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Upper extremity deep vein thrombosis (UEDVT) accounts for 5% of all deep vein thromboses (DVTs). UEDVT may be complicated by post thrombotic syndrome and pulmonary embolism, and early recognition and prompt start of anticoagulant treatment are key. Primary UEDVT, also known as Paget-von Schrötter syndrome, is associated with repeated or sudden physical activity of the upper arm and venous outflow obstruction due to anatomical variations. Secondary UEDVT is often associated with malignancy or use of intravenous devices, such as central venous catheters or pacemaker leads. Although the diagnosis and treatment of UEDVT have many similarities with DVT of the lower extremities, knowledge of specific aspects regarding UEDVT is important to guide optimal management. In this review, we will discuss the epidemiology, diagnosis, and treatment of UEDVT based on the current literature. [ABSTRACT FROM AUTHOR]

Immunothrombosis—immune-mediated activation of coagulation—is protective against pathogens, but excessive immunothrombosis can result in pathological thrombosis and multiorgan damage, as in severe coronavirus disease 2019 (COVID-19). The NACHT-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome produces major proinflammatory cytokines of the interleukin (IL)-1 family, IL-1β and IL-18, and induces pyroptotic cell death. Activation of the NLRP3 inflammasome pathway also promotes immunothrombotic programs including release of neutrophil extracellular traps and tissue factor by leukocytes, and prothrombotic responses by platelets and the vascular endothelium. NLRP3 inflammasome activation occurs in patients with COVID-19 pneumonia. In preclinical models, NLRP3 inflammasome pathway blockade restrains COVID-19-like hyperinflammation and pathology. Anakinra, recombinant human IL-1 receptor antagonist, showed safety and efficacy and is approved for the treatment of hypoxaemic COVID-19 patients with early signs of hyperinflammation. The non-selective NLRP3 inhibitor colchicine reduced hospitalization and death in a subgroup of COVID-19 outpatients but is not approved for the treatment of COVID-19. Additional COVID-19 trials testing NLRP3 inflammasome pathway blockers are inconclusive or ongoing. We herein outline the contribution of immunothrombosis to COVID-19-associated coagulopathy, and review preclinical and clinical evidence suggesting an engagement of the NLRP3 inflammasome pathway in the immunothrombotic pathogenesis of COVID-19. We also summarize current efforts to target the NLRP3 inflammasome pathway in COVID-19, and discuss challenges, unmet gaps, and the therapeutic potential that inflammasome-targeted strategies may provide for inflammation-driven thrombotic disorders including COVID-19. [ABSTRACT FROM AUTHOR]

Recently, leptin has been suggested as a possible cause of atherosclerotic disease. In the present study, we have investigated in postmenopausal women (n=60; age: 52±13) the relationship between circulating levels of leptin, oxidized LDL (Ox-LDL) and other biochemical and anthropometric variables of atherosclerotic risk. In addition, we have evaluated soluble thrombomodulin (sTM) as a marker of endothelial damage. An additional study was conducted in a subgroup of obese subjects to determine the short-term effects of weight loss on selected variables. Ox-LDL showed a positive correlation with leptin circulating levels (r=0.65, P<0.0001). A significant association was also found between Ox-LDL and body mass index (r=0.69, P<0.0001), waist-to-hip ratio (r=0.50, P<0.0001), insulin levels (r=0.65, P<0.0001), HOMA index (r=0.55, P<0.0001) and sTM (r=0.74, P<0.0001) levels. After multivariate regression analysis leptin was still related to Ox-LDL levels (P=0.007). In obese women who completed the program of weight reduction, leptin changes persisted as a significant predictor of plasma changes in Ox-LDL levels. These findings suggested a novel link between leptin and Ox-LDL, possibly involved in atherosclerotic disease. [Copyright &y& Elsevier]