Beyond hemostasis, platelets’ immune and inflammatory role is recognized and thrombocytosis is generally regarded as a marker of the inflammatory response. However, the immune functions of platelets remain beneath the surface, and previous studies have reported conflicting findings regarding the significance of thrombocytosis in infection-related diseases. Can reactive thrombocytosis be viewed as a “higher-is-worse or higher-is-better” predictor of clinical outcome? We analyzed 2754 patients discharged from the respiratory and infectious-disease wards between 1 January 2021 and 11 June 2025, and patients from the MIMIC-IV 3.1 database were used as validation cohorts, grouped by peak platelet counts (< 90, ≥ 400, 90–399 × 10⁹/L). Cox regression and multivariate logistic regression were performed to analyze the relationship between platelet count and in-hospital mortality. Multivariate linear regression was used to analyze the relationship between platelet count and length of hospital stay (LOS). Patients with reactive thrombocytosis had longer hospital stays (13 vs. 10 days; p < 0.001) and higher inflammatory markers than those with normal platelet counts CRP (90.2 vs. 28.6 mg/L; p < 0.001), PCT (0.195 vs. 0.092 ng/mL; p < 0.001), WBC (12.6 vs. 8.4 × 10⁹/L; p < 0.001). Despite these differences, mortality (3.4

The C-reactive protein-triglyceride-glucose index (CTI) has emerged as a novel biomarker to assess metabolic-inflammatory disorders. However, the relationship between CTI and cardiovascular disease (CVD) in people living with HIV (PLWH) remains unexplored. This cross-sectional study enrolled 505 PLWH who initiated antiretroviral therapy (ART) at Beijing Ditan Hospital between January 2016 and December 2020. Multivariate logistic regression models were constructed to assess the relationship between CTI and CVD prevalence, adjusting for potential confounding factors. Receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive performance of CTI for CVD, with the area under the curve (AUC) serving as the primary metric. Furthermore, restricted cubic spline (RCS) analysis was performed to explore the dose–response relationship between CTI and CVD. After adjusting for potential confounders, higher CTI was significantly associated with an increased prevalence of CVD. Each standard deviation (SD) increase in CTI was associated with a 189.0

INTRODUCTION:Pregnancy induces significant physiological changes in the hemostatic system, leading to a hypercoagulable state to prevent postpartum hemorrhage. These adaptations involve alterations in coagulation and fibrinolysis, which can be further modified in complicated pregnancies such as gestational diabetes mellitus (GDM) and preeclampsia (PE). AIM:This study investigated coagulation and fibrinolysis parameters in healthy pregnancies across different gestational stages and compared them to GDM and PE in the third trimester. METHODS:In this retrospective study, 293 pregnant women undergoing prenatal check-ups were enrolled. Coagulation parameters (prothrombin time, PT; activated partial thromboplastin time, APTT; thrombin time, TT; and fibrinogen, FIB) and fibrinolysis parameters (fibrin/fibrinogen degradation products, FDP; D-dimer; plasminogen activator inhibitor-1, PAI-1; tissue plasminogen activator, tPA; and plasmin-α2-plasmin inhibitor complex, PIC) were measured and compared across groups: non-pregnant controls, healthy pregnancies (first trimester, third trimester, delivery), GDM, and PE. RESULTS:In normal pregnancy, all gestational stages showed significantly shortened PT, APTT, and TT and elevated FIB, FDP, D-dimer, PAI-1, and tPA compared to non-pregnant controls. FDP and D-dimer increased progressively with gestation. Compared to the third trimester, GDM was characterized by significantly higher PAI-1 and tPA but lower PIC, whereas PE was characterized by significantly higher PAI-1 and PIC, prolonged APTT, and lower tPA. Furthermore, among healthy women at delivery and those with GDM, overweight and obesity were associated with significantly increased PAI-1 levels. CONCLUSION:As pregnancy progresses, enhanced coagulation with hypofibrinolysis occurs in normal pregnancy, and further hypofibrinolysis is the primary thrombotic driver in GDM and obesity. PE presents a more complex alteration in both coagulation and fibrinolytic pathways.

BACKGROUND:Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with a high incidence of thrombosis. Coagulation factor 3 (F3) plays a key role in initiating the coagulation pathway. This study identified cell subpopulations that highly express F3 and explored their potential roles in PDAC. METHODS:This study evaluated 1837 patients with PDAC from two cancer hospitals between November 1, 2023, and November 30, 2024. The analyses included assessing coagulation and fibrinolysis indicators, and employing single-cell sequencing technology to examine the tumor microenvironment in freshly resected PDAC tissues. Findings were validated using the Gene Expression Omnibus database. RESULTS:Over half of the patients (54.98%) with PDAC showed abnormal coagulation indicators. F3 mRNA and protein levels were higher in PDAC tissues than in normal tissues. This high F3 expression in PDAC was associated with a poor prognosis (p < 0.01). Analysis of 33,300 cells from freshly resected PDAC tissues showed high F3 expression in cancer-associated fibroblasts (CAFs) and ductal cells. Subsequent subtype analysis indicated that ductal cell 1 (tumor cells) and inflammatory CAFs (iCAFs) exhibited high F3 expression. Pseudotime trajectory analysis showed that iCAFs were prevalent in the earlier part of the pseudotime pathway. Notably, pathways associated with inflammation, phosphoinositide 3-kinase/Akt signaling, and coagulation and complement were significantly enriched in iCAFs. In addition, the interaction between iCAFs and tumor cells was regulated by growth factor receptor-ligand pairings. "GSE212966" and "GSE197177" data confirmed these results. CONCLUSION:The high expression of F3 in specific iCAF subtypes suggests a role in PDAC hypercoagulability and tumor progression. Targeting these iCAF subtypes could provide potential strategies for treating PDAC.

Due to platelet storage lesions (PSL), transfused platelets are unable to function properly in the prevention and treatment of bleeding in critically ill patients. It is a traditional assumption that PSL is closely related to platelet activation during storage because of the exposure of CD62P, phosphatidylserine (PS), etc. In this standpoint, activated platelets in vitro cannot be reactivated in vivo to exert their hemostatic function and exposed PS accelerates platelet clearance. Therefore, reducing platelet activation is helpful to alleviate PSL. Diannexin is the dimer of annexin that has a higher affinity for PS. CD39 is an ADP hydrolase produced by the vascular endothelium. As a result, we construct CD39-Diannexin (CD39-DA) fusion protein and hypothesize that CD39-DA can reduce platelet activation during storage to alleviate PSL. CD39-DA can bind to the exposed PS on the surface of stored platelets by immunofluorescence. Compared to the control groups, CD39-DA reserves part of stored platelets’ aggregation function confirmed by platelet aggregation assay, induced by AA, ADP and collagen. Additionally, CD39-DA reduces lactic dehydrogenase (LDH) levels and CD62P-positive events after three-day storage. Interestingly, we preliminarily discover that CD39-DA may reduce stored platelets’ apoptosis and increase aggregatory platelets after activation by thrombin, collagen and calcium, which is marked by GSAO. In conclusion, we confirm that CD39-DA can alleviate PSL by reducing platelet activation.

Studies of ancient DNA from cemeteries provide valuable insights into early human societies, and have strongly indicated patrilocality1-10. Here, we analysed ancient DNA alongside archaeological contexts and multiple stable isotopic data from 60 individuals in 2 separate cemeteries at the Fujia archaeological site in eastern China, dating between 2750 and 2500 BCE. Our findings suggest the existence of an early-described matrilineal community in the Neolithic period, characterized by high endogamy and a population practicing millet agriculture near the coast. Evidence of intermarriage between individuals in the two cemeteries and the presence of both primary and secondary burials, organized strictly according to maternal clans, underscore a strong sense of social cohesion and identity at Fujia. Bayesian modelling of radiocarbon dates indicates that the two cemeteries were used for approximately 250 years, implying a stable matrilineal lineage spanning at least 10 generations. This study contributes to the ongoing debate in anthropology and archaeology11, not only suggesting the existence of a matrilineal society in early human history but also revealing a pair of Neolithic cemeteries organized around two matrilineal clans, furthering our understanding of the early evolution of human societies through kinship systems.

BACKGROUND:Preeclampsia (PE), as a pathological pregnancy process, is still unclear in its precise pathophysiology. The current consensus on PE pathogenesis is that it is an immune-inflammatory response due to placental dysfunction leading to multiorgan involvement in the mother. Macrophages can polarize into different phenotypes under the influence of distinct microenvironments, secreting various cytokines or chemokines with distinct functions. These phenotypes play roles in either promoting inflammation or facilitating tissue repair. Studies have observed the increase in M1 polarization of decidual macrophages during the occurrence of PE, with this polarization imbalance contributing to the immuno-inflammatory response involved in placental formation. Therefore, understanding the polarization characteristics of macrophages provides a valuable direction for research related to the prevention and treatment of PE. METHODS:Authors searched for related literature on PubMed using the professional terms "preeclampsia" and "macrophage polarization". The obtained literature was categorized according to its research. Similar articles are summarized in the same sections, which are divided into different small sections according to their specific contents. RESULTS:Different studies have explored the metabolic characteristics, surface markers, secretions, signaling pathways, and functions of different macrophage polarization types, highlighting the critical role of polarization imbalance and excessive inflammatory responses in the development of PE. Intervening in inflammatory responses at the maternal-fetal interface holds significant value for the prevention and treatment of PE. CONCLUSION:Understanding the metabolic characteristics of different macrophage polarization types, combined with their polarization imbalance during the development of PE, can facilitate targeted prevention of PE.

BackgroundPlatelet concentrate (PC) transfusions are crucial in prevention and treatment of bleeding in infection, surgery, leukemia, and thrombocytopenia patients. Although the technology for platelet preparation and storage has evolved over the decades, there are still challenges in the demand for platelets in blood banks because the platelet shelf life is limited to 5 days due to bacterial contamination and platelet storage lesions (PSLs) at 20-24 degrees C under constant horizontal agitation. In addition, the relations between some adverse effects of platelet transfusions and PSLs have also been considered. Therefore, understanding the mechanisms of PSLs is conducive to obtaining high quality platelets and facilitating safe and effective platelet transfusions.ObjectiveThis review summarizes developments in mechanistic research of PSLs and their relationship with clinical practice, providing insights for future research.MethodsAuthors conducted a search on PubMed and Web of Science using the professional terms "PSL" and "platelet transfusion." The obtained literature was then roughly categorized based on their research content. Similar studies were grouped into the same sections, and further searches were conducted based on the keywords of each section.ResultsDifferent studies have explored PSLs from various perspectives, including changes in platelet morphology, surface molecules, biological response modifiers (BMRs), metabolism, and proteins and RNA, in an attempt to monitor PSLs and identify intervention targets that could alleviate PSLs. Moreover, novel platelet storage conditions, including platelet additive solutions (PAS) and reconsidered cold storage methods, are explored. There are two approaches to obtaining high-quality platelets. One approach simulates the in vivo environment to maintain platelet activity, while the other keeps platelets at a low activity level in vitro under low temperatures.ConclusionUnderstanding PSLs helps us identify good intervention targets and assess the therapeutic effects of different PSLs stages for different patients. Some major biological response modifiers (BMRs) and the potential mechanisms of platelet storage lesions (PSLs). (1) During storage, platelet morphology transforms from discoid to sphere with pseudopodia and lysis at extended storage. (2) Changes in molecules on the surface are reduced G-protein-coupled protease-activated receptors (PAR4), exposure and shedding of CD42b (GPI b alpha) and GPVI, and inverse phosphatidylserine (PS), which are different from classical platelet activation. In parallel, alpha-granules release CD62P to the membrane and soluble CD40 ligand (sCD40L) and regulated on normal activation T cells expressed and secreted (RANTES) to the extracellular space. Platelet microparticles (PMPs) are also produced by platelets. (3) These BMRs including GPI b alpha, GPVI, PS and PMPs may be associated with reactive oxygen species (ROS) as demonstrated by elevated O2- level. microRNAs (miRNAs) that may be derived from precursor miRNAs (pre-miRNAs) and proteins that are synthesized in the existing process of translation (4) can be detected. (5) The proportion of glucose that can access the tricarboxylic acid cycle (TCA) decreases contributes to the accumulated lactate due to mitochondrial dysfunction.image

Preeclampsia (PE) is a placenta-mediated thrombotic-inflammatory syndrome. Procoagulant platelets are the main source of platelet microparticles (PMPs), which can result in both pro-inflammatory and pro-thrombotic effects. Therefore, we hypothesized that targeted inhibition of procoagulant platelets would prevent PE via the reduction of PMPs generation. The procoagulant platelet levels in 49 healthy pregnant women and 39 pregnant women with PE were measured and compared. High-performance liquid chromatography coupled with mass spectrometry (LC–MS/MS) was used to investigate the differential proteomes of the platelet proteins isolated from 6 healthy pregnant women and 6 pregnant women with PE. Recombinant protein CD39-Diannexin was constructed for the targeted inhibition of procoagulant platelets. A PE mouse model was developed to investigate whether targeted inhibition of procoagulant platelets could prevent PE. PE patients showed elevated levels of procoagulant platelets and platelet microparticle generation; their platelet proteomics revealed that the proteins involved in complement, coagulation, and inflammation responses were downregulated. Recombinant protein CD39-Diannexin can target the inhibition of procoagulant platelet function both ex vivo and in vivo. This can prevent the PE-like phenotype, characterized by decreased blood pressure, protein/creatine (P/C) ratio, soluble fms-like tyrosine kinase (sFlt-1), decreased pregnancy failure, and reduced placenta inflammasome activation. To conclude, procoagulant platelets are involved in the mechanism underlying PE and the recombinant protein CD39-Diannexin may help prevent PE via the targeted inhibition of procoagulant platelets.

INTRODUCTION:The increase in fibrinogen levels is vital for the formation of a prothrombotic state during gestation to counter-bleeding challenges at delivery. However, pregnancy complications characterized by systemic inflammatory response syndrome may consume fibrinogen, resulting in elevated D-dimer levels. METHODS:Our study is based on a total of 16 768 pregnant women who delivered between December 1, 2013, and December 1, 2018, to study fibrinogen and D-dimer changes during gestation under normal and multiples of pathogenic states. RESULT:Compared with nonpregnant women (3.04[3.02-3.08]), pregnant women depicted higher fibrinogen levels throughout gestation (p < 0.001). In the uncomplicated group, fibrinogen levels increased throughout the first (3.28[3.26-3.29]), second (4.04[4.01-4.07]), and third trimesters (4.40[4.38-4.41]) but dropped at delivery (4.30[4.28-4.31]), similar to the changing pattern of the pregnancy-related complication group and pre-existing disorder group. Women with pregnancy-related complications showed significantly higher mean fibrinogen levels throughout gestation (p < 0.001), except for placental abruption, where, it decreased from the third trimester and was lower than that of uncomplicated pregnancies (3.89[3.60-4.17] vs. 4.40 [4.38-4.41], p = 0.001). Among uncomplicated pregnancies, D-dimer grew rapidly throughout the first trimester (0.09[0.06-0.15]), second trimester (0.28[0.19-0.40]), third trimester (0.51[0.36-0.78]), and delivery (0.70[0.47-1.03]). CONCLUSION:Women with pregnancy-related complications and pre-existing disorders shared similar changing patterns; however, the D-dimer of women with placenta accreta presented higher levels than those with uncomplicated pregnancies since the first trimester. We concluded that fibrinogen levels are expected to increase steadily, but in patients with placental abruption, fibrinogen levels dropped during the third trimester. D-dimer levels typically rise consistently throughout pregnancy, yet in patients with placenta accreta, they show abnormal elevation since an early stage of pregnancy.

Parkinson's disease (PD), being the second largest neurodegenerative disease, poses challenges in early detection, resulting in a lack of timely treatment options to effectively manage the disease. By the time clinical diagnosis becomes possible, more than 60% of dopamine neurons in the substantia nigra (SN) of patients have already degenerated. Therefore, early diagnosis or identification of warning signs is crucial for the prompt and timely beginning of the treatment. However, conducting invasive or complex diagnostic procedures on asymptomatic patients can be challenging, making routine blood tests a more feasible approach in such cases. Numerous studies have been conducted over an extended period to search for effective diagnostic biomarkers in blood samples. However, thus far, no highly effective biomarkers have been confirmed. Besides classical proteins like α-synuclein (α-syn), phosphorylated α-syn and oligomeric α-syn, other molecules involved in disease progression should also be given equal attention. In this review, we will not only discuss proposed biomarkers that are currently under investigation but also delve into the mechanisms underlying the disease, focusing on processes such as α-syn misfolding, intercellular transmission and the crossing of the blood-brain barrier (BBB). Our aim is to provide an updated overview of molecules based on these processes that may potentially serve as blood biomarkers.

ObjectiveThe purpose of this manuscript was to conclude the role of platelets in immune inflammation and discuss the complex mechanisms of pyroptosis in platelets as well as their related diseases. MethodsThis article reviewed the existing literature to see the development of pyroptosis in platelets. ResultsPlatelets have been shown to be capable of activating inflammasomes assembled from NOD-like receptor family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC) and caspase-1. Recently, they were also implicated in pyroptosis. Cleaved by caspase-1, N-terminal gasdermin D (N-GSDMD) could form pores in the cell membrane, inducing nonselective intracellular substance release. This programmed cell death induced thrombocytopenia and inflammatory cytokine release such as IL-1 beta and IL-18, promoting platelet aggregation, vaso-occlusion, endothelial permeability and cascaded inflammatory response. ConclusionPyroptosis in platelets contributes to thrombocytopenia and inflammation.

Background: Lupus anticoagulants (LA) increase the risk of thrombotic and obstetric events in patients with antiphospholipid syndrome than in those with other antiphospholipid antibodies. Anti-phosphatidylserine/ prothrombin (aPS/PT) complex antibodies are thought to cause LA positivity. Therefore, we aimed to explore whether aPS/PT antibodies could prolong phospholipid (PL)-dependent clotting time and increase the risk of thrombosis or pregnancy complications based on LA positivity. Methods: We recruited 222 patients with positive LA and estimated their aPS/PT, anticardiolipin (aCL), anti-82glycoprotein I (a82GPI), and anti-82GPI domain I (anti-D1) antibody (IgM and IgG) titers and PL-dependent clotting time. Results: PT was longer in aPS/PT IgG-positive patients than in aPS/PT IgM-negative patients (P < 0.001), while there was no significant difference between aPS/PT IgM-positive and IgM-negative patients (P = 0.100). Both SCT-S and dRVVT-S were prolonged in aPS/PT (IgG and IgM)-positive patients compared to aPS/PT-negative patients (P < 0.001, P = 0.010, P < 0.001, P = 0.002, respectively). Similarly, the associations between aPS/ PT IgG or IgM antibody titers and SCT-S or dRVVT-S were significant. SCT-C and dRVVT-C did not show any significant differences. The incidence of thrombosis in the aPS/PT IgG-positive group was much higher than that in the IgG-negative group (P = 0.012). Likewise, the incidence of thrombosis was higher in the anti-D1- and aPS/ PT IgG-positive patients than in the negative controls (40 % vs 14.3 %, x2 = 3.934, P = 0.047). Furthermore, the aPS/PT IgG-positive group showed the strongest association with thrombosis [OR 2.584, 95 % CI (1.213, 5.505)]. Conclusion: The aPS/PT antibodies prolonged PL-dependent clotting time, especially SCT-S and dRVVT-S. In addition, the presence of aPS/PT IgG antibodies increased the risk of thrombosis in LA positivity.

体外膜肺氧合(ECMO)治疗时,非生物材料表面与血液接触后引发的凝血系统和补体系统等激活,会导致血栓形成和炎症反应,这种反应与全身炎症反应综合征有相似之处,是血栓、出血、器官衰竭等并发症的主要原因,也是导致ECMO治疗预后不佳、死亡率高的主要原因.除了抗凝剂的使用,人们同时希望通过改进ECMO管路材料的生物相容性来解决这一问题.该文综述了 ECMO中血栓炎症反应的机制,并总结了现有的ECMO管路生物相容性改进方式,希望为ECMO治疗和相关研究提供参考.

BACKGROUND:Lupus anticoagulants (LA) increase the risk of thrombotic and obstetric events in patients with antiphospholipid syndrome than in those with other antiphospholipid antibodies. Anti-phosphatidylserine/prothrombin (aPS/PT) complex antibodies are thought to cause LA positivity. Therefore, we aimed to explore whether aPS/PT antibodies could prolong phospholipid (PL)-dependent clotting time and increase the risk of thrombosis or pregnancy complications based on LA positivity. METHODS:We recruited 222 patients with positive LA and estimated their aPS/PT, anticardiolipin (aCL), anti-β2-glycoprotein I (aβ2GPI), and anti-β2GPI domain I (anti-D1) antibody (IgM and IgG) titers and PL-dependent clotting time. RESULTS:PT was longer in aPS/PT IgG-positive patients than in aPS/PT IgM-negative patients (P < 0.001), while there was no significant difference between aPS/PT IgM-positive and IgM-negative patients (P = 0.100). Both SCT-S and dRVVT-S were prolonged in aPS/PT (IgG and IgM)-positive patients compared to aPS/PT-negative patients (P < 0.001, P = 0.010, P < 0.001, P = 0.002, respectively). Similarly, the associations between aPS/PT IgG or IgM antibody titers and SCT-S or dRVVT-S were significant. SCT-C and dRVVT-C did not show any significant differences. The incidence of thrombosis in the aPS/PT IgG-positive group was much higher than that in the IgG-negative group (P = 0.012). Likewise, the incidence of thrombosis was higher in the anti-D1- and aPS/PT IgG-positive patients than in the negative controls (40 % vs 14.3 %, χ2 = 3.934, P = 0.047). Furthermore, the aPS/PT IgG-positive group showed the strongest association with thrombosis [OR 2.584, 95 % CI (1.213, 5.505)]. CONCLUSION:The aPS/PT antibodies prolonged PL-dependent clotting time, especially SCT-S and dRVVT-S. In addition, the presence of aPS/PT IgG antibodies increased the risk of thrombosis in LA positivity.

目的 探讨产前24 h内凝血指标、妊娠并发症、产妇合并症对产后出血的早期预测价值.方法 回顾性分析北京大学第三医院2013-2018年入院分娩的产妇17 024例,根据是否发生产后出血分为产后出血组(n=2 211)和非产后出血组(n=14 813).比较两组产妇的人口学特征、临床诊断资料及产前24 h内凝血指标,用单因素及多因素Logistic回归模型分析产后出血的危险因素,用ROC曲线评估其对产后出血的早期预测价值.结果 单因素Logistic回归分析显示,两组间年龄、孕周、多胎、纤维蛋白原(Fib)、活化部分凝血活酶时间(APTT)、凝血酶时间(TT)、国际标准化比值(INR)、子痫前期、胎盘早剥、前置胎盘、胎盘植入差异均有统计学意义(P均＜0.05).多因素Logistic回归模型分析显示,年龄、孕周、INR的增加,以及多胎、子痫前期、胎盘早剥、前置胎盘、胎盘植入是产后出血发生的独立危险因素(P均＜0.05).多指标联合预测产后出血的ROC曲线下面积(AUCROC)为0.685(95％CI:0.672～0.698),准确度为87.7％.结论 综合分析产妇年龄、孕周、多胎、分娩前24 h内凝血指标(Fib、APTT、INR)、胎盘介导妊娠并发症种类有助于发现产后出血高风险人群.

血栓栓塞性疾病的栓塞和出血风险并存已成为临床困境.疾病的多元化与药物更迭使抗栓治疗日益复杂和专业化,单一学科已不能胜任疑难病例的抗栓治疗.为更好地整合医疗资源,确保患者从规范化抗栓治疗中获益,北京大学第三医院突破学科间壁垒,组建了以心内科为主体,联合药剂科、检验科、神经内科、急诊科、消化科、心脏外科、呼吸科、介入血管外科、神经外科、风湿免疫科和血液科等12个科室参与的抗栓诊治专业团队,致力于制定合理的抗栓策略,着力解决临床血栓性疾病抗凝、抗血小板治疗中的关键问题,旨在探索一个"以心房颤动患者为中心"的多学科联合诊疗和精细化管理模式.

目的 建立检测血小板促凝亚群的方法,通过该方法检测并比较PE孕妇和健康妊娠孕妇中血小板促凝亚群的差异.方法 通过流式细胞术构建促凝血小板检测方法;自2020年10月至2021年6月,连续入选北京大学第三医院49例健康育龄女性、39例健康妊娠孕妇和34例PE孕妇并检测其促凝血小板形成水平.结果 利用全血作为样本,在静息及激活时检测促凝血小板的CV值分别为10.11％及3.13％;利用洗涤血小板作为样本,在静息及激活时检测促凝血小板的CV值分别为12.86％及6.75％.在静息和激活状态下,PE的促凝血小板水平均高于健康妊娠孕妇[2.30％(1.90％,2.80％)vs 1.35％(1.13％,1.50％),P<0.001;16.90％(15.25％,18.85％)vs 8.50％(7.92％,9.50％),P<0.001].而利用洗涤血小板检测,只有在激活状态下,PE促凝血小板水平高于健康妊娠孕妇[19.25％(15.98％,24.08％)vs 16.50％(15.00％,17.50％),P=0.047].利用全血检测,在静息和激活状态下检测促凝血小板,其AUCROC分别为0.951和0.993;而利用洗涤血小板检测,在激活状态下,其AUCROC为0.691.结论 利用流式细胞术成功构建促凝血小板检测方法,其中采用全血检测的方案性能优于洗涤血小板检测方案.PE孕妇的促凝血小板形成水平显著高于健康妊娠孕妇,提示促凝血小板可能参与子痫前期发生.

Genetic and acquired risk factors are extremely important mechanisms in the development of venous thromboembolism (VTE). Inherited antithrombin (AT) deficiency due to mutations in the SERPINC1 gene is a well-known risk factor for genetic thrombophilia. In this case, we reported a 28-year young abroad student who presented with refractory and recurrent VTE in-hospital. This patient presented with a 2-month history of right lower limb pain and 1 week of fever. The ultrasound showed deep venous thrombosis in the right common and superficial femoral veins. The CTPA confirmed acute pulmonary embolism with multiple filling defects in both pulmonary arteries. He was diagnosed with “pulmonary embolism, pneumonia, lower extremity venous thrombosis”. The level of serum antithrombin was normal, yet gene sequencing revealed a heterozygous missense mutation of SERPINC1, c.1277C>T (p.Ser426Leu). The patient underwent anticoagulant therapy of heparin and inferior vena cava filter implantation. The patient had undergone recurrent VTE despite adequate anticoagulation with heparin during the first 2 weeks. The swelling, pain, and thrombosis of lower extremity veins got resolved from warfarin and rivaroxaban. Inherited antithrombin deficiency due to mutations in the SERPINC1 gene is the genetic basis of this patient, and warfarin/rivaroxaban, other than heparin, is beneficial.