冷上清在治疗血栓性血小板减少性紫癜中的应用

目的探讨冷上清在治疗血栓性血小板减少性紫癜中的临床应用价值。方法用冷上清做置换液,采用血浆置换疗法,对20例血栓性血小板减少性紫癜（TTP）患者进行治疗,判定治疗效果。结果20例TTP患者的治疗有效率达90％。结论冷上清做置换液对TTP患者进行血浆置换的疗效显著,且节约血液资源。     

血浆置换治疗血栓性血小板减少性紫癜14例分析

目的观察血浆置换（PE）治疗血栓性血小板减少性紫癜（TTP）的疗效。方法对14例患者进行血浆置换治疗,并结合免疫抑制剂、抗血小板药物及营养支持等治疗。结果血浆置换14例患者中11例存活。存活患者血浆置换治疗后清醒,发热消退,皮下无新鲜出血点和淤斑,黄疸消失。结论血浆置换治疗TTP疗效好,可明显改善TTP的预后,是治疗TTP的首选有效方法。     

血浆置换治疗血栓性血小板减少性紫癜疗效分析

目的 观察血浆置换(PE)治疗血栓性血小板减少性紫癜(TTP)的疗效.方法 12例TTP患者进行PE治疗,观察其临床症状、血液学指标缓解及不良反应.结果 10例患者临床症状缓解,外周血破碎RBC消失、Hb、PLT、LDH、sCr恢复正常,2例死亡.104次PE治疗中过敏反应3次.结论 PE治疗TTP安全有效.     

血浆置换治疗血栓性血小板减少性紫癜及影响因素研究

目的 探讨血浆置换(PE)治疗血栓性血小板减少性紫癜(TTP)临床疗效评价及影响因素的相关性研究.方法 对12例TTP患者进行PE治疗,每例连续进行3次以上,每次置换60～80 ml/kg,治疗期间同时运用免疫抑制剂.结果 12例TTP患者中,2例死亡,1例转院,9例患者贫血纠正,出血症状好转,发热消退,血小板计数上升至正常水平,肾功能(肌肝、尿素氮)指标恢复正常,乳酸脱氢酶(LDH)下降至400 U/L以下,6例痊愈出院,3例临床症状得到缓解和控制,有效率达75%.结论 PE治疗对TTP患者疗效显著,禁忌输注血小板与冷沉淀.     

血浆置换辅助治疗重症肌无力的临床疗效分析

目的评价血浆置换辅助治疗重症肌无力患者的临床效果。方法应用CS-3000PLUS全自动血细胞分离机对肌无力危象、为胸腺摘除术准备以及撤呼吸机困难患者进行血浆置换,以"706"代血浆和新鲜冰冻血浆作为置换液,每次置换血浆量为2 000 ml。结果 103名患者中每例进行PE 2～18次,平均(4.27±1.98)次,除1名肌无力危象患者因突发心肌梗塞死亡外,其余患者经过血浆置换单独或辅助治疗后均有显效或者好转,基本达到治疗目的。其中63名患者在93次血浆置换过程中出现不同程度副作用,包括口周麻木、四肢麻木、荨麻疹、寒战和发热等,经对症处理后均好转。结论血浆置换辅助治疗MG患者的肌无力危象、为胸腺摘除术准备以及撤呼吸机困难的1种有效治疗手段。     

血浆置换治疗在儿科危重患者抢救中的经验

目的探讨血浆置换治疗在儿科危重症患者的应用价值和治疗方案。方法应用GAMBR0-PRISMA床旁血滤机和TPE2000膜式血浆分离器对15例危重症患儿（1岁10月～15岁，平均6．8岁）进行39次血浆置换治疗；以新鲜冰冻血浆作置换液，置换量为40-70ml／（kg·次），血泵速度为50～120ml／min，治疗时间2～3h／次：结果39次血浆置换治疗均顺利成功实施，无明显并发症出现；14例在治疗后临床症状及生化指标好转，5例痊愈。结论血浆置换可以应用于多种危重症儿科疾病，治疗方案需根据病情制定。     

血浆置换术联合冷上清输注治疗血栓性血小板减少性紫癜

血栓性血小板减少性紫癜(TTP)是一组由于微循环中形成了血小板血栓,血小板数目因大量消耗而减少所形成的紫癜.广泛微血栓而致重要器官的功能障碍、衰竭与梗塞,后果严重.笔者用血浆置换术(PE)结合冷上清输注治疗4例TTP患者,取得了良好的临床效果.     

血栓性血小板减少性紫癜9例临床分析

目的:总结血栓性血小板减少性紫癜(TTP)的临床特点及治疗,以提高对该病早期诊治的能力.方法:回顾性分析2005年1月至2012年1月收治的9例,TTP患者的临床资料.结果:6例早期确诊患者给予输注新鲜冰冻血浆或血浆置换治疗,5例存活,1例死亡;未能早期确诊的3例均死亡.结论:TTP多具有血小板减少、微血管病性溶血性贫血和神经异常,但早期确诊困难,及时输注血浆和血浆置换是治疗TTP的有效方法.     

血浆置换在神经内科自身免疫性疾病临床治疗中的不良反应分析

目的 观察血浆置换在神经内科自身免疫性疾病临床治疗中的应用安全性.方法 回顾性分析我科2007年3月～2012年5月应用血浆置换治疗的神经内科89名患者(男性55例,女性34例),观察每次治疗期间患者的不良反应出现情况.结果 根据所患疾病类型与严重程度,置换次数在4～6次/人,共416人次,每次置换血浆量1500～3000ml.血浆置换治疗期间过敏反应最为常见,共69次;其次为心脑血管症状,共12次;输血后枸橼酸盐中毒反应6次,最早出现于置换2个循环后,最迟在置换结束后输注新鲜冰冻血浆过程中;另有低血压性休克的严重不良反应2次,均出现于急性格林-巴利综合征患者.结论 1)没有致死病例;2)出现临床不良反应症状较轻,经及时对症治疗后短时间内可恢复正常.血浆置换治疗神经内科的自身免疫性疾病是安全的.     

冷上清治疗复发性血栓性血小板减少性紫癜1例

血小板减少性紫癜(TTP)是一种少见而严重的疾病.起病急,病情重,易反复发作,不积极治疗,死亡率可达100%[1].我科1999年10月成功救治1名危重的TTP患者,与国内其它病例报告不同的是,该患者在经血浆置换救治成功后,在维持治疗中4次复发,予以冷上清治疗后,症状得以缓解,至今未再复发,现报告如下.     

Fresh-frozen plasma, pathogen-reduced single-donor plasma or bio-pharmaceutical plasma?

Three types of therapeutic plasma are available that differ in their manufacturing processes, composition, clinical efficacy, and side effects. Quarantine-stored, not pathogen-reduced fresh-frozen plasma (QFFP) is prepared from single whole blood or plasma donations. The manufacture of pathogen-reduced single-donor plasmas such as methylene blue-light treated (MLP) or amotosalen-ultraviolet light treated plasma (ALP) involves the addition of a chemical followed by irradiation and subsequent removal of the chemical. Both plasma types show substantial fluctuation of clotting factor and inhibitor levels according to interindividual variations, and both carry the risk of inducing transfusion-associated lung injury (TRALI). Photo-oxidation in pathogen-reduced single-donor plasmas reduces clottable fibrinogen and other clotting factors markedly, and there is a lack of clear evidence showing whether this is harmful or not. MLP also appears to be less effective clinically than QFFP. Like clotting factor or inhibitor concentrates, solvent/detergent-treated plasmas (SDP) are bio-pharmaceutical preparations derived from large plasma pools, and variations in plasma protein levels from batch-to-batch are for that reason low. The SD manufacturing process inevitably involves a considerable reduction of plasmin inhibitor (PI), and moderate reduction of all other clotting factors and inhibitors in the final plasma bags. Clinical studies and broad clinical use have however shown that this does not significantly reduce clinical efficacy or increase adverse events. SDPs obviously do not induce TRALI and the risk of allergic reactions is significantly lower than for QFFP. Common to all three plasma types is that the time between donation and freezing the plasma, and whether plasma from whole blood or apheresis plasma is used as starting material, are decisive determinants for the clotting factor and inhibitor potencies in the final bags. Plasma frozen 3-6h after donation, and apheresis plasma, contain markedly greater amounts of clotting factors and inhibitors than plasma frozen 15-24h after collection or plasma from whole blood. Lyophilisation and the pooling of single-donor plasma units with ABO blood group in suitable proportions (Uniplas) facilitate SDP handling and logistics without loss of clinical efficacy. SDP is obviously at least as cost-effective as QFFP if non-infectious adverse events including TRALI are taken into account, at least in younger patients and patients with good prognosis.     

Partial plasma protein replacement in therapeutic plasma exchange

We wished to determine whether subtotal replacement of protein in plasma removed at plasma exchange would be adequate to prevent hypovolemia and hypoproteinemia. Seven well nourished outpatients with chronic progressive multiple sclerosis underwent 60 plasma exchanges in which two liters of plasma were replaced with 750 ml saline followed by 1250 ml of a 5% albumin solution (62.5% albumin replacement). Total serum protein, protein electrophoresis, and immunoglobulin levels were measured before and after each exchange. Clinically, the exchanges were well tolerated. Total serum protein dropped by a mean of only 18% during the study and mean preexchange serum albumin levels were unchanged, even though immunoglobulins decreased by 57–72%. We conclude that in well nourished patients, partial albumin replacement of this magnitude is an adequate substitute for plasma removed in a plasma exchange.     

Range of fractionated plasma products to optimize plasma resources

<正>HUMAN PLASMA is a source material that is crucial for the production of unique therapeutic fractionated products.Indeed,plasma contains hundreds of proteins ensuring many physiological functions.The most abundant proteins,albumin and immunoglobulin G (IgG),are present at about 35 and 10 g/L,respectively,representing about 80% of all plasma proteins.However,other important therapeutic proteins include the coagulation factors (factor Ⅷ (FⅧ); FⅨ; Von Willebrand Factor (VWF),fibrinogen) various protease inhibitors (alpha 1-antitrypsin; antithrombin; C1-esterase) and anticoagulants (protein C) which exhibit potent physiological activity.Currently over 10 different protein therapeutics can be extracted from plasma to treat life-threatening diseases or injuries associated to bleeding and thrombotic disorders,immunological diseases,infectious conditions as well as tissue degenerating diseases,thus addressing the clinical needs of many patients.Considering that plasma is a very valuable resources available in limited supply at national levels,it is important,for ethical,medical,and economical reasons,to optimize its use by producing,at satisfactory yields,an appropriate range of safe products meeting the needs of patients.     

Dissemination of contact activation in plasma by plasma kallikrein

The dissemination of contact activation of plasma was examined by measuring the cleavage of Hageman factor (HF) molecules on two separate sets of kaolin particles, one of which contained all of the components of the contact activation system, HF, prekallikrein (PK) and high molecular weight kininogen (HMWK) in whole normal plasma, and the second set of particles containing only HF and HMWK, being prepared with PK-deficient plasma. After mixing of the particles, cleavage of HF on the second set of particles occurred at a rate similar to that occurring on the first set of particles. This indicated that rapid dissemination and burst of activity of the contact reaction takes place in fluid phase. A supernatant factor, responsibel for the dissemination of the contact reaction, was identified as kallikrein. A rapid appearance of cleaved PK (kallikrein) and HMWK on both the kaolin surface and in the supernate was observed. Within 40 s, > 70-80% of the PK and HMWK in the supernate was cleaved. On the surface, approximately 70% of each radiolabeled protein was cleaved at the earliest measurement. Cleavage of PK by activated HF occurred at least 17 times faster on the surface than in the fluid phase, as virtually no cleavage of PK occurred in fluid phase. Each molecule of surface-bound, activated HF was calculated to cleave at a minimum, 20 molecules of PK per minute. It is concluded that the contact activaton of plasma may be divided into three phases: (a) the reciprocal activation of a few molecules of zymogen HF and PK on the surface, with HMWK acting as cofactor to bring these molecules into apposition; (b) the rapid release of kallikrein into the fluid phase and the continued conversion of PK to kallikrein by each surface-bound molecule of activated HF; and (c) the activation by fluid-phase kallikrein of multiple surface-bound HF molecules, and the cleavage of multiple molecules of MHWK both in fluid phase and on the surface by the soluble kallikrein. The evidence suggests that steps b and c account for a great majority of the generation of contact activation of plasma.