Prevention of thromboembolic events after radical prostatectomy in patients with hereditary thrombophilia due to a factor V Leiden mutation by multidisciplinary coagulation management

Objective:To examine the perioperative impact of factor V Leiden mutation on thromboembolic events'risk in radical prostatectomy(RP)patients.With an incidence of about 5%,factor V Leiden mutation is the most common hereditary hypercoagulability among Caucasians and rarer in Asia.The increased risk of thromboembolic events is three-to seven-fold in heterozygous and to 80-fold in homozygous patients.Methods:Within our prospectively collected database,we analysed 33006 prostate cancer patients treated with RP between December 2001 and December 2020.Of those,patients with factor V Leiden mutation were identified.All patients received individualised recommendation of haemostaseologists for perioperative anticoagulation.Thromboembolic complications(deep vein thrombosis and pulmonary embolism)were assessed during hospital stay,as well as according to patient reported outcomes within the first 3 months after RP.Results:Overall,85(0.3%)patients with known factor V Leiden mutation were identified.Median age was 65(interquartile range:61-68)years.There was at least one thrombosis in 53(62.4%)patients and 31(36.5%)patients had at least one embolic event in their medical history before RP.Within all 85 patients with factor V Leiden mutation,we experienced no thromboembolic complications within the first 3 months after surgery.Conclusion:In our cohort of patients with factor V Leiden mutation,no thromboembolic events were observed after RP with an individualised perioperative coagulation management concept.This may reassure patients with this hereditary condition who are counselled for RP.

Arterial and Venous Thrombosis following Vaccination against COVID-19 with Astra-Zeneca Vaccine Revealing Thrombophilia

Vaccination against COVID-19 is the most recognised means of containing the pandemic. Vaccines are not without side effects, particularly vascular thrombosis. But before blaming the vaccines, a thorough assessment of thrombotic risk factors is necessary. We report a case of arterial and venous thrombosis after vaccination with AstraZeneca revealing an exaggeration of factor VIII in a 37-year-old female patient. The angioscanner showed a venous thrombosis of the right subclavian, a pulmonary embolism and the presence of a thrombus in the aorta. The biology was in favour of a high level of factor VIII. The patient was treated with an antivitamin K, and the clinical evolution was favourable.

Thrombophilia Caused by Beta2-Glycoprotein I Deficiency： In Vitro Study of a Rare Mutation in APOH Gene

This study aimed to explore the mechanism of a novel mutation （p.Lys38Glu） in apolipoprotein H （APOH） gene causing hereditary beta2-glycoprotein I （β2GPI） deficiency and thrombosis in a proband with thrombophilia. The plasma level of β2GPI was measured by ELISA and Western blotting, and anti-β2GPI antibody by ELISA. Lupus anticoagulant （LA） was assayed using the dilute Russell viper venom time. Deficiency of the major natural anticoagulants including protein C （PC）, protein S （PS）, antithrombin （AT） and thrombomodulin （TM） was excluded from the proband. A mutation analysis was performed by amplification and sequencing of the APOH gene. Wild type and mutant （c.112A〉G） APOH expression plasmids were constructed and transfected into HEK293T cells. The results showed that the thrornbin generation capacity of the proband was higher than that of the other family members. Missense mutation p.Lys38Glu in APOH gene and LA coexisted in the proband. The mutation led to β2GPI deficiency and thrombosis by impairing the protein production and inhibiting the platelet aggregation. It was concluded that the recurrent thrombosis of the proband is associated with the coexistence ofp.Lys38Glu mutation in APOH gene and LA in plasma.

Aspirin responsive platelet thrombophilia in essential thrombocythemia and polycythemia vera

Essential thrombocythemia(ET) and polycythemia vera(PV) frequently present with erythromelalgia and acrocyanotic complications, migraine-like microvascular cerebral and ocular transient ischemic attacks(MIAs) and/or acute coronary disease. The spectrum of MIAs in ET range from poorly localized symptoms of transient unsteadiness, dysarthria and scintillating scotoma to focal symptoms of transient monocular blindness, transient mono- or hemiparesis or both. The attacks all have a sudden onset, occur sequentially rather than simultaneously, last for a few seconds to several minutes and are usually associated with a dull, pulsatile or migraine-like headache. Increased hematocrit and blood viscosity in PV patients aggravate the microvascular ischemic syndrome of thrombocythemia to major arterial and venous thrombotic complications. Phlebotomy to correct hematocrit to normal in PV significantly reduces major arterial and venous thrombotic complications, but fails to prevent the platelet-mediated erythromelalgia and MIAs. Complete long-term relief of the erythromelalgic microvascular disturbances, MIAs and major thrombosis in ET and PV patients can be obtained with low dose aspirin and platelet reduction to normal, but not with anticoagulation. Skin punch biopsies from the erythromelalgic area show fibromuscular intimal proliferation of arterioles complicated by occlusive plateletrich thrombi leading to acrocyanotic ischemia. Symptomatic ET patients with erythromelalgic microvascular disturbances have shortened platelet survival, increased platelet activation markers β-thromboglobulin(β-TG), platelet factor 4(PF4) and thrombomoduline(TM), increased urinary thromboxane B2(TXB2) excretion, and no activation of the coagulation markers thrombin fragments F1+2 and fibrin degradation products. Inhibition of platelet cyclooxygenase(COX1) by aspirin is followed by the disappearance and no recurrence of microvascular disturbances, increase in platelet number, correction of the shortened platelet survival times to normal, and reduction of increased plasma levels of β-TG, PF4, TM and urinary TXB2 excretion to normal. These results indicate that platelet-mediated fibromuscular intimal proliferation and platelet-rich thrombi in the peripheral, cerebral and coronary end-arterial microvasculature are responsible for the erythromelalgic ischemic complica-tions, MIAs and splanchnic vein thrombosis. Baseline platelet P-selectin levels and arachidonic acid induced COX1 mediated platelet activation showed a highly significant increase of platelet P-selectin expression(not seen in ADP and collagen stimulated platelets), which was significantly higher in JAK2V617 F mutated compared to JAK2 wild type ET.

Primary myelofibrosis with thrombophilia as first symptom combined with thalassemia and Gilbert syndrome:A case report

BACKGROUND A 46-year-old Han man first had sigmoid sinus and transverse sinus venous thrombosis at the age of 42.At the age of 44,he once again developed thrombosis.Genetic testing showed heterozygous SERPINC1 mutation,bone marrow biopsy showed fibrosis grade 1(MF-1),and JAK2 V617F mutation was positive,accompanied by UGT1A1 mutation andβ-thalassemia gene mutation.CASE SUMMARY A 46-year-old Han man was first found to have sigmoid sinus and transverse sinus venous thrombosis at the age of 42 but had no individual or family thrombosis history,and he had been regularly taking warfarin anticoagulant therapy for a long period of time.At the age of 44,venous thrombosis reappeared in parts of the intrahepatic vein,main portal vein,splenic vein,and superior mesenteric vein,and his spleen was obviously enlarged.He had a history of jaundice for many years,and genetic testing revealed that he carried a heterozygous SERPINC1 mutation.Bone marrow biopsy showed multifocal fibrous tissue hyperplasia among trabeculae and focal fibrosis.He was positive for the JAK2 V617F mutation.At the same time,UGT1A1 andβ-thalassemia gene mutations existed,and a SERPINC1 mutation and UGT1A1 mutation were both found in his parents.CONCLUSION The patient in this case had thrombophilia as the primary symptom,JAK2V617-positive myeloproliferative neoplasm(MPN)was the main potential cause,and hereditary AT-III deficiency may have been one of multiple secondary causes.It remains to be determined whether UGT1A1 andβ-thalassemia gene mutations are related to thrombophilia.However,the clinical features of MPN in this patient were hidden,and the relevant clinical features of coexisting thalassemia and hereditary Gilbert syndrome,reported here for the first time domestically and abroad,were complicating factors,causing great difficulties for a clear diagnosis.Thus,when thrombophilia has been determined,it is necessary to screen the relevant latent problems overall.When the clinical features cannot be perfectly explained by one etiology,a relevant comprehensive examination should also be initiated from the perspective of multiple etiologies.

Inherited Thrombophilia and Early Recurrent Pregnancy Loss among Egyptian Women

Inherited thrombophilia has been implicated as a possible cause of recurrent pregnancy loss. Although numerous studies are available in literature, thrombophilia rate seems to vary fromstudy to another. The aim of our study was to determine the frequency of FII Prothrombin(G20210A), Factor V Leiden (G1691A), as well as methyl tetrahydrofolate reductase (MTHFR?C677T) polymorphisms, protein C, protein S and antithrombin III deficiency in a series of patients with unexplained RPL compared to control. Patients and Methods: 100 patients of unexplained RPL and 43 age-matched healthy controls were investigated for inherited thrombophilia. Results: MTHFR and Factor V Leiden were the commonest gene defects among cases studied (63%, 60% respectively) and control groups (41.9%, 41.9% respectively) (p = 0.019, p = 0.046 respectively). The least common deficiencies were protein S and protein C deficiency in cases (3%, 2% respectively) as well as in controls (1%, 0% respectively). 4 cases were homozygous for MTHFR and 2 cases homozygous for Factor V Leiden mutation. Odds ratio for MTHFR and Factor V mutation was 2.36 and 2.08 respectively (CI 95%). Combined defects were seen in cases and controls (p < 0.05). Conclusion: Our study found an association between MTHFR and Factor V Leiden mutations in patients with unexplained RPL among Egyptian women. Further studies are needed to define the management of genetic thrombophilia in cases of recurrent pregnancy loss.

Laboratory Diagnostic Strategy for Thrombophilia

Thrombophilia is described as a tendency to develop thrombosis as a consequence of predisposing factors that may be genetically determined, acquired, or both. The risk factors associated with venous thromboembolism are different from those associated with arterial thrombosis.

重视非肝硬化内脏静脉血栓的病因筛查

非肝硬化内脏静脉血栓(NC-SVT)主要包括门静脉血栓、肠系膜上静脉血栓、脾静脉血栓和肝静脉血栓(布加综合征),其患病率随着相关基础疾病发病率升高而呈现上升趋势。由于NC-SVT严重的危害性,临床医生对其诊断意识和诊断能力也明显提高。但在治疗上往往只重视抗凝、介入等针对血栓的处理,而忽视对导致SVT的危险因素或基础疾病的筛查,一定程度上影响部分患者的血栓治疗效果,也将延误对基础疾病的诊断和治疗。本文简要介绍了与NC-SVT发生相关的获得性、遗传性及系统性、局部性基础疾病。

Are all primary omental infarcts truly idiopathic?Five case reports

BACKGROUND Idiopathic omental infarction(IOI)is challenging to diagnose due to its low incidence and vague symptoms.Its differential diagnosis also poses difficulties because it can mimic many intra-abdominal organ pathologies.Although hypercoagulability and thrombosis are among the causes of omental infarction,venous thromboembolism scanning is rarely performed as an etiological investigation.CASE SUMMARY The medical records of the 5 cases,who had the diagnosis of IOI by computed tomography,were examined.The majority of the patients were male(n=4,80%)and the mean age was 31 years(range:21-38).The patients had no previous abdominal surgery or a history of any chronic disease.The main complaint of all patients was persistent abdominal pain.Omental infarction was detected in all patients with contrast-enhanced computed tomography.Conservative treatment was initially preferred in all patients,but it failed in 1 patient(20%).After discharge,all patients were referred to the hematology department for thrombophilia screening.Only 1 patient applied for thrombophilia screening and was homozygous for methylenetetrahydrofolate reductase(A1298C mutation)and heterozygous for a factor V Leiden mutation.CONCLUSION IOI should be considered in the differential diagnosis in patients presenting with progressive and/or persistent right side abdominal pain.Investigating risk factors such as hypercoagulability in patients with IOI is also important in preventing future conditions related to venous thromboembolism.

多普勒超声子宫动脉血流参数联合凝血相关指标对易栓症所致复发性流产妊娠结局的预测价值

目的:探讨多普勒超声子宫动脉血流参数联合凝血相关指标对易栓症所致复发性流产妊娠结局的预测价值。方法:选取2020年1月至2023年1月北京市海淀医院妇科门诊就诊的82例复发性流产患者,所有患者均进行相关治疗,并统计随访结果。所有患者于入院次日治疗前均进行子宫动脉搏动指数(PI)、阻力指数(RI)、收缩压最大血流速度(S)与舒张末期最大血流速度(D)比值(S/D),以及活化部分凝血活酶时间(APTT)、凝血酶原时间(PT)、纤维蛋白原(FIB)、凝血酶时间(TT)及D二聚体(D-D)检测。采用Pearson相关性分析PI、RI与S/D与APTT、PT、FIB、TT、D-D的相关性;采用受试者工作特征(ROC)曲线下面积(AUC)分析PI、RI、S/D、APTT、PT、FIB、TT及D-D单独检测及联合检测预测易栓症所致复发性流产妊娠结局的价值。结果:随访结果显示,82例复发性流产患者妊娠成功49例,妊娠丢失33例,妊娠成功孕妇的PI、RI与S/D均明显低于妊娠丢失孕妇,差异有统计学意义(t=10.598、6.693、3.059,P<0.05);APTT、PT、FIB、TT、D-D水平均明显低于妊娠丢失孕妇,差异有统计学意义(t=9.552、96.462、22.767、5.100、95.805,P<0.05);PI与APTT、PT、FIB、TT及D-D均存在正相关性(r=3.178,P<0.05),RI与APTT、PT、FIB、D-D均存在正相关性(r=3.246,P<0.05),S/D与PT、FIB、TT、D-D均存在正相关性(r=3.246,P<0.05);PI、RI、S/D、APTT、PT、FIB、TT及D-D单独检测及联合检测预测易栓症所致复发性流产妊娠结局灵敏度分别为42.40%、48.50%、39.40%、48.50%、63.60%、72.70%、42.40%、39.40%、84.80%,特异性分别为98.00%、71.40%、55.10%、75.50%、59.20%、71.40%、77.60%、85.70%、98.80%,AUC分别为0.674、0.685、0.409、0.646、0.784、0.788、0.566、0.563和0.941。结论:PI、RI及S/D子宫动脉血流参数与APTT、PT、FIB、TT和D-D凝血相关指标单独及联合检测预测易栓症所致复发性流产妊娠结局均具有一定的价值,且联合检测的预测价值更高。

口服抗凝治疗增加易栓症患者异常子宫出血的发生风险:一项单中心回顾性研究

目的 探讨女性易栓症患者口服抗凝治疗期间异常子宫出血(abnormal uterine bleeding,AUB)的发生率及其不良影响。方法 以2013年1月—2023年5月于北京协和医院血液内科出凝血疾病门诊就诊,并接受口服利伐沙班或华法林抗凝治疗的女性易栓症患者为研究对象。回顾性收集抗凝治疗前及治疗后患者的一般临床资料及AUB情况,并根据抗凝治疗药物不同将患者分为利伐沙班治疗组和华法林治疗组。采用广义估计方程分析女性易栓症患者抗凝治疗前后AUB的发生率,探讨不同抗凝治疗药物对AUB发生率的影响。结果 共入选符合纳入与排除标准的女性易栓症患者106例,相较于用药前,AUB的发生率显著增加(56.6%比26.4%,P<0.001),以月经过多(48.1%)和经期延长(21.7%)为主要临床表现。相较于华法林,利伐沙班更易导致AUB(OR=3.3,95%CI:1.5~7.4,P=0.003)。在发生月经过多和经期延长的54例患者中,72.2%(39/54)采取了干预措施,其中经期暂停服用抗凝药是主要干预措施(37.0%),相较于华法林治疗组,利伐沙班治疗组患者更易在经期停药(OR=10.4,95%CI:1.2~87.2,P=0.019)。结论 口服抗凝治疗可显著增加女性易栓症患者AUB的发生风险,且利伐沙班相关AUB的发生风险明显高于华法林。

1例直肠癌病人术后并发肠系膜部位易栓症的护理

总结1例直肠癌病人术后并发易栓症(肠系膜血栓)的护理经验,护理要点包括:组建多学科团队,制订诊疗和护理方案;实施重症管理策略,纠正应激性高血糖,酸碱失衡电解质紊乱,做好重要脏器的监测和保护,做好镇痛等舒适管理;积极控制腹腔感染;促进肠道功能恢复,早期营养支持干预;给予血栓再发的评估,抗凝管理和非药物预防措施;实施早期个性化康复训练;针对病人心理需求提供积极心理干预。经过多学科的精心治疗和护理,病人病情好转,住院16 d后转出重症监护室,26 d后出院。

胎儿心脏定量分析技术评估获得性易栓症孕妇胎儿心脏形态和功能的临床价值

目的应用胎儿心脏定量分析技术(Fetal HQ)评估获得性易栓症孕妇胎儿心脏形态和收缩功能,探讨其临床应用价值。方法选取我院确诊为获得性易栓症的孕妇24例(病例组)和同期就诊的健康孕妇40例(对照组),应用频谱多普勒测量胎盘功能相关参数,包括脐动脉收缩期峰值流速与舒张末期峰值流速比值(UA S/D)、脐动脉搏动指数(UA PI)、大脑中动脉搏动指数(MCA PI)、静脉导管搏动指数(DV PI)、脑胎盘比值;应用Fetal HQ测量胎儿心脏形态参数[整体球形指数(GSI)]和功能参数[左、右室整体纵向应变(LVGLS、RVGLS)、面积变化分数(LVFAC、RVFAC)、游离壁应变(LVFWS、RVFWS)及左室间隔壁应变(LVSWS)、左室射血分数(LVEF)],比较两组上述参数的差异;分析胎盘功能参数与Fetal HQ参数的相关性。结果病例组胎儿UA S/D高于对照组,差异有统计学意义(P=0.007);两组胎儿UA PI、MCA PI、DV PI、脑胎盘比值比较,差异均无统计学意义。病例组胎儿RVGLS、RVFAC、RVFWS均较对照组减低,差异均有统计学意义(均P<0.05);两组胎儿GSI、LVEF、LVGLS、LVFAC、LVFWS、LVSWS比较,差异均无统计学意义。相关性分析显示,病例组胎儿UA S/D与RVGLS、RVFAC、RVFWS均呈负相关(r=-0.534、-0.624、-0.570,均P<0.05)。结论Fetal HQ可准确评估获得性易栓症孕妇胎儿心脏形态和右室收缩功能,具有较好的临床应用价值。

基于“虚气留滞”中医病机假说阐释易栓症致复发性流产

复发性流产易栓症是人体凝血功能异常所引起的病理状态,中医并无确切名称,高发于育龄期女性,一直是临床治疗的难点与重点。本文结合“虚气留滞”病机理论,分析复发性流产易栓症的病因病机。气血亏虚,脏腑虚弱是其发病的基础,痰湿、气滞、血瘀等病理物质伤及冲任胞络致屡孕屡堕,是其发病依据。“虚气”为本,“留滞”为标,前因后果,相互影响,为复发性流产易栓症提供新的辨病思路。

西安地区582例16岁青少年血液易栓症基因筛查结果分析

目的分析相关易栓基因抗磷脂抗体(antiphosphdipid antibody,APOH)、血栓调节蛋白(thrombo-regulatory protein,THBD)、PC抗凝蛋白(PC anticoagulant protein,PROC)等在青少年群体中的突变率,为易栓基因筛查用于青少年血栓性疾病预防诊治提供相应的理论依据。方法选取2019年5~12月接受体检的16岁青少年582例作为研究对象,采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)基因分型检测技术及基因测序技术,对PROC c.574_576del,THBD c.-151G>T,APOHc.461G>A等基因位点进行检测,并对突变率进行统计分析。结果582例样本中经PCRRFLP基因分型检测发现,PROC c.574_576del突变率约为0.69%(4/582),低于中国人群的整体突变率2.4%;THBD c.-151G>T突变率为2.92%(17/582),高于中国人群的整体突变率0.97%;APOHc.461G>A突变率约为12.71%(74/582),高于中国人群的整体突变率10.27%。测序分析发现,APOHc.461G>A突变与APOHc.422T>C,APOHc.1004G>C突变连锁出现。结论青少年群体中易栓症基因突变率与整体人群易栓症基因突变率有明显差异,APOHc.461G>A,THBD c.-151G>T突变率明显高于中国人群的整体突变率,因此,对青少年血栓性疾病诊疗时应及时进行易栓症基因检测。

军事飞行员易栓症1例并文献复习

目的探究易栓症的诊断、治疗以及对空军飞行员飞行的影响及医学鉴定。方法对1例军事飞行员易栓症的诊治及航空医学鉴定过程进行分析,并文献复习。结果该飞行员因左下肢肿痛诊断左下肢静脉血栓,之后又先后出现右下肢静脉血栓、肺动脉分支血栓形成;易栓症检查:蛋白S下降,血管性血友病因子(von willebrand factor,vWF)活性、vWF抗原、Ⅷ因子(factorⅧ,FⅧ)活性升高;血栓性疾病相关基因二代测序检测:HABP2突变,c.1518+1G>C突变频率50%,血、口腔黏膜上皮细胞HABP2突变一代测序检查阳性。诊断:易栓症,蛋白S缺陷症。给予利伐沙班口服。航空医学鉴定结论为飞行不合格。结论飞行人员反复出现静脉血栓、动脉血栓,应查易栓症相关指标,尽早明确诊断,易栓症患者需要长期口服抗凝药物治疗,以预防血栓再发。该类飞行人员在航空环境下,存在再发血栓风险及口服抗凝药物所致的自发出血风险,建议停飞。

Acute myocardial infarction after initially diagnosed with unprovoked venous thromboembolism: A case report

BACKGROUND Protein C deficiency is typically associated with venous thromboembolism;however,arterial thrombosis has been reported in several cases.We report the case of a patient with pulmonary thromboembolism and deep vein thrombosis following acute myocardial infarction with high thrombus burden.CASE SUMMARY A 40-year-old man was diagnosed with pulmonary thromboembolism and deep vein thrombosis without any provoking factors.The patient was treated with anticoagulants for six months,which were then discontinued.Three months after the discontinuation of anticoagulant therapy,the patient was hospitalized with chest pain and diagnosed with acute myocardial infarction with high thrombus burden.Additional tests revealed protein C deficiency associated with thrombophilia.The patient was treated with anticoagulants combined with dual antiplatelet agents for 1 year after percutaneous coronary intervention,and no recurrent events were reported during a follow-up period of 5 years.CONCLUSION Recurrent thromboembolic events including acute myocardial infarction with thrombus should be considered an alarming sign of thrombophilia.

类风湿关节炎合并易栓症致肺栓塞1例

高凝状态是易栓症的特征性描述,发生静脉血栓的风险较高,由此产生的深静脉血栓涉及肺动脉及下肢深静脉。易栓症可由自身基因突变引起,也可继发于自身免疫性疾病,且在多次的血栓事件后才可被诊断。本文报道1例67岁男性患者,既往类风湿关节炎病史10年,此次主因“间断胸闷、气短3 d”就诊,通过病史采集,体格检查及相关辅助检查,明确诊断为急性肺栓塞、易栓症、类风湿关节炎。经过溶栓和抗凝等治疗,患者症状好转。临床中引起肺栓塞的病因较多,当我们怀疑存在易栓症时,应重点询问家族史、既往史和个人史,达到早诊断、个体化治疗和提高患者生活质量的目的。

Effect of heparin on recurrent IVF-ET failure patients

Objective:To elucidate the possible role of unfractionated heparin in patients with failed repeated in in vitro fertilization and embryo transfer(IVF-ET)and thrombophilia.Methods:This case control study evaluated the efficacy of the unfractionated heparin in increasing the pregnancy and implantation ratio in women with recurrent IVF-ET failures.Eighty-six women received in vitro fertilization/intracytoplasmic sperm injection(IVF/ICSI)with a record of three or more previous IVF-ET failures.Participants were randomly distributed into two groups.Group A(n=43)received unfractionated heparin 5000 IU twice daily,and group B(n=43)did not take any antithrombotic drugs.Coagulation abnormalities such as factor桋Leiden(FVL)mutation,methylene tetra hydro folate reductase(MTHFR)mutation and prothrombin mutation(F栻)were evaluated.Age,body mass index,basal follicular stimulating hormone,basal estradiol,duration of infertility,and number of IVF-ET failures were compared between two groups.Results:45.0%and 17.4%of women were pregnant with and without MTHFR and prothrombin mutation,respectively,when they received unfractionated heparin treatment.The implantation rate was more in group A(12.5%)than group B(4.3%)and differences in the fertilization rate of the two groups were observed(27.7%vs.35.9%).The clinical pregnancy rate per cycle was remarkably more in group A(30.2%)than group B(14.0%).Conclusions:Heparin is a safe and valuable treatment for patients with repeated IVF-ET failures.The clinical pregnancy and implantation rates are higher in the heparin-treated group in contrast with the control group.

基于易栓症相关风险因素的视网膜静脉阻塞发病机制

视网膜静脉阻塞是一种异质性疾病,其中血栓的形成导致视网膜静脉系统狭窄或阻塞视网膜静脉回流。其发病机制复杂且多种多样,我们尚未完全了解,但目前多认为其与局部、全身两方面相关。易栓症伴随着血液中的高凝状态,血小板进而易于聚集,常导致深静脉血栓事件,而诱发易栓症血液高凝状态的相关因子及血小板相关参数与视网膜静脉阻塞的关联性目前尚无系统总结。本文就此以已发现的易栓症相关风险因子为基础,讨论其与视网膜静脉阻塞之间的关系及相关性,为科研及临床提供新的思路与方法。