Thromboinflammation is a complex pathology associated with inflammation and coagulation. In cases of cardiovascular disease, in particular ischemia-reperfusion injury, thromboinflammation is a common complication. Increased understanding of thromboinflammation depends on an improved concept of the mechanisms of cells and proteins at the axis of coagulation and inflammation. Among these elements are activated protein C and platelets. This review summarizes the complex interactions of activated protein C and platelets regulating thromboinflammation in cardiovascular disease. By unraveling the pathways of platelets and APC in the inflammatory and coagulation cascades, this review summarizes the role of these vital mediators in the development and perpetuation of heart disease and the thromboinflammation-driven complications of cardiovascular disease. Furthermore, this review emphasizes the significance of the counteracting effects of platelets and APC and their combined role in disease states.

Bleeding events are feared complications in patients with advanced liver diseases and are associated with morbidity and mortality. In this context, gastrointestinal bleeding, particularly upper gastrointestinal bleeding, has a special clinical importance. In addition to endoscopic measures for hemostasis, reducing portal pressure in particular is a key component of treatment. Although the standard coagulation parameters are often altered in patients with liver diseases, optimizing coagulation plays a secondary role. Typically, a bundle of measures are employed in patients with portal hypertensive bleeding, which nowadays in most cases can halt the bleeding and stabilize the situation. The measures include endoscopy, antibiotic treatment, vasopressor treatment and, if necessary, shunt placement (transjugular intrahepatic portosystemic shunt).
UNASSIGNED: Blutungsereignisse sind gefürchtete Komplikationen bei Patient:innen mit fortgeschrittenen Lebererkrankungen. Sie sind mit Morbidität und Mortalität vergesellschaftet. Die (obere) gastrointestinale Blutung hat hier besondere klinische Bedeutung. Neben endoskopischen Maßnahmen zur Blutstillung ist vor allem die Senkung des Pfortaderdrucks ein zentraler therapeutischer Baustein. Obwohl die Standardgerinnungsparameter bei Patient:innen mit Lebererkrankungen häufig verändert sind, spielt die Optimierung der Gerinnung eine untergeordnete Rolle. Typischerweise kommt bei Patienten mit portal-hypertensiver Blutung ein Bündel an Maßnahmen zum Einsatz, wodurch die Blutung heute in den meisten Fällen zum Stillstand gebracht und die Situation stabilisiert werden kann. Die Maßnahmen beinhalten unter anderem Endoskopie, antibiotische Therapie, Vasopressortherapie und gegebenenfalls eine Shuntanlage (transjugulärer intrahepatischer portosystemischer Shunt).

Venous thromboembolism (VTE) is a major cause of morbidity and mortality in the United States. VTE is caused by genetic and acquired conditions, but the genetic variants that increase the risk of VTE are not fully characterized. Recent genome-wide association studies (GWAS) have discovered novel genetic loci linked to VTE. Some of these loci have been characterized, uncovering new pathways that regulate VTE. Functional characterization of candidate genes discovered by GWAS may reveal new therapeutic targets to treat and prevent abnormal thrombosis or bleeding.

There has been an expansion in our understanding of the multifaceted roles of circulating blood cells in regulating haemostasis and contributing to thrombosis. Notably, there is greater recognition of the interplay between coagulation with inflammation and innate immune activation and the contribution of leucocytes. The full blood count (FBC) is a time-honoured test in medicine; however, its components are often viewed in isolation and without consideration of their haemostatic and thrombotic potential. Here, we review how the individual components of the FBC, that is, haemoglobin, platelets and leucocytes, engage with the haemostatic system and focus on both their quantitative and qualitative attributes. We also explore how this information can be harnessed into better management of people with multiple long-term conditions because of their higher risk of adverse clinical events.

BACKGROUND: Titanium dioxide nanoparticles (TiO2NPs) are widely used in medical application. However, the relevant health risk has not been completely assessed, the potential of inducing arterial thrombosis (AT) in particular.
METHODS: Alterations in platelet function and susceptibility to arterial thrombosis induced by TiO2NPs were examined using peripheral blood samples from healthy adult males and an in vivo mouse model, respectively.
RESULTS: Here, using human platelets (hPLTs) freshly isolated from health volunteers, we demonstrated TiO2NP treatment triggered the procoagulant activity of hPLTs through phosphatidylserine exposure and microvesicles generation. In addition, TiO2NP treatment increased the levels of glycoprotein IIb/IIIa and P-selectin leading to aggregation and activation of hPLTs, which were exacerbated by providing physiology-mimicking conditions, including introduction of thrombin, collagen, and high shear stress. Interestingly, intracellular calcium levels in hPLTs were increased upon TiO2NP treatment, which were crucial in TiO2NP-induced hPLT procoagulant activity, activation and aggregation. Moreover, using mice in vivo models, we further confirmed that TiO2NP treatment a reduction in mouse platelet (mPLT) counts, disrupted blood flow, and exacerbated carotid arterial thrombosis with enhanced deposition of mPLT.
CONCLUSIONS: Together, our study provides evidence for an ignored health risk caused by TiO2NPs, specifically TiO2NP treatment augments procoagulant activity, activation and aggregation of PLTs via calcium-dependent mechanism and thus increases the risk of AT.

Coagulation disorders are common in Kawasaki disease (KD). The main objectives of the present study were to probe the associations of coagulation profiles with clinical classification, IVIG responsiveness, coronary artery abnormalities (CAAs) in the acute episode of KD. A total of 313 KD children were recruited and divided into six subgroups, including complete KD (n = 217), incomplete KD (n = 96), IVIG-responsive KD (n = 293), IVIG-nonresponsive KD (n = 20), coronary artery noninvolvement KD (n = 284) and coronary artery involvement KD (n = 29). Blood samples were collected within 24-h pre-IVIG therapy and 48-h post-IVIG therapy. Coagulation profiles, conventional inflammatory mediators and blood cell counts were detected. Echocardiography was performed during the period from 2- to 14-day post-IVIG infusion. In addition, 315 sex- and age-matched healthy children were enrolled as the controls. (1) Before IVIG therapy, coagulation disorders were more prone to appear in KD patients than in healthy controls, and could be overcome by IVIG therapy. FIB and DD significantly increased in the acute phase of KD, whereas reduced to normal levels after IVIG therapy. (2) PT and APTT were significantly longer in patients with complete KD when compared with their incomplete counterparts after IVIG therapy. (3) The larger δDD, δFDP and the smaller δPT, δINR predicted IVIG nonresponsiveness. (4) The higher δDD and δFDP correlated with a higher risk for CAAs (DD: r = -0.72, FDP: r = -0.54). Coagulation disorders are correlated with complete phenotype, IVIG nonresponsiveness and CAA occurrence in the acute episode of KD, and can be rectified by synergistic effects of IVIG and aspirin.

The advanced-PRF+ (A-PRF+) is a platelet concentrate, showing a higher concentration of growth factors, an increased number of cells and looser structure of the fibrin clot than leukocyte-PRF. A high variability in the size of PRF associated with patients, haematological features and centrifugation protocols was reported. The aims of this study were to evaluate the feasibility of A-PRF+ production in the field and the correlation between haematological parameters, macroscopic and microscopic features in equine A-PRF+. Samples from twenty Standardbred horses (3-7 years) were harvested with glass tubes without anticoagulants, previously heated at 37 °C. Blood samples were centrifugated at 1300 rpm for 8 min with a fixed-angle centrifuge and a horizontal centrifuge in the field, at a temperature of 15-17 °C. Clots were measured and placed on the Wound Box® for a 2-min compression. Membranes were measured and fixed in 10% formalin for histological examination. Clot and membrane surface did not differ between sex and centrifuge. Haematological parameters did not show a significant correlation to clot and membrane size. Membranes obtained from both centrifugation protocols showed a loose fibrin structure and cells evenly distributed throughout the clot. Tubes\' warming was effective to obtain A-PRF+ clots from all samples, regardless the environmental temperature. Further studies are needed to evaluate the influence of other blood molecules on the A-PRF+ structure and size.

BACKGROUND: Despite an increase in knowledge, blood loss during burn excisional surgery remains a major challenge and is an independent predictor of mortality. During burn surgery, limited measures are available to control the bleeding. Increased fibrinolysis could be one of the contributing factors of blood loss during burn excisional surgery. Tranexamic acid inhibits the fibrinolytic response, and a small body of evidence shows positive effects of tranexamic acid on the volume of blood loss.
METHODS: The main objectives of this study are twofold, (1) to investigate whether tranexamic acid reduces blood loss and (2) to investigate the changes in coagulation after burn trauma and during burn excisional surgery. This study is a multicenter double-blind randomized clinical trial in patients scheduled for burn excisional surgery within the Dutch burn centers. All adult patients scheduled for burn surgery with an expected blood loss of ≥ 250 are eligible for inclusion in this study. The study is powered on a blood loss reduction of 25% in the intervention group. In total, 95 subjects will be included. The intervention group will receive 1500 mg tranexamic acid versus placebo in the other group. Primary endpoint is reduction of blood loss. Secondary endpoints include occurrence of fibrinolysis during surgery, graft take of the split skin graft, and differences in coagulation and blood clot formation.
CONCLUSIONS: This protocol of a randomized controlled trial aims to investigate the efficacy of tranexamic acid in reducing blood loss during burn excisional surgery. Furthermore, this study aims to clarify the coagulation status after burn trauma and during the surgical process.
BACKGROUND: EudraCT: 2020-005405-10; ClinicalTrial.gov: NCT05507983 (retrospectively registered in August 2022, inclusion started in December 2021).

暂无摘要。

The term \'routine coagulation\' typically applies to hemostasis tests routinely performed in hematology laboratories, often available 24/7, and potentially ordered urgently. These tests would comprise of the prothrombin time (PT), the PT converted to an international normalized ratio, the activated partial thromboplastin time (often called partial thromboplastin time in North American laboratories) and potentially the thrombin time, the D-dimer assay, and fibrinogen assays. Although other tests could feasibly be offered (testing feasible), there are good reasons for not including all of these other tests in all routine coagulation laboratories.