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Endothelium dysfunction and thrombosis in COVID-19 with type 2 diabetes

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Abstract

SARS-CoV-2 can directly or indirectly damage endothelial cells. Endothelial injury, especially phosphatidylserine (PS) exposure on the outer membrane of cells, can more easily promote thrombosis. Type 2 diabetes(T2D) patients were more susceptible to COVID-19, they had more severe symptoms, higher risk of thrombotic complications, and longer duration of post-COVID-19 sequelae. This review provided a detailed overview of the mechanisms underlying endothelial dysfunction in T2D patients with COVID-19 (including long COVID), which may be influenced by hyperglycemia, hypoxia, and pro-inflammatory environments. The mechanisms of thrombosis in T2D patients with COVID-19 are also explored, particularly the effects of increased numbers of PS-exposing particles, blood cells, and endothelial cells on hypercoagulability. Given the high risk of thrombosis in T2D patients with COVID-19, early antithrombotic therapy can both minimize the impact of the disease on patients and maximize the chances of improvement, thereby alleviating patient suffering. We provided detailed guidance on antithrombotic drugs and dosages for mild, moderate, and severe patients, emphasizing that the optimal timing of thromboprophylaxis is a critical factor in influencing prognosis. Considering the potential interactions between antidiabetic, anticoagulant, and antiviral drugs, we proposed practical and comprehensive management recommendations to supplement the incomplete efficacy of vaccines in the diabetic population, reduce the incidence of post-COVID-19 sequelae, and improve patient quality of life.

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This work was supported by grants from the National Natural Science Foundation of China (81970924).

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M.L. wrote first drafts and combined all contributions into the first and subsequent drafts. X.W. revised the manuscript and selected magazine. J.S. designed the study and revised the manuscript and read and contributed to successive drafts. Y.N. was involved in the conception and design of the study and revised the manuscript and read and contributed to successive drafts.

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SEARCH STRATEGY AND SELECTION CRITERIA: We identified references for this Review through searches of PubMed for articles published in English from Jan 1, 2020, to Jan 18, 2022, using the terms “COVID-19”, “COVID-19 sequelae”, “long COVID”“type 2 diabetes”, “hypercoagulation”, “hypercoagulability”, “thrombosis”, “hypoxia”, “macrophage”, “endothelial cells”, “aspirin”, “thrombolysis”, “LWWH”, “anticoagulation”, “antidiabetic drugs”, “antithrombosis”, and “blood glucose monitoring”. Relevant articles were also identified through searches of the authors’ personal files, Google Scholar, as well as from reference lists of identified articles. Articles were initially selected for inclusion based on the opinion of the contributing authors, with each section covered by two or three authors with particular expertise. The chosen references were also reviewed by the wider group when reading successive drafts

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Li, M., Wu, X., Shi, J. et al. Endothelium dysfunction and thrombosis in COVID-19 with type 2 diabetes. Endocrine 82, 15–27 (2023). https://doi.org/10.1007/s12020-023-03439-y

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