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.

Frequency of the C677T Polymorphism of MTHFR, G20210A of Prothrombin and R506Q of Factor V Leiden in Type 2 Diabetics in Abidjan

In Africa, the prevalence of diabetes is escalating and remains a concern due to the numerous complications it causes. Vascular damage associated with diabetes leads to a prothrombotic state observed in diabetic individuals. Diabetes is a complex and multifactorial disease involving genetic components. With the aim of preventing complications and contributing to an efficient management of diabetes, we investigated genes likely to lead to a risk of thrombosis, in particular the C677T of MTHFR, G20210A of prothrombin, and R506Q of factor V Leiden in type 2 diabetics in Abidjan receiving ambulatory care. A descriptive cross-sectional study was carried out on consenting type 2 diabetic patients. Mutation detection was carried out using the PCR-RFLP method employing restriction enzymes. Hemostasis tests (fibrinogen, D-dimers, fibrin monomers, and von Willebrand factor) were performed using citrate tubes on the Stage? Star Max automated system. Plasminogen activator inhibitor was assayed by ELISA method, and biochemical parameters were determined using the COBAS C311. The study population consisted of 45 diabetic patients, 51.1% of whom presented vascular complications, mainly neuropathy. Disturbances in hemostasis parameters were observed, with 15.5% of patients showing an increase in fibrin monomers. Mutation analysis revealed an absence of factor V mutation (factor V Leiden) and of G20210A mutation of the prothrombin gene. However, 15.6% of subjects had a heterozygous C677T mutation of MTHFR, with 57% of them being anemic. The exploration of biological and genetic factors associated with thrombotic risk is of significant interest in the optimal management of African type 2 diabetics.

Mesenteric and portal vein thrombosis associated with hyperhomocysteinemia and heterozygosity for factor V Leiden mutation

A 79-year-old man was hospitalized because of worsening upper abdominal pain which started two days before admission and was continuously present. His personal and family historywas uneventful, he did not smoke and denied toxic habits or using any medications, including overthe-counter medications, herbal remedies or any vitamin supplements.

Prevalence of factor V Leiden and prothrombin G20210A in patients with gastric cancer

AIM： To analyze the prevalence of the two commonest thrombophilic mutations, factor V Leiden and prothrombin G20210A, in patients with gastric cancer. METHODS： One hundred and twenty-one patients with primary gastric carcinoma and 130 healthy subjects, comparable for age and sex, were investigated. Factor V Leiden was detected by using polymerase chain reaction and restriction enzyme digestion, and prothrombin G20210A gene mutation by allele-specific PCR. RESULTS： Among the 121 cancer patients, factor V Leiden was found in 4 cases （GA genotype： 3.3%） and prothrombin G20210A in 10 cases （GA genotype： 8.3%）. Of the 130 control subjects, factor V Leiden was detected in 6 cases （GA genotype： 4.6%） and prothrombin G20210A in 8 cases （GA genotype： 6.1%）. No double heterozygous carriers of both mutations were found in either group. The prevalence of both factor V Leiden and prothrombin G20210A variant was not statistically different between the cancer patients and the healthy subjects. CONCLUSION： Our study suggests that, in gastric cancer, the risk factors of thrombophilic cancer state are on acquired rather than on a genetic basis and that prothrombin G20210A does not seem to be a cofactor in gastric cancer pathogenesis.

Effect of Factor V Leiden on Thrombosis in Childhood Leukemia

Thromboembolism is an important complication in children undergoing therapy for ALL as it has the potential to impact adversely on both their survival and quality of life. The incidence of thrombosis in children with ALL varies between 1.1% and 36.7% and the actual mean is 3.2%. The aim of our study is to review the available reported data on the effect of FVL on thrombotic risk in pediatric patients with acute leukemia.

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.

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。

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

Resistance to activated protein C is a risk factor for fibrostenosis in Crohn’s disease

AIM: To evaluate the effect of resistance to activated protein C (aPCR), the most common known inherited thrombophilic disorder, on the risk of intestinal operation of fi brostenosis in patients with Crohn’s disease (CD). METHODS: In a previous study, we assessed the prevalence of aPCR in CD. In a retrospective case- controlled study, 8 of these CD patients with aPCR were now compared with 24 CD patients without aPCR, matched by gender, age at diagnosis and duration of disease in a 1:3 fashion. The primary end point was the occurrence of an intestinal CD-related operation with evidence of fibrostenosis in the bowel resection specimen. RESULTS: The Kaplan-Meier analysis revealed that patients with aPCR had a lower probability of remaining free of operation with f ibrostenosis than patients without aPCR (P = 0.0372; exact log-rank test) resulting in a signifi cantly shorter median time interval from diagnosis of CD to the fi rst operation with fi brostenosis (32 vs 160 mo). At 10 years, the likelihood of remaining free of operation with fi brostenosis was 25% for patients with aPCR and 57.8% for patients without aPCR. CONCLUSION: CD patients with aPCR are at higher risk to undergo intestinal operation of fi brostenosis than those without aPCR. This supports our hypothesis of aPCR being a possible risk factor for fi brostenosis in CD.

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.

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.

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。

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.

FvLeiden突变与我国汉族人布-加综合征的相关性及其临床意义

目的 研究FvLeiden突变 (FvL突变 )与我国汉族人散发性布 加综合征 (BCS)、家族性BCS的相关性 ,以及FvL突变在家族性BCS发病中的意义。方法 对 2 5例散发BCS、6例家族性BCS(来自A、B两个家系 )及其家系成员 (39人 )、31名健康对照者进行FvL突变分析。并对两个BCS家系进行病因调查。结果 2 5例我国汉族人散发BCS中无 1例FvL突变阳性。 6例家族性BCS中 ,4例FvL突变阳性。其中家系A两先证者 (四女儿、八女儿AⅢ7,15)及六女儿 (AⅢ11)均有FvL突变 ;家系B先证者之一 (五女儿BⅡ10 )FvL突变阳性 ,另一先证者 (二女儿BⅡ3)阴性。两家系成员中 ,AⅡ2 、BⅢ5存在FvL突变。突变类型均为杂合性突变。经系谱分析两家系FvL突变符合孟德尔遗传规律 ,与BCS发病密切相关。对照组无一例阳性。 31例BCS病例组与对照组间FvL突变频率差异无显著意义 ,而家族性BCS病例组与对照组间FvL突变频率差异有显著意义。A家系中 ,10例有程度不同下肢静脉曲张 ,其中 8例为中度以上静脉曲张 ,符合常染色体显性遗传特征。结论 我国汉族人家族性BCS与FvL突变相关 ,散发性BCS与FvL突变无关。FvL突变可能是家族性BCS的内因。

血栓栓塞症患者抗活化的蛋白C的研究

目的 探讨抗活化的蛋白 Ｃ（ＡＰＣＲ）现象在中国人血栓栓塞症发病中的作用。方法 用 ＡＰＴＴ法检测 ＡＰＣＲ敏感 比率（ＡＰＣＲ－ＳＲ）来研究４０例深静脉血栓症（ＤＶＴ）患者、５２例脑血栓形成患者和１００例正常人的ＡＰＣＲ发生率；用多聚酶 链反应－限制性内切酶长度多态性（ＰＣＲ－ＲＦＬＰ）来检测ＦＶ Ｌｅｉｄｅｎ突变；用免疫火箭电泳测血浆总蛋白Ｓ和游离蛋白Ｓ。结 果 正常人的正常化ＡＰＣＲ－ＳＲ（ｎ－ＡＰＣＲ－ＳＲ）为０．９３±０．３２，ＤＶＴ组和脑血栓组各有６例ｎ－ＡＰＣＲ－ＳＲ＜０．６１，ＡＰＣＲ发生率分 别为１５％和１１．５％，与正常对照组相比有显著差别；没有检测到ＦＶ Ｌｅｉｄｅｎ突变；ＤＶＴ组的蛋白Ｓ测值与正常人没有显著差 别。结论 ＡＰＣＲ可能是中国人群血栓栓塞症发病的一个危险因素，在不同种族中，致病机理不同。

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.

Like father, like son: Pulmonary thromboembolism due to inflammatory or hereditary condition? Two case reports

BACKGROUND Venous thromboembolism,which includes deep venous thrombosis and pulmonary embolism,is a well-known causal disorder with high morbidity and mortality rates.Inherited or acquired conditions affecting components of coagulation and fibrinolysis systems have been linked to venous thromboembolism pathogenesis as they may lead to a pro-inflammatory state in human bodies.Toxoplasmosis is a zoonosis that potentially leads to acute systemic cachectic-inflammatory effects in experimental animal models but is not yet proven in humans.It is known that venous thrombosis can occur during acute inflammatory/infectious diseases,although it is not well established with regard to toxoplasmosis alone.CASE SUMMARY A 70-year-old Caucasian man and his 32-year-old son developed general malaise,chills,fever,and myalgia,having established a diagnosis of toxoplasmosis.Twenty days later,they presented dry cough leading to further investigations that revealed an incidental deep venous thrombosis plus pulmonary embolism in them both.Thrombophilia screening showed both patients had a factor V Leiden mutation heterozygosis.Father and son completely recovered without any sequalae after anticoagulant treatment.They have not presented symptom recurrence of either medical disorder during 1 year of follow-up.CONCLUSION Toxoplasmosis may enhance the risk of venous thromboembolism in patients showing factor V Leiden mutation heterozygosis.

Anatomy of Free Flap Failures: Dissection of a Series

Introduction: Free flap success rates have remained stable in recent years ranging 93% to 98%. Historically, the causes of free flap failures were attributed to the surgeon’s inexperience and technique. However, there are factors beyond the surgical anastomosis that contribute to flap failure. The purpose of this study is to review each case of total flap loss in detail to develop a better understanding of complications. Methods: A retrospective study was performed over eleven years in a single surgeon’s practice, a predominantly head and neck reconstructive practice. All charts were independently reviewed. In patients who sustained total flap loss, a review was conducted of patient comorbidites, anesthesia records, perioperative and follow-up notes. Results: A total of 514 free flaps were performed. 76% (392) of these flaps were for head and neck reconstruction. There were 22 total flap losses (4%) and 26 partial flap losses (5%). Of the 22 total flap losses, four flaps were avulsed, five flaps were in patients later found to have coagulation disorders (homozygous mutations of the MTHFR gene and factor V Leiden), four patients were exposed to neosynephrine, two patients remained hypotensive perioperatively, and four delayed flap losses were attributed to pseudomonal infection. Five losses were technical or related to flap inexperience. Several representative case scenarios are illustrated. Conclusion: Careful review of free flap failures indicates that a thorough workup (particularly coagulation disorders), flap selection, surgeon to anesthesia communication, proper securing of the flap, and postoperative patient blood pressure and infection control have a greater part to play in this new era of anastomotic success.

血栓相关基因缺陷在体内的相互作用

目的 探讨血栓相关基因缺陷之间在体内的相互作用.方法 由α-半乳糖苷酶A（α-galactosidase A,Gla）缺乏和凝血因子V Leiden（factor V I.eiden,Fvl）基因突变小鼠建立二者复合基因突变小鼠,通过器官组织学分析,评价致病基因表现型-纤维蛋白沉积和血栓形成情况.结果 Gla缺乏与Fvl复合基因突变小鼠的器官纤维蛋白沉积较二者之一单独突变明显增加.复合突变比Gla缺乏=Gla/0FvQ/Q和Gla/FvQ/Q 比Gla-/0 Fv＋/＋=（0.28±0.03）%vs.（0.07±0.007）%,P〈0.01;复合突变比Fvl 突变=Gla/0FvQ/Q和Gla-/- FvQ/Q 比Gla＋/0 FvQ/Q和Gla＋/＋ FvQ/Q=（0.28±0.03）%vs.（0.11±0.02）%,P〈0.01.同时,Gla缺乏与Fvl复合基因突变小鼠的器官断面血栓形成数日也分别较二者之一明显增加.复合突变比Gla缺乏=1.9±0.7 vs.0.0±0.0,P〈0.05;复合突变比Fvl突变=1.9±0.7 vs.0.3±0.1,P〈0.05.结论 Gla缺乏与Fvl突变在小鼠体内相互加重血栓前状态和血栓形成,临床上GLA缺乏、FVL突变或其它血栓相关基因缺陷患者出现早发和严重的血栓疾病可能合并其它遗传性血栓相关的基因缺陷.

冠心病患者活化蛋白C敏感率及抵抗现象的研究

目的检测冠心病(CHD)患者活化蛋白C敏感率(APC-SR)并计算活化蛋白C抵抗(APCR)阳性率,探讨APC-SR及APCR在CHD中的临床意义。方法选取2006年1月至7月华中科技大学同济医学院附属协和医院心内科住院的56例CHD患者为研究对象,对照组为同期在本院耳鼻喉科住院的患者54例,采用全自动血凝分析仪测定APC-SR,计算APCR阳性率;同时采用免疫酶联吸附试验检测血浆中蛋白C、总蛋白S和游离蛋白S。结果CHD患者APC-SR平均值(2.44±0.18)显著低于对照组(2.68±0.15)(P<0.01);CHD组APCR阳性率与对照组比较,差异无显著性意义。CHD组APC-SR<2.4的阳性率显著高于对照组(P<0.01)。蛋白C、总蛋白S和游离蛋白S在CHD组和对照组之间差异无显著性意义。结论低水平APC-SR与CHD的发病相关,可考虑将该指标作为CHD危险人群的筛查指标。