Homozygous factor Ⅴ Leiden mutation in type Ⅳ Ehlers-Danlos patient

Ehlers-Danlos syndrome(EDS) is a group of inherited connective tissue disorders caused by collagen synthesis defects. Several hemostatic abnormalities have been described in EDS patients that increase the bleeding tendencies of these patients. This case report illustrates a patient with an unusual presentation of a patient with type Ⅳ EDS, platelet δ-storage pool disease and factor Ⅴ Leiden mutation. Young woman having previous bilateral deep vein thrombosis and pulmonary emboli coexisting with ruptured splenic aneurysm and multiple other aneurysms now presented with myocardial infarction. Presence of factor Ⅴ Leiden mutation raises the possibility that the infarct was due to acute coronary thrombosis, although coronary artery aneurysm and dissection with myocardial infarction is known to occur in vascular type EDS. This is the first report in the medical literature of factor Ⅴ Leiden mutation in an EDS patient which made the management of our patient challenging with propensity to both bleeding and clotting.

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.

Down Regulated Protein C Plasma Levels in the Absence of Factor V Leiden Mutation in HIV Patients: An Observational Study in Maiduguri, North-Eastern Nigeria

Background: As life expectancy of HIV-infected patients increases with use of highly active antiretroviral therapy (HAART), protean haematologic manifestation including decreased activity of natural anticoagulants such as protein C may occur in the absence of genetic risk factors. Based on this preposition, we assessed the plasma level of protein C, and prevalence of factor V Leiden mutation among HIV-infected individuals. Our cohort consisted of 499 HIV-infected patients, of which 250 had AIDS, while 249 were either asymptomatic or had minor mucocutaneous infection consistent with WHO clinical stages I and II without features of AIDS. We also evaluated 251 healthy, HIV-negative subjects as controls. All participants were tested for plasma protein C levels and factor V Leiden (FVL) mutation (Arg 506 Gln) by automation and amplification created restriction enzyme site (ACRES) polymerase chain reaction, respectively. The prevalence of reduced protein C plasma levels among HIV positive patients was 20%;it was more prevalent among those that had AIDS compared with those without features of AIDS, but within WHO clinical stage I and II, (93.3% vs 6.7%) respectively. None of the control patients had either reduced protein C nor FVL mutation. All participants that demonstrated reduced protein C plasma levels demonstrated normal FVL genotype (1691G/G). Conclusion: Decreased protein C plasma levels can occur in HIV-infected patients in the absence of factor V Leiden mutation. The risk increases with severity of the disease. Deranged protein C plasma level increases the risk of hypercoagulable state in patients with advanced HIV disease;it should be considered among the causes of thrombo embolism in this group of patients.

Mesenteric vein thrombosis in a patient heterozygous for factor Ⅴ Leiden and G20210A prothrombin genotypes

Mesenteric venous thrombosis(MVT)is a rare but life threatening form of bowel ischemia.It is implicated in 6%-9% of all cases of acute mesenteric ischemia.The proportion of patients with primary(or idiopathic)MVT varies from 0% to 49%,with a decrease in frequency secondary to more recent availability of newer investigations for hypercoagulability.The presence of factor Ⅴ Leiden(FVL)and prothrombin G20210A mutations(PGM)have been well documented in these cases.However,there have been scarce case reports describing MVT in heterozygotes of both these mutations occurring simultaneously and its implications on long term management.Our case describes acute MVT in a previously asymptomatic young patient with no prior history of venous thromboembolism.The patient was found to be heterozygous for FVL and PGM and treated with lifelong anticoagulation with warfarin(goal international normalized ratio:2-3)and avoidance of hormonal contraceptives.

国人布-加综合征与FⅤ Leiden突变的相关研究

目的 :探讨国人布 -加综合征 (BCS)与凝血第 因子 L eiden(F L)突变的相关性。方法 :收集 2 9例国人BCS(其中 2 5例为散发 BCS、4例为家族性 BCS)和 2 9名健康对照者 ,并对其血样进行 PCR- RFL P的 F L 突变分析。结果 :2 9例 BCS中 ,共有 3例 F L 突变阳性 ,均为家族性 BCS病例。其中家系 A姐妹均有 F L 突变 ,家系 B妹妹突变阳性 ,均为杂合性突变。散发病例无 1例阳性。对照组无 1例阳性。 2 9例国人 BCS中 ,F L 突变频率为0 .0 5 17,而 4例家族性 BCS的 F L 突变频率则为 0 .375 0。2 9例 BCS病例组与 2 9例对照组间 F L 突变频率无统计学差别 ,但家族性 BCS病例组与对照组间 F L 突变频率有显著统计学差别。结论 :国人家族性 BCS与 F L 突变相关 ,国人散发性 BCS与 F L

FⅤ Leiden突变与缺血性卒中

F Ⅴ Leiden突变可导致活化蛋白C抵抗现象,是引起白种人静脉血栓栓塞的最常见遗传因素。但对这一突变与缺血性卒中的关系尚存有争议。文章综述了F Ⅴ Leiden突变的分子机制及近年来在缺血性卒中方面的研究情况。

汉族人深静脉血栓形成患者FV Leiden突变检测

目的 ;探讨汉族人FV基因 16 91位点多态分布情况及FVLeiden突变与深静脉血栓形成的关系。方法 :利用聚合酶链反应和限制性片段长度多态性 (PCR RFLP)方法 ,检测 10 3例深静脉血栓形成 (DVT)患者与 10 6例正常对照的FVLeiden突变 ,并进行对比分析。结果 :2组FV基因第 16 91位点的基因型为G/G ,全部为野生型 ,未见突变类型。结论

FVLeiden和FIIG20210A与中国人群肺血栓栓塞症的相关性

目的:探讨凝血因子V基因突变(FVLeiden)和凝血酶原G20210A基因突变(FIIG20210A)与中国人群肺血栓栓塞症的关系。方法:选取45例经过核素肺灌注显像和(或)螺旋CT肺动脉造影(CTPA)确诊的肺血栓栓塞症患者为实验组,85例正常健康人群为对照组。对实验组和对照组分别进行凝血因子V基因突变和凝血酶原G20210A基因突变检测。结果:FVL和凝血酶原G20210A基因杂合子及纯合子突变在PTE患者组及对照组中基因型频率均为0,提示病例组及对照组上述基因型变异频率及突变等位基因频率均为0。结论:凝血因子V基因G1691A突变和凝血因子G20210A基因突变可能与中国人群肺血栓栓塞症无关。

口服避孕药与凝血因子的变化及因子Ⅴ基因突变的关系

目的 探讨国产复方口服避孕药 (COC)与凝血因子的变化及因子V基因突变的关系。方法 测定 14 1例健康妇女凝血因子Ⅱ、Ⅴ、Ⅶ、Ⅷ、Ⅹ活性 ;分析女性脑卒中患者因子Ⅴ基因多态性。结果 炔诺酮组和炔诺孕酮组凝血因子X活性均数均显著高于对照组 (97 0 8± 14 78,P <0 0 5 ;98 5 8± 13 2 8,P <0 0 1) ;炔诺酮组凝血因子Ⅷ活性均显著高于对照组 (15 0 96± 5 7 11,P <0 0 5 ) ;二服药组凝血因子Ⅱ、Ⅴ、Ⅶ活性均数与对照组相似 ,差异无显著性 ;女性脑卒中患者中服避孕药者和非服避孕药者均未发现因子Ⅴ基因多态性。结论 长期服用国产低剂量COC对妇女的凝血因子有一些负面影响 ,不同避孕药的影响略有不同 ;COC不会引起中国妇女凝血因子ⅤLeiden突变。

Thrombosis and inflammatory bowel disease-the role of genetic risk factors

Thromboembolism is a significant cause of morbidity and mortality in patients with inflammatory bowel disease （IBD）. Recent data suggest thromboembolism as a disease-specific extraintestinal manifestation of IBD, which is developed as the result of multiple interactions between acquired and genetic risk factors. There is evidence indicating an imbalance of procoagulant, anticoagulant and fibrinolitic factors predisposing in thrombosis in patients with IBD. The genetic factors that have been suggested to interfere in the thrombotic manifestations of IBD include factor V Leiden, factor Ⅱ （prothrombin, G20210A）, methylenetetrahydrofolate reductase gene mutation （MTHFR, 6777T, plasminogen activator inhibitor type 1 （PAI-1） gene mutation and factor X Ⅲ （val34leu）. In this article we review the current data and future prospects on the role of genetic risk factors in the development of thromboembolism in TBD.

复合杂合突变致遗传性凝血因子Ⅴ缺陷症家系的表型与基因型分析

目的:通过检测复合杂合突变导致遗传性凝血因子Ⅴ(FⅤ)缺陷家系的表型和基因突变分析,探讨其分子发病机制。方法:检测先证者及其家系成员(共3代10人)血浆凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(FIB)、FⅤ促凝活性(FⅤ∶C)、FⅤ抗原(FⅤ∶Ag)及其他相关凝血指标以明确诊断。采用DNA直接测序分析F5基因的所有外显子、侧翼、5'和3'非翻译区及家系成员相应的突变位点区域,发现突变位点用反向测序证实。使用ClustalX-2.1-win软件分析突变氨基酸的保守性,PROVEAN和MutationTaster在线生物信息学软件预测突变对蛋白质功能的影响,Swiss-PdbViewer软件在突变位点上进行蛋白质模型和氨基酸相互作用分析。结果:先证者PT和APTT较正常对照健康体检者显著延长,分别为34.2 vs 13.2 s和119.3 vs 36.0 s;FⅤ∶C和FⅤ∶Ag极度降低,分别为3%和6%。先证者的第二子、第三子、女儿和孙子的PT和APTT略有延长,FⅤ∶C和FⅤ∶Ag均有不同程度的降低,其他家庭成员的相关凝血参数均在正常范围内。先证者6号外显子上存在c.911G>A杂合错义突变,导致p.Gly276Glu;16号外显子上存在c.5343C>G杂合错义突变,导致p.Ser1781Arg。其第二子、第三子和孙子均携带p.Gly276Glu的杂合子,其女儿携带p.Ser1781Arg的杂合子,其他家庭成员均为野生型。保守分析结果表明,Gly276和Ser1781在同源物种中高度保守。2种生物信息学软件的预测结果相同,PROVEAN(得分-6.214和-12.79)表明,该复合杂合突变是一种有害突变;MutationTaster(得分0.976和0.999)提示,这些突变可能引起相应疾病。p.Gly276Glu蛋白质模型分析显示,Glu侧链延长,分子量变大,这将增加它与周围氨基酸之间的空间位阻,影响FⅤ蛋白的正常局部折叠,最终导致蛋白质活性和含量降低。由于尚无16号外显子FⅤ的X射线3D结构文件,本研究无法对p.Ser1781Arg突变蛋白进行空间结构分析。结论:在本研究中鉴定的新型复合杂合突变(p.Gly276Glu和p.Ser1781Arg)是该家系FⅤ水平下降的主要原因,其中p.Ser1781Arg国内外鲜见报道。

Lman1基因复合杂合突变导致的凝血因子Ⅴ、Ⅷ联合缺乏症

凝血因子Ⅴ和Ⅷ(FⅤ、FⅧ)联合缺乏症(F5F8D)是一种罕见的常染色体隐性遗传性出血性疾病。近年的研究发现,该病病因在于基因lman1或mcfd2的突变。本研究的目的是对1名F5F8D先证者及其家系成员的lman1、mcfd2基因进行扩增、测序,以查找潜在的致病突变。采集了先证者及其父母的外周血样本,进行了凝血功能相关检查,包括活化部分凝血活酶时间(APTT)、凝血酶原时间(PT)、凝血酶时间(TT)、血浆纤维蛋白原(Fg)、FⅤ促凝活性(FⅤ∶C)、FⅧ促凝活性(FⅧ∶C),并提取基因组DNA,通过PCR法对先证者lman1基因的13个外显子及侧翼序列、mcfd2基因的4个外显子及侧翼序列进行特异性扩增,产物经纯化后直接测序,以检测致病突变。根据先证者突变所在位点,选择性扩增其父、母的相应片段,纯化、测序,以便进行家系分析。结果表明:先证者APTT82.2秒、PT19.6秒、TT18.6秒,Fg2.9 g/l,FⅤ∶C 7.1%,FⅧ∶C 18.7%。先证者及其母亲lman1基因第8外显子区出现杂合性单碱基插入c.912_913insA,导致蛋白序列改变p.Glu305fsX20;先证者及其父亲lman1基因11外显子区出现杂合性无义突变c.1366C>T,导致p.Arg456X。结论:先证者lman1基因的复合杂合突变c.912_913insA、c.1366C>T是导致其发病的原因;前者继承自其母,后者继承自其父。这种复合杂合突变的组合方式尚未见有报道。

V因子Leiden突变及蛋白S、蛋白C与脑静脉窦血栓抗凝有效性相关性分析

目的:分析V因子Leiden突变及蛋白S、蛋白C低下与脑静脉窦血栓行抗凝治疗有效性的关系。方法:选取2017年5月至2022年2月蚌埠市第三人民医院收治的脑静脉窦血栓的103例患者为研究对象,根据DNA检测及酶联免疫吸附沉淀检测判定患者是否存在V因子Leiden突变及蛋白S、蛋白C水平,分别以单纯V因子突变为观察A组33例,单纯蛋白S、蛋白C低下为观察B组34例,无V因子Leiden突变及蛋白S、蛋白C低下为对照组36例,记录三组在给予抗凝治疗的第3、7、15 d的血栓弹力图参数及INR、APTT的水平,研究比较V因子Leiden突变及蛋白S、蛋白C与脑静脉窦血栓抗凝有效性的关系。结果:观察A组在抗凝治疗第3、7、15 d时凝血反应时间(R)延长水平不明显、血凝块形成速率(K)延长水平不明显、最大血凝块强度(MA)减少水平不明显及凝血功能指标INR升高水平不明显、APTT延长水平不明显,与对照组及观察B组比较,差异具有统计学意义(P<0.05),而观察B组仅在抗凝治疗3 d R延长水平、K延长水平与对照组相比,差异有统计学意义(P<0.05),观察B组在抗凝治疗第7、15 d时R延长水平明显、K延长水平明显、MA减少水平明显及INR升高水平明显、APTT延长水平明显,但和对照组相比,两者差异无统计学意义(P>0.05)。结论:对于V因子Leiden突变的脑静脉窦血栓的患者行抗凝治疗效果较差,对于蛋白S、蛋白C低下的患者行抗凝治疗效果较好,对于无V因子Leiden突变及蛋白S、蛋白C低下的患者抗凝治疗效果最好,V因子Leiden突变及蛋白S、蛋白C低下与脑静脉窦血栓的抗凝有效性存在相关性。

肺栓塞与凝血因子Ⅴ Leiden突变关系的研究

目的 探讨凝血因子ⅤLeiden突变与具有易栓症的肺栓塞之间的关系。方法 经放射性核素肺通气 灌注扫描、螺旋CT和 (或 )肺动脉造影检查并结合临床资料确诊的肺栓塞患者 2 0例 ,所有患者均符合易栓症条件 ,同时选取性别、年龄匹配的健康对照者 2 0例。采用酚 氯仿抽提技术提取基因组DNA ,聚合酶链反应 (PCR)扩增DNA ,用测序技术测定扩增基因序列。结果 肺栓塞组及对照组均不存在凝血因子ⅤLeiden突变。结论 (1)我国凝血因子ⅤLeiden突变频率可能很低。(2 )凝血因子ⅤLeiden突变可能不是国人肺栓塞的危险因素。

FⅤ Leiden突变、抗心磷脂抗体与缺血性脑血管病

目的 探讨国人凝血因子Ⅴ外显子 10中一个固定的错义突变 (FⅤLeiden突变 )发生率及其与抗心磷脂抗体 (aCL)和缺血性脑血管病 (ICVD)的关系。方法 应用聚合酶链反应和限制性片段长度多态性 (PCR RFLP)分析方法对国人 118例ICVD患者及 75名健康者进行FⅤLeiden突变检测 ,86例ICVD患者检测aCL ,2 7例进行抗活化蛋白C(APC R)检测。结果 (1) 6例 (5 1% )ICVD患者出现FⅤLeiden突变 ,且皆为杂合子 ,对照组中无一例发生突变 ,FⅤLeiden突变患者年龄较轻 ,平均年龄5 0岁。 (2 )ICVD组 2 7例检测了APC R ,8例阳性。 (3)aCL阳性患者FⅤLeiden突变发生率高于aCL阴性患者 ,本组FⅤLeiden突变患者共 6例 ,其中aCL阳性者 3例。结论 虽然FⅤLeiden突变在ICVD患者中发生率不高 ,但在血栓形成中起重要作用 ,年轻ICVD患者FⅤLeiden突变发生率更高。ICVD患者FⅤLeiden突变可能与aCL阳性有关。对于aCL阳性患者 ,特别是年轻、病因不明的ICVD患者应进行FⅤLeiden突变和APC R检测 ,以期指导诊断、预防和治疗。

长链RT-PCR在若干遗传病基因突变分析中的应用

目的 以 3个遗传病为例 ,探讨长链 RT- PCR在基因突变分析中的应用。 方法 采用长链 RT- PCR扩增 AL D、ATP7B和 FV的 m RNA编码区。从凝胶中回收预期扩增产物 ,再以分段或全长方式进行二次 PCR。对二次 PCR产物进行直接序列测定 ,查找序列突变。 结果 在长链 RT- PCR中 ,三种 m RNA的编码区全长均得到扩增 ,预期扩增产物分别为 2 4 4 0 ,4 4 80 ,6 789bp。在二次 PCR中 ,分段扩增策略和全长扩增策略均可获得大量的特异性产物 ,后者均可直接用于序列测定。 结论 长链 RT- PCR对于长链 m RNA的序列分析是一个简便可靠的方法。

遗传性因子V缺乏症的基因研究

研究一个遗传性凝血因子 (FV)缺乏症重型患者的基因缺陷。方法 :采用 RT- PCR及 PCR技术 ,对先证者FV c DNA序列全长和基因组 DNA中第 11和第 13外显子的序列进行了 PCR扩增 ,PCR产物回收纯化后直接测序。结果 :对先证者 FV基因组 DNA的部分序列的 PCR扩增 ,经 DNA测序 ,发现有两个基因突变位点 ,其中 2 86 3G→ A为中性多态性位点 ,另一个 336 6 C→ G为同义突变。对先证者 FV c DNA序列全长进行分段扩增均未见目的条带。结论 :推测先证者 FV缺乏可能为 FV基因某种新的突变导致 m RNA不稳定或转录调控异常所致。

Epidemiological aspects of Budd-Chiari in Egyptian patients:A single-center study

AIM： TO describe the socio-demographic features, etiology, and risk factors for Budd-Chiari syndrome （BCS） in Egyptian patients. METHODS： Ninety-four Egyptian patients with confirmed primary Budd-Chiari syndrome were presented to the Budd-Chiari Study Group （BCSG） and admitted to the Tropical Medicine Department of Ain Shams University Hospital （Cairo, Egypt）. Complete clinical evaluation and laboratory investigations, including a thrombophilia workup and full radiological assessment, were performed to determine underlying disease etiologies.RESULTS： BCS was chronic in 79.8% of patients, acute or subacute in 19.1%, and fulminant in 1.1%. Factor V Leiden mutation （FVLM） was the most common etiological cause of disease （53.1%）, followed by mutation of the gene encoding methylene tetrahydrofolate reductase （MTHFR） （51.6%）. Current or recent hormonal treatment was documented in 15.5% of females, and BCS associated with pregnancy was present in 17.2% of females. Etiology could not be determined in 8.5% of patients. Males had significantly higher rates of MTHFR gene mutation and Behcet＇ s disease, and females had significantly higher rates of secondary antiphospholipid antibody syndrome. A highly significant positive relationship was evident between the presence of Behcet＇s disease and inferior vena caval occlusion, either alone or combined with occlusion of the hepatic veins （,0 〈 0.0001）. CONCLUSION： FVLM is the most common disease etiology and MTHFR the second most common in Egyptian BCS patients. BCS etiology tends to vary with geographic region.

Risk assessment of venous thromboembolism in inflammatory bowel disease by inherited risk in a population-based incident cohort

Inflammatory bowel disease(IBD),including Crohn’s disease(CD)and ulcerative colitis(UC),is a chronic inflammatory disease of the digestive tract with increasing prevalence globally.Although venous thromboembolism(VTE)is a major complication in IBD patients,it is often underappreciated with limited tools for risk stratification.AIM To estimate the proportion of VTE among IBD patients and assess genetic risk factors(monogenic and polygenic)for VTE.METHODS Incident VTE was followed for 8465 IBD patients in the UK Biobank(UKB).The associations of VTE with F5 factor V leiden(FVL)mutation,F2 G20210A prothrombin gene mutation(PGM),and polygenic score(PGS003332)were tested using Cox hazards regression analysis,adjusting for age at IBD diagnosis,gender,and genetic background(top 10 principal components).The performance of genetic risk factors for discriminating VTE diagnosis was estimated using the area under the receiver operating characteristic curve(AUC).RESULTS The overall proportion of incident VTE was 4.70%in IBD patients and was similar for CD(4.46%),UC(4.49%),and unclassified(6.42%),and comparable to that of cancer patients(4.66%)who are well-known at increased risk for VTE.Mutation carriers of F5/F2 had a significantly increased risk for VTE compared to non-mutation carriers,hazard ratio(HR)was 1.94,95%confidence interval(CI):1.42-2.65.In contrast,patients with the top PGS decile had a considerably higher risk for VTE compared to those with intermediate scores(middle 8 deciles),HR was 2.06(95%CI:1.57-2.71).The AUC for differentiating VTE diagnosis was 0.64(95%CI:0.61-0.67),0.68(95%CI:0.66-0.71),and 0.69(95%CI:0.66-0.71),respectively,for F5/F2 mutation carriers,PGS,and combined.CONCLUSION Similar to cancer patients,VTE complications are common in IBD patients.PGS provides more informative risk information than F5/F2 mutations(FVL and PGM)for personalized thromboprophylaxis.

视网膜中央静脉阻塞与凝血酶原基因G20210A及凝血因子Ⅴ基因Leiden突变的关系

目的:检测视网膜中央静脉阻塞(CRVO)患者凝血酶原(PT)基因G20210A及凝血因子Ⅴ(FⅤ)基因Leiden的突变情况,并探究二者突变情况与CRVO疾病的关系。方法:选取2016年6月至2018年12月本院收治的CRVO患者82例作为研究组,选取同期健康体检者80例作为对照组,应用全自动生化分析仪检测血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)水平;应用全自动化学发光仪检测血清同型半胱氨酸(Hcy)、叶酸(FA)水平;检测PT基因G20210A和FⅤ基因Leiden的限制性长度多态性。采用向后法Logistic回归分析影响CRVO疾病发生的危险因素。结果:研究组与对照组性别、年龄、饮酒情况比较,差异无统计学意义(P> 0. 05);研究组血清Hcy、TC、TG、HDL-C、LDL-C检测值显著高于对照组(P <0. 05),FA检测值显著低于对照组(P <0. 05)。研究组与对照组均仅检测到PT基因G20210A野生型和FⅤ基因Leiden野生型,均未见突变。Logistic回归分析显示,血清FA、TC、TG、LDLC水平均可能为CRVO发生的危险因素(P <0. 05)。结论:血清FA、TC、TG、LDL-C为CRVO发生的危险因素,而PT基因G20210A和FⅤ基因Leiden突变与CRVO发生无关。