低脂联素血症是冠状动脉粥样硬化严重程度的重要标志

目的　探讨人血浆脂联素水平与冠状动脉粥样硬化病变程度的关系。方法　根据冠状动脉造影结果和临床表现,将 172例临床可疑的冠心病患者进行分组,用放射免疫法检测血浆脂联素水平,同时监测患者血脂、血压、血糖及体重指数(BMI)等相关指标。结果　 (1)动脉粥样硬化病变患者血浆脂联素水平〔10. 7mg/L(1. 5~40. 5mg/L)〕明显低于阴性对照〔14. 3mg/L(2. 4~39. 8)mg/L,P<0. 01〕。脂联素水平随动脉粥样硬化程度的加重呈进行性下降。(2)血浆脂联素水平与冠状动脉的狭窄程度、BMI及甘油三酯呈负相关,与胰岛素敏感性指数及高密度脂蛋白胆固醇呈正相关 (P<0. 05)。结论　血浆脂联素水平随动脉粥样硬化的发展呈进行性下降,低脂联素血症是动脉粥样硬化发生发展的独立危险因素。     

亚甲蓝光化学法病毒灭活对新鲜冰冻血浆有效成分的影响

目的了解亚甲蓝光化学法病毒灭活对新鲜冰冻血浆有效成分的影响,为临床治疗提供依据。方法取50袋（400 ml/袋）新鲜无偿献血者血液,在6 h内完成血浆分离,并立即行亚甲蓝光化学法病毒灭活（灭活条件为光照度35 000 LUX、温度4℃、作用时间30 min）,灭活前后留取小辫,贴好标签后立即置速冻冰箱冻存;冻存1周后37℃依次解冻,采用凝固法检测Ⅷ因子含量、双缩脲法检测总蛋白含量,以灭活后含量/灭活前含量计算有效成分保有率。结果亚甲蓝光化学法病毒灭活前后血浆Ⅷ因子及总蛋白含量均较灭活前显著降低（P均〈0.05）,其保有率分别为80.88%、95.69%。结论对血浆进行亚甲蓝光化学法病毒灭活可导致Ⅷ因子含量减低;由新鲜冰冻血浆和普通冰冻血浆制备的病毒灭活血浆需考虑用于不同患者。     

宜昌地区病毒灭活血浆的质量监控及临床应用

目的:探讨宜昌地区亚甲蓝/光照法病毒灭活血浆临床应用的安全性和有效性。方法:随机抽取30袋新鲜冰冻血浆,检测其亚甲蓝病毒灭活前、后的总蛋白、凝血因子Ⅷ、APTT、PT、Fbg、亚甲蓝残留量;临床随机抽取400例输注亚甲蓝病毒灭活血浆的受血者,观察输注亚甲蓝病毒灭活血浆前后的体温、脉搏、呼吸、血压等生理指标。结果:未经亚甲蓝病毒灭活的新鲜冰冻血浆其总蛋白含量为(59.72±2.13)g/L、凝血因子Ⅷ(0.981 1±0.275 3)IU/ml、Fbg(2.64±0.52)g/L、APTT(13.20±0.19)s、PT(34.80±1.98)s;经亚甲蓝病毒灭活后其总蛋白含量为(57.02±3.13)g/L,回收率为95.5%、凝血因子Ⅷ(0.707 4±0.187 7)IU/ml,回收率为72.11%、Fbg(1.97±0.63)g/L,回收率为74.6%、APTT(17.3±0.27)s、PT(37.4±3.12)s、亚甲蓝残留量(0.162 7±0.102 6)mol/L;患者输注亚甲蓝病毒灭活血浆前后体温、脉搏、呼吸、血压差异无统计学意义。结论:宜昌地区亚甲蓝病毒灭活血浆的临床应用是安全有效的。     

4种原料血浆制备的冷沉淀质量分析

目的:探讨4种原料血浆制备的冷沉淀中部分凝血因子含量,为临床提供优质的冷沉淀制剂。方法:选取400ml ACD-B保存液全血20袋,将每袋400ml全血分为2份,制备成悬浮红细胞和滤白悬浮红细胞。制备悬浮红细胞得到的100ml血浆又分2份,制备成新鲜冰冻血浆(FFP)和新鲜病毒灭活冰冻血浆(灭活FFP);制备滤白悬浮红细胞得到的100ml新鲜滤白血浆又分2份,制备成新鲜滤白冰冻血浆(滤白FFP)和新鲜滤白病毒灭活冰冻血浆(滤白灭活FFP)。4种血浆在液体状态下留样,冰冻,备检。1周后将4种冰冻血浆对应制备成4种冷沉淀:FFP冷沉淀、滤白冷沉淀、灭活冷沉淀、滤白灭活冷沉淀。冷沉淀冰冻1周后37℃度水浴溶化后留样。检测Ⅷ因子含量(FⅧ)及纤维蛋白原(Fg)含量。结果:FFP、灭活FFP、滤白FFP、滤白灭活FFP的FⅧ及Fg回收率依次为100%、89.8%、74.3%、50.1%和100%、89.5%、52.1%、48.3%。FFP冷沉淀、滤白冷沉淀、灭活冷沉淀、滤白灭活冷沉淀的FⅧ及Fg回收率依次为100%、89.7%、78.6%、48.1%和100%、91.7%、54.7%、50.8%。结论:不同原料血浆及其制备成的冷沉淀凝血因子回收率差别较大。制备冷沉淀时应优选原料血浆,保证输血疗效。     

12w太极拳训练对绝经妇女血清脂联素的影响

目的探讨脂联素在运动防治代谢综合征中的作用及其机制。方法募集绝经后女性15名〔年龄(61.2±8.9)岁〕为运动组,10名女性〔年龄(57.1±8.4)岁〕为对照组,对运动组进行为期12 w的太极拳训练干预,干预前后分别进行人体测量指标、血液指标的测量,并检测血清脂联素水平。结果运动组干预后体质指数〔(23.43±2.86)kg/m2〕、腰围〔(79.80±7.33)cm〕、腰围身高比(50.16±4.55)、总胆固醇〔(5.36±1.00)mmol/L〕与干预前〔体质指数(24.49±2.95)kg/m2、腰围(81.67±6.82)cm、腰围身高比(51.35±3.94)、总胆固醇(6.06±0.76)mmol/L〕相比,显著降低(P<0.05);运动组干预验后高密度脂蛋白胆固醇〔(1.52±0.23)mmol/L〕与干预前〔(1.34±0.19)mmol/L〕相比,显著升高(P<0.01);运动组干预后血清脂联素水平〔(17.18±4.66)μg/ml〕显著高于对照组〔(11.41±7.91)μg/ml〕(P<0.05)。结论太极拳训练能够降低代谢综合征的危险因素,提高脂联素水平。     

脑梗死患者血浆对氧磷酯酶-1和氧化低密度脂蛋白水平的变化及意义

目的探讨脑梗死患者血浆对氧磷酯酶-1(PON-1)活性和氧化低密度脂蛋白(ox-LDL)含量变化以及它们在脑梗死发生发展过程中的作用。方法用对氧磷为底物的速率法和酶联免疫吸附法(ELISA)分别测定75例急性期脑梗死患者血浆PON-1活性和ox-LDL水平,并与35例脑出血患者及46例健康对照组比较。结果(1)脑梗死患者血浆PON-1活性为(138.2±25.3)U/L,明显低于脑出血组〔(168.2±28.2)U/L〕及健康对照组〔(171.1±28.5)U/L〕(P<0.01);脑梗死患者血浆ox-LDL水平为〔(615.3±253.2)μg/L〕,明显高于脑出血组〔(460.9±193.0)μg/L〕及健康对照组〔(437.7±187.4)μg/L〕(P<0.01)。(2)大梗死灶组血浆PON-1活性明显低于中梗死灶组和小梗死灶组。而大梗死灶组血浆ox-LDL水平明显高于中梗死灶组和小梗死灶组(P<0.01)。(3)相关分析表明,脑梗死时血浆PON-1活性与ox-LDL水平呈负相关(r=-0.556,P<0.01),而与血脂水平无明显的相关关系。结论脑梗死患者血浆PON-1活性降低和ox-LDL水平升高,提示血浆PON-1可能通过降低抗氧化能力机制参与了脑梗死的病理生理过程。     

4种新鲜冰冻血浆质量分析

目的:分析4种新鲜冰冻血浆(FFP)部分有效成分的含量,为临床使用提供实验依据。方法:随机抽取20袋新鲜全血,每袋(400±40)ml,按照标准操作规程分别制备出4种FFP,分别为:FFP、去白细胞新鲜冰冻血浆(去白细胞FFP)、病毒灭活新鲜冰冻血浆(病毒灭活FFP)、去白细胞病毒灭活新鲜冰冻血浆(去白细胞病毒灭活FFP)。采用凝固法检测凝血因子Ⅷ含量(FⅧ:C)及纤维蛋白原含量(Fg);采用双缩脲法检测血浆蛋白含量。结果:血浆经过单纯滤除白细胞后Fg含量为(1.913±0.209)g/L,与FFP比较差异有统计学意义(t=3.797,P0.01);经过单纯病毒灭活之后FⅧ:C含量及Fg含量分别为(0.699±0.174)IU/ml、(1.114±0.232)g/L,与FFP比较t值分别为4.071、16.201,差异均有统计学意义(均P0.01);经过滤除白细胞及病毒灭活2道工序之后,则FⅧ:C含量、Fg含量及血浆蛋白含量分别为(0.471±0.071)IU/ml、(1.033±0.159)g/L、(55.6±2.7)g/L,与FFP比较t值分别为9.860、21.819、2.882,差异均有统计学意义(均P0.01);与病毒灭活FFP比较,去白细胞病毒灭活FFP FⅧ:C含量下降了32.6%。结论:4种FFP中,去白细胞病毒灭活FFP有效成分含量最低,其中FⅧ:C含量低于国家标准。在临床使用这4种FFP时应注意其区别,作为冷沉淀凝血因子原料血浆时应注意其质量的不同。     

吡格列酮联合利拉鲁肽对老年2型糖尿病合并非酒精性脂肪肝患者血浆脂联素、转化生长因子-β1水平的影响

目的探讨吡格列酮联合利拉鲁肽对老年2型糖尿病合并非酒精性脂肪肝患者血浆脂联素、转化生长因子(TGF)-β1水平的影响。方法选择老年2型糖尿病合并非酒精性脂肪肝患者62例,按照随机表法分为对照组与治疗组,各31例。对照组给予利拉鲁肽治疗,观察组在对照组基础上结合吡格列酮治疗。两组疗程均为12 w。比较两组疗效,治疗前后糖代谢变化、肝功能、脂联素和TGF-β1水平变化。结果治疗组治疗总有效率显著高于对照组(χ^2=5.415,P<0.05)。治疗组治疗后空腹血糖(FPG,6.73±0.43)mmol/L、糖化血红蛋白(HbA1c,7.08%±0.32%)和2 h餐后血糖(2 h PG,9.21±0.76)mmol/L显著低于对照组〔(7.21±0.28)mmol/L、(7.71±0.41)%和(10.63±0.89)mmol/L,t=5.208、6.744、6.756,P<0.05〕。治疗组治疗后谷丙转氨酶(ALT,37.76±3.37)U/L、γ谷氨酰转肽酶(GGT,43.19±3.26)U/L和谷草转氨酶(AST,28.93±2.24)U/L显著低于对照组〔(42.18±2.78)U/L、(48.42±3.78)U/L和(32.26±2.37)U/L,t=5.633、5.834、5.686,P<0.05〕。治疗组治疗后血清脂联素(6.32±0.61)mg/L显著高于对照组〔(5.49±0.46)mg/L〕,而TGF-β1〔(7.43±0.76)μg/L〕显著低于对照组〔(9.89±1.02)μg/L,t=6.049、10.768,均P<0.05〕。结论吡格列酮联合利拉鲁肽对老年2型糖尿病合并非酒精性脂肪肝患者疗效明显,可改善患者糖代谢和肝功能,且可提高脂联素水平及降低TGF-β1水平。     

B超检测老年冠心病患者颈动脉内-中膜厚度和肱动脉舒张功能的变化

目的　观察老年冠心病患者的颈动脉内 中膜厚度 (IMTc)及高脂餐后肱动脉舒张功能的变化。　方法　采用高分辨超声检测技术观察老年冠心病患者 (30例 )、老年健康人 (2 2例 )及非老年健康人 (11例 )的IMTc及高脂餐前后肱动脉血流介导的血管舒张功能 (FMD)的变化。　结果　老年冠心病组的IMTc〔(1 13± 0 2 3)cm〕显著高于老年健康组〔(0 94± 0 2 0 )cm〕及非老年健康组〔(0 78± 0 14)cm〕 ,差异均有非常显著性 (均为P <0 0 1)。老年冠心病组的空腹FMD〔(3 4± 1 7) %〕显著低于老年健康组〔(5 3± 3 3) % ,P <0 0 5〕及非老年健康组〔(8 1± 3 9) % ,P <0 0 1〕。年龄与IMTc呈正相关 (r=0 44 4,P <0 0 5 ) ,与空腹FMD呈负相关 (r =- 0 6 5 0 ,P <0 0 0 1) ;高脂餐后 3组受试者的FMD显著减弱〔分别为 (0 6± 0 7) %、(2 6± 2 0 ) %及 (4 2± 2 8) % ;均为P <0 0 0 1〕 ,其中老年冠心病组的FMD下降程度〔ΔFMD % ,(76 7± 10 4) %〕显著高于老年健康组〔(5 4 1± 3 7) %〕及非老年健康组〔(5 0 8± 3 3) %〕 ,差异有显著性 (均为P <0 0 5 )。　结论　老年冠心病患者存在严重的颈动脉粥样硬化与血管舒张功能失调 ,高脂餐后血管舒张功能的进一步减弱 ,可能是诱发急性冠状动脉事     

样品热灭活对HIV抗体筛查和确证试验结果的影响研究

目的研究血浆样品经热灭活(56℃30min)后,其艾滋病病毒(HIV)抗体筛查和确证试验结果是否会受到影响。方法取5份HIV抗体阳性血浆样品,各分为2管,其中1管进行热灭活处理,然后对这2组样品分别进行10倍系列稀释,用1种HIV抗体酶联免疫吸附试验(ELISA)试剂检测,比较S/CO比值。取300份血浆样品,分为灭活组和普通组,分别用5种HIV抗体ELISA试剂(其中第三代试剂3种、第四代试剂2种)和3种HIV抗体快速检测试剂进行筛查检测,出现筛查阳性反应的样品进一步做确证试验。结果随着稀释度的增加,5份HIV抗体阳性样品灭活前后的ELISA检测结果(S/CO比值)都逐渐减小,直至转为阴性反应,其中4份样品灭活后比灭活前早一个稀释度转阴,1份同时转阴,提示灭活过程会略微降低HIV抗体的浓度。用5种ELISA试剂、3种快速检测试剂检测300份样品,样品灭活前后的检测结果差异均无统计学意义;对出现筛查阳性反应的所有样品,灭活前后的确证试验检测结果一致。结论经56℃30min热灭活后,尽管HIV阳性血浆样品中的HIV抗体浓度略有降低,但对于未经稀释的常规临床血浆样品来说,热灭活处理不会明显影响目前常用筛查、确证试剂的检测结果。     

Rapid reversal of oral anticoagulation with warfarin by a prothrombin complex concentrate (Beriplex): efficacy and safety in 42 patients

Beriplex, a prothrombin complex concentrate (PCC), was administered to 42 patients requiring immediate reversal of their oral anticoagulant therapy. The dose administered was determined using the pretreatment International Normalized Ratio (INR). Blood samples were obtained before treatment and at 20, 60 and 120 min after treatment. The following investigations were performed on all samples - INR, clotting factors II, VII, IX and X, coagulation inhibitors protein C (PC) and antithrombin (AT), and other markers of disseminated intravascular coagulation, plasma fibrinogen, D-dimer and platelet count. Immediate reversal of the INR, the vitamin K-dependent clotting factors and PC was achieved in virtually all patients. Reduced AT levels were present in 18 patients before treatment. Further slight AT reductions occurred in four patients, but other associated abnormalities of haemostasis were observed in only one of the four patients. One patient with severe peripheral vascular disease, sepsis and renal and cardiac failure died of a thrombotic stroke following leg amputation, 48 h after receiving Beriplex. No other arterial and no venous thromboembolic events occurred within 7 d of treatment. Beriplex is effective in rapidly reversing the anticoagulant effects of warfarin, including PC deficiency, without inducing coagulation activation. Caution should continue to be exercised in the use of these products in patients with disseminated intravascular coagulation, sepsis or liver disease.     

A comparison of the efficacy and rate of response to oral and intravenous Vitamin K in reversal of over-anticoagulation with warfarin

The role of oral Vitamin K administration in the reversal of anticoagulation is not yet clear because of a paucity of data on the early effects of treatment, apparent differences in efficacy between preparations and a lack of data comparing oral with intravenous administration. We have compared the effects on the International Normalized Ratio (INR) and activities of the Vitamin K-dependent clotting factors II, VII, IX and X at 4 h and 24 h after administration of three oral Vitamin K preparations and of intravenous Vitamin K in 64 anticoagulated patients who required non-urgent partial correction of anticoagulation. Our data confirm that correction of anticoagulation is more rapid after intravenous administration of Vitamin K than after oral administration of similar or larger doses. At 24 h, satisfactory correction of INR can be achieved using low-dose Vitamin K given by either the intravenous or oral route. Our data, and that from previous studies, suggest that there may be differences in efficacy between orally administered products. Administration of Vitamin K by either route was accompanied by changes in the activities of the Vitamin K-dependent clotting factors that reflected their respective biological half-lives. In the 24 h after treatment, the relationship between the INR and the individual Vitamin K-dependent clotting factors was similar to that described previously in stable anticoagulated patients. We conclude that the reversal of anticoagulation with warfarin is achieved more rapidly by intravenous administration of Vitamin K. Satisfactory, but slower, reversal of anticoagulation can be effected using oral Vitamin K, but there may be differences in efficacy between the products tested in our study.     

Prothrombin complex concentrates in emergency bleeding disorders

The use of prothrombin complex concentrates (PCCs), a heterogeneous combination of coagulation factors and counterbalancing inhibitor components, has broadened in recent years beyond single‐factor replacement in conditions such as hemophilia B, to encompass emergency reversal of anticoagulation secondary to oral vitamin K antagonists, ie, warfarin therapy. PCCs also have been studied in other bleeding disorders, such as surgery‐related and trauma‐related bleeding. This review provides an updated examination of the differences among PCC formulations, their potential role in the management of bleeding disorders, and the primary safety issues affecting their use. Am. J. Hematol. 2012. © 2012 Wiley Periodicals, Inc.     

Emergency reversal of anticoagulation: from theory to real use of prothrombin complex concentrates. A retrospective Italian experience

Background

Prothrombin Complex Concentrates (PCC) are administered to normalise blood coagulation in patients receiving oral anticoagulant therapy (OAT). Rapid reversal of OAT is essential in case of major bleeding, internal haemorrhage or surgery.The primary end-point was to evaluate whether PCC in our hospital were being used in compliance with international and national guidelines for the reversal of OAT on an emergency basis. The secondary end-point was to evaluate the efficacy and safety of PCC.

Materials and methods

All patients receiving OAT who required rapid reversal anticoagulation because they had to undergo emergency surgery or urgent invasive techniques following an overdose of oral anticoagulants were eligible for this retrospective observational study.

Results

Forty-seven patients receiving OAT who needed rapid reverse of anticoagulation were enrolled in our study. The patients were divided in two groups: (i) group A (n=23), patients needed haemostatic treatment before neurosurgery after a head injury and (ii) group B (n=24), patients with critical haemorrhage because of an overdose of oral anticoagulants. The International Normalised Ratio (INR) was checked before and after infusion of the PCC. The mean INR in group A was 2.7 before and 1.43 after infusion of the PCC; in group B the mean INR of 6.58, before and 1.92 after drug infusion. The use of vitamin K, fresh-frozen plasma and red blood cells was also considered. During our study 22 patients died, but no adverse effects following PCC administration were recorded.

Discussion

In our study three-factor-PCC was found to be effective and safe in rapidly reversing the effects of OAT, although it was not always administered in accordance with international or national guidelines. The dose, time of administration and monitoring often differed from those recommended. In the light of these findings, we advocate the use of single standard protocol to guide the correct use of PCC in each hospital ward.     

Acute Iron Intoxication with Abruptly Reduced Levels of Vitamin K-Dependent Coagulation Factors

A 17-year-old girl swallowed at least 50 Duroferon duretter®. Each tablet contains ferrous sulphate equivalent to 0.1 g Fe²⁺. Thus, a total of 5 g Fe²⁺ was ingested. Vitamin K-dependent coagulation factors dropped within the next hours to very low levels. Thrombotest showed less than 3% of normal coagulation activity 8 h after oral intake. Recovery was uneventful except for laboratory evidence of transient liver damage. The rapidity by which the early coagulation deficiencies developed and the lack of evidence of disseminated intravascular coagulation suggested a direct effect of iron on coagulation factors. In vitro studies confirmed that iron in concentrations that may have been attained in vivo, altered the functional activity of several coagulation factors. Monitoring the vitamin K-dependent coagulation factors may be a simple and useful parameter in acute iron intoxication.     

Warfarin resistance associated with parenteral nutrition

Warfarin is widely used as an oral anticoagulant for the prevention and long-term treatment of venous thromboembolism and for the prevention of thromboembolic complications associated with atrial fibrillation, heart valve replacement and myocardial infarction. Warfarin exerts its anticoagulation effect by inhibiting the enzymes responsible for the cyclic interconversion of vitamin K in the liver. Vitamin K serves as a cofactor required for the carboxylation of the vitamin K-dependent coagulation proteins. By inhibiting the supply of vitamin K in the production of these proteins, warfarin indirectly slows their rate of synthesis. The authors describe a 46-year-old patient readily anticoagulated for a deep venous thrombosis who then required large doses of warfarin after initiation of total parenteral nutrition, which included lipid preparation that contained vitamin K, in addition to vitamin K required for the daily parenteral nutrition. The effect of total parenteral nutrition with vitamin K on anticoagulation is discussed.     

Long-chain n-3 fatty acids specifically affect rat coagulation factors dependent on vitamin K: relation to peroxidative stress

Fatty acids of marine origin have been shown to affect blood coagulation in the rat. In an attempt to gain insight into the mechanisms of this phenomenon, we studied the effects of dietary linseed and fish oils on the liver antioxidant status and plasma coagulation parameters in rats on a time-course basis. Dietary enrichment in eicosapentaenoic and docosahexaenoic acids resulted in strong hypocoagulation after only 1 week and a concomitant increase in liver lipid peroxidation and tocopherolquinone content. Enrichment in linolenic acid induced similar increases in lipid peroxidation and tocopherol catabolism but negligible alteration of coagulation. A significant correlation between plasma factor II coagulant activity and liver tocopherolquinone was found in fish oil- but not in linseed oil-fed rats. Although ingestion of tocopherolquinone led to high levels of this compound in the liver, it had only marginal effects on coagulation factors. Thus, it seems unlikely that this vitamin E metabolite could be involved in the lowering of vitamin K-dependent clotting factors through inhibition of gamma-glutamylcarboxylase. Rather, our results indicate that the effects of the n-3 fatty acids of fish oil on vitamin K-dependent coagulation factors are specific and independent of liver tocopherolquinone levels.     

Effect of oral anticoagulant treatment on markers for calcium and bone metabolism

Vitamin K-dependent proteins regulate blood coagulation as well as bone growth and calcification. Here, we have compared the effects of oral anticoagulants on circulating vitamin K-dependent proteins and on markers for calcium and bone metabolism. Patients with a clinical indication for antithrombotic therapy were randomized into three groups and treated with either aspirin, regular-intensity anticoagulation [target international normalized ratio (INR) values: 2.5-3.5] or low-intensity anticoagulation (target INR values: 1.1-1.6). At the start and after 1 year of treatment, various biochemical markers were assessed. Both the circulating levels and the degree of carboxylation of the various gamma-carboxyglutamate (Gla)-containing proteins were affected differently by oral anticoagulant treatment. Circulating osteocalcin was more sensitive to poor vitamin K status than other Gla proteins. From the fact that - except for osteocalcin - neither markers for osteoblast nor osteoclast function were affected by oral anticoagulant treatment, we conclude that bone turnover remained unaltered, which is indicative of an unchanged rate of bone loss. Whether the long-term production of undercarboxylated bone Gla proteins may have a negative effect on the quality of bone (e.g. bone strength) cannot be concluded from this study.     

Heterozygous protein C deficiency type I

Summary Protein C is a vitamin K-dependent plasma protein which has anticoagulatory and profibrinolytic properties as a result of inactivating coagulation factors Va and VIIIa and enhancing fibrinolysis. Heterozygous protein C deficiency is well known to be a risk factor for thromboembolic diseases. We here present a family with 16 members deficient in protein C, out of which only two persons were suffering from thromboembolic disorders. In patients suffering from heterozygous protein C deficiency thromboembolic complications in childhood are rare and are not obligatory in adults. These patients should therefore not be treated with oral anticoagulants unless thromboembolic complications have already occurred or are imminent. Coumarin anticoagulation implicates a serious risk of coumarin skin necrosis in protein C deficient patients during the initial therapeutic phase. This risk may be avoided by initiating coumarin therapy with low doses of the drug and in cases of thromboembolic complications by overlapping with heparin anticoagulation.     

Vitamin K2 (Menaquinone-7) supplementation does not affect vitamin K-dependent coagulation factors activity in healthy individuals

Background:Vitamin K has long been regarded as a procoagulant drug by physicians, and concerns have been raised with regard to its effects on hemostasis. Although many studies have shown that vitamin K supplementation is safe for thrombotic events, the effect of vitamin K supplementation on the activities of vitamin K dependent procoagulation factors in healthy individuals is not available.Objectives:This study aimed to investigate whether vitamin K2 supplementation at recommended doses affects the activity of vitamin K dependent procoagulation factors in healthy individuals without any anticoagulation treatment.Design:Forty healthy volunteers between 25 and 40 years of age were recruited. Menaquinone-7 (MK-7) was administrated at 90 μg for 30 days. Prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), and blood coagulation factors II, VII, IX, and X activities and Protein induced by vitamin K absence or antagonist-II (PIVKA-II) were measured on days 0 and 30 after MK-7 administration.Results:PT, APTT, and TT showed no significant differences on day 30 when compared with baseline. The activities of coagulation factors II, VII, IX, and X on day 30 showed no significant differences with those at baseline. PIVKA-II levels were unchanged after 30 days of MK-7 supplementation.Conclusions:MK-7 supplementation at recommended dosage does not affect vitamin K-dependent coagulation factors’ coagulation activity, and does not enhance the carboxylation of prothrombin in healthy individuals. This indicated that MK-7 administration does not alter hemostatic balance in healthy populations without anticoagulation treatment.