylserine/prothrombin (anti‐PS/PT) antibodies were detected in the serum by enzyme‐linked immunosorbent assay. Results Of the 66 COVID‐19 patients in critical condition, aPLs were detected in 31 (47% ). Antiphospholipid antibodies were not present among COVID‐19 patients who were not in critical condition. The IgA anti‐β2GPI antibody was the most commonly observed aPL in patients with COVID‐19 and was present in 28.8% (19 of 66) of the critically ill patients, followed by IgA aCLs (17 of 66, or 25.8%) and IgG anti‐β2GPI (12 of 66, or 18.2%). For multiple aPLs, IgA anti‐β2GPI + IgA aCLs was the most common antibody profile observed (15 of 66, or 22.7%), followed by IgA anti‐β2GPI + IgA aCL + IgG anti‐β2GPI (10 of 66, or 15.2%). Antiphospholipid antibodies emerge ~35–39 days after disease onset. A dynamic analysis of aPLs revealed 4 patterns based on the persistence or transient appearance of the aPLs. Patients with multiple aPLs had a significantly higher incidence of cerebral infarction compared to patients who were negative for aPLs (P = 0.023). Conclusion Antiphospholipid antibodies were common in critically ill patients with COVID‐19. Repeated testing demonstrating medium to high titers of aPLs and the number of aPL types a patient is positive for may help in identifying patients who are at risk of developing cerebral infarction. Antiphospholipid antibodies may be transient and disappear within a few weeks, but in genetically predisposed patients, COVID‐19 may trigger the development of an autoimmune condition similar to the antiphospholipid syndrome (APS), referred to as “COVID‐19–induced APS‐like syndrome.” Long‐term follow‐up of COVID‐19 patients who are positive for aPLs would be of great importance in understanding the pathogenesis of this novel coronavirus.

CD39/CD73-adenosine pathway has been recently defined as an important tumor-induced immunosuppressive mechanism. We here documented a fraction of CD11bCD33 myeloid-derived suppressor cells (MDSCs) in peripheral blood and tumor tissues from non-small cell lung cancer (NSCLC) patients expressed surface ectonucleotidases CD39 and CD73. Tumor TGF-β stimulated CD39 and CD73 expression, thereby inhibited T cell and NK cell activity, and protected tumor cells from the cytotoxic effect of chemotherapy through ectonucleotidase activity. Mechanistically, TGF-β triggered phosphorylation of mammalian target of rapamycin, and subsequently activated hypoxia-inducible factor-1α (HIF-1α) that induced CD39/CD73 expression on MDSCs. CD39 and CD73 on MDSCs, therefore, link their immunosuppressive and chemo-protective effects to NSCLC progression, providing novel targets for chemo-immunotherapeutic intervention.