两种血小板制剂应用于儿科血液病的临床观察

目的观察并比较机器单采法及手工法分离制备血小板制剂用于儿科血液病输注的效果。方法输注机器单采血小板患儿463例次为机采制剂组,输注手工分离血小板制剂患儿155例次为手工制剂组,分别在输注后24、48及72h作外周血血小板计数,观察临床止血效果、有无输血反应发生,计算血小板计数增加校正指数(CCI)、血小板回升率(PPR)、输注无效率、输血反应发生率等指标。结果输注后24、48、72h,机采制剂组:CCI分别为18.9、15.4、14.1,PPR分别为33.4%、27.8%、25.0%;手工制剂组:CCI分别为11.3、9.4、2.9,PPR分别为20.3%、10.3%、3.8%;机采法制剂组均明显高于手工制剂组(P<0.01)。机采制剂组输注无效率10.58%、输血反应发生率3.02%,手工制剂组相应为32.90%及11.61%,机采组虽都明显低于手工组,但两组均达到较好的临床止血目的,组间无差异。结论输注机器单采血小板制剂能更有效地提高血液病患儿的血小板值,减少其血小板输注无效及输血反应的发生。     

手工与机采血小板疗效的临床观察

目的 比较手工血小板和机采血小板的疗效,为临床输血提供参考依据.方法 样本来源于该院经过血小板输注治疗的住院患者,其中134例患者输用6 756 U手工血小板为A组;74例患者输用2 880 U机采血小板为B组.分别观察两组患者输注24 h后血小板校正增加指数（CCI）、血小板回收率（PPR）、临床出血症状有无改善、有无输血反应等进行输注后疗效判断.结果 与B组比较,A组CCI、PPR、总的输注有效率、输注反应率比较差异均无统计学意义（P〉0.05）.结论 对于未产生同种免疫的患者,输注手工血小板或机采血小板,具有同等的安全性和有效性.因此,手工血小板的应用能够节约血液资源,缓解血小板供应紧张的现状.     

3种血小板制剂临床输注效果的研究

目的观察不同血小板制剂在临床上的输注效果,为临床合理应用不同种类的血小板制剂提供参考。方法174名患者输注新鲜机采血小板制剂(组1),116名患者输注冰冻机采血小板制剂(组2),48名患者输注手工采集血小板制剂(组3)。在输注后24h,观察临床止血效果、有无输血反应发生,比较计算血小板增加数校正值(CCI)、血小板回升率(PPR)、输注无效率、止血率及输血反应率。结果CCI的各组间比较均有差异。PPR的组间比较:组1与组2,组1与组3均有差异。血小板输注无效率的3组间比较无差异。血小板输注后止血率的组间比较:组1与组3有差异。输血反应发生率的组间比较:组1与组3、组2与组3有差异。结论3种血小板制剂在临床上都有明确疗效,但新鲜机采血小板的作用优于其它两种血小板制剂。但需综合考虑患者情况,合理使用血小板制剂,才能更好地满足患者治疗需要。     

机采血小板输注疗效观察

目的 比较出血性血液病患者机采血小板与手工血小板榆注效果.方法 将42例血小板减少患者分别输注机采血小板和手工血小板后检测外周血小板计数,以校正血小板计数增值(CCI)判定输注效果.结果 机采组输注后1h,输注后24h,CCI高于手工采组,机采组输血无效率低于手工采组,均有统计学意义(p＜0.01).结论 机采血小板输注疗效优于手工血小板.     

血液病反复输血患者血小板抗体、交叉配型结果与血小板输注效果的相关性分析

目的探讨血液病反复输血患者血小板抗体、交叉配型试验结果与血小板输注效果的关系。方法回顾性分析112例血液病反复输血患者临床资料,根据入院时血小板抗体检验结果将其分为阳性组与阴性组,配型到阴性或弱阳性供者标本纳入相合亚组,多次配型均为阳性供者标本纳入不合亚组。比较阳性组与阴性组首次输注后,相合亚组与不合亚组本次输注后,1 h、24 h血小板校正增高计数(CCI)及血小板回收率(PPR)差异,采用Spearman相关系数模型分析1 h、24 h血小板CCI及PPR与血小板抗体检验、交叉配型试验结果的相关性。结果阳性组1 h CCI、24 h CCI、1 h PPR、24 h PPR水平均明显低于阴性组(P<0.05),相合亚组1 h CCI、24 h CCI、1 h PPR、24 h PPR水平均明显高于不合亚组(P<0.05)。血小板抗体测试结果与1 h CCI、24 h CCI、1 h PPR、24 h PPR水平均呈显著负相关(P<0.05);交叉配型试验结果与1 h CCI、24 h CCI、1 h PPR、24 h PPR水平均呈显著正相关(P<0.05)。结论血小板抗体检测及交叉配型结果与反复输血患者血小板输注效果关系较为密切,临床需积极开展上述试验以避免不必要的血小板资源浪费。     

冰冻血小板和新鲜血小板临床输注效果的差异分析

目的 比较冰冻血小板和新鲜血小板用于治疗血液病及创伤性失血后患者在止血与血小板计数方面存在的差异.方法 40例患者输注冰冻血小板,40例患者输注新鲜血小板.对血小板增高指数(CCI)和血小板回收率(PPR)、患者输注前后出血改善程度三方面进行评价.结果 输注冰冻血小板1 h CCI(5.8±1.4)×109、PPR 36%,24 h CCI(2.9±1.0)×109、PPR 18%.输注新鲜血小板1 h CCI(20.1±4.8)×109、PPR 72%,24 h CCI(16.0±6.1)×109、PPR 56%.CCI值和PPR值比较,P＜0.05,提示外周血小板计数差异有统计学意义.输注冰冻血小板组平均提高血小板计数能力不及输新鲜血小板组高,但两组输注后患者出血情况均有改善.结论 在提高外周血小板计数方面两种制剂有差异,输新鲜血小板提升外周血小板计数效果好,输冰冻血小板效果差.评判冰冻血小板的效果,不以单纯外周血小板的计数指标评价,应综合评价.冰冻血小板只适用于应急止血,不适合常规使用,新鲜血小板是血液病患者的首选制剂.两种制剂在有效止血方面差异无统计学意义.     

血液病患者两种血小板输注的临床疗效比较

目的 探讨单采和手工分离血小板输注对血液病患者的临床疗效差异,为临床合理、有效使用血小板提供参考依据.方法 选择62例(256例次)输注血小板的血液病患者,其中输注单采血小板患者39例为单采组,输注手工分离血小板患者23例为手工组,于输注前、输注后24 h进行外周血小板计数,根据血小板计数增高指数(CCI)、血小板回收率(PPR)等指标来判断临床疗效.结果 输注有效率、输血不良反应率、输注后24 h CCI和PPR在两组间比较差异有统计学意义(P＜0.05).结论 对需反复输血的血液病患者,输注血小板次数影响血小板输注疗效,输注单采血小板的临床疗效明显优于手工分离血小板,应首选单采血小板输注.     

血小板抗体检测在新生儿血小板减少症诊治中的应用

目的探讨血小板抗体检测在新生儿血小板减少症(NT)诊治中的应用。方法采用固相凝集法(MASPAT)对2014年5月-2016年10月本院新生儿科收治的110名NT患儿和其中18名患儿的母亲做血小板抗体检测,根据检测结果将其分为血小板抗体阳性组(观察组)和阴性组(对照组),比较2组患儿发病时间、颅内出血情况,分析组间差异,对比2组随机输注患儿的24 h血小板纠正计数增加值(24 h CCI)。结果本组患儿血小板抗体阳性率20.91%(23/110)。观察组与对照组NT发病时间:≤72 h者分别为82.61%(19/23)vs 49.43%(43/87),72 h者分别为17.39%(4/23)vs 50.57%(44/87)(P0.05);颅内出血:60.87%(14/23)vs 31.03%(27/87)(P0.05);对34名Plt50×109/L需输注血小板的重症NT患儿采取随机输注,24 h CCI(×109/L)组间比较:≥7.5者分别为100%(7/7)vs 85.19%(23/27)(P0.05)。结论免疫性NT患儿多为重症,发病时间急,伴有严重的颅内出血;免疫因素所致NT患儿可不做配型随机输注血小板,亦能达到预期疗效。对围生期血小板减少孕妇做免疫性血小板抗体监测有助于降低NT发病率。     

单采血小板与浓缩血小板的临床疗效比较

目的 比较单采血小板与浓缩血小板的临床疗效.方法 对212例患者输注血小板前后的血小板数值进行检测,根据血小板计数增加指数(CCI)、血小板回收率(PPR)以及临床症状进行疗效评估.结果 单采血小板和浓缩血小板均有输注疗效,单采血小板有效率CCI 89.09%,PPR 93.64%,浓缩血小板有效率CCI 63.73%,PPR 69.61%;单采血小板组和浓缩血小板组在输注后1 h CCI、24 h CCI以及1 h PPR比较,差异有统计学意义(P<0.05),24 h PPR比较差异有统计学意义(P<0.01);两组在临床出血症状疗效比较差异有统计学意义(P<0.01).结论 对血小板减少的患者,输注单采血小板可明显提升外周血中的血小板数量,并能迅速起到止血的目的,防止大出血并发症,而浓缩血小板效果不显著.     

冰冻机采血小板临床疗效分析

目的探讨冰冻机采血小板在临床上的疗效.方法对预防性输注冰冻机采血小板病人,检测血小板输注前和输后1h及24h血小板计数,计算出血小板增值(CCI);治疗性急性出血输注冰冻机采血小板病人检测血小板输注前及输后1h出血时间.以输注新鲜机采血小板的患者作平行对照.结果预防性输注组中,测定1h CCI＞7.5×109/L的百分率,冰冻机采血小板组86.7%(13/15),新鲜机采血小板组90.9%(20/22),两组比较差别无显著性(P>0.05);24h CCI＞4.5×109/L的百分率,冰冻机采血小板组53.3%(8/15),新鲜机采血小板组86.4%(19/22),两组比较差别有显著性(P<0.05);治疗性急性出血组输注血小板前两组出血时间无显著性差别(t=0,P＞0.05),输注后1h两组出血时间差别有显著性(P＜0.05).结论冰冻血小板治疗急性出血患者效果优于新鲜血小板,预防性输注效果显著差于新鲜血小板.     

Frozen platelets

The technical limitations on platelet shelf life and storage have driven research for alternatives, including cryopreservation of platelets. Over the past 60 years, product development has adopted freezing platelets in 6% dimethyl sulfoxide (DMSO) and storage in mechanical freezers at ?80?°C for up to 2 years. Frozen platelets show a primed, hypercoagulable in vitro phenotype post-thaw when assayed using morphology, flow cytometry for marker expression, and thrombin capacity. In vivo studies show a role for frozen platelets in the maintenance of hemostasis and data from limited clinical trials show frozen platelets are safe and appear beneficial. As research continues to address the functional role of in vitro assays for clinical outcomes, frozen platelet product development represents a good alternative to room temperature platelets for many applications.     

Physiology of cold-stored platelets

Platelet transfusions are a life-saving medical intervention used for the treatment of thrombocytopenia or hemorrhage. Extensive research has gone into trying to understand how to store platelets prior to the transfusion event. Much has been learned about storage bag materials, synthetic solutions, and how temperature impacts platelet viability and function. While room temperature storage of platelets preserves 24-hour in vivo platelet recovery and survival there is a greater risk for bacterial growth. Therefore, cold storage of platelets has become attractive due to the reduction in potential bacterial proliferation and the maintenance of platelet function beyond 5 days of storage. Cold stored platelets, however, have their own set of challenges. Cold stored platelets become activated through several mechanisms. The morphological and molecular changes that occur due to cold exposure enhance their ability to participate in the hemostatic process at the cost of rapid clearance from circulation. This review focuses on the underlying mechanisms leading to cold platelet activation and the receptor modifications involved in platelet clearance.     

Coagulation activity of platelets

Haemostasis is the concerted action of blood components aimed at prevention of blood loss after vessel injury. Thrombosis is the other side of the coin, a misled physiological process, i.e. a haemostatic reaction occurring at a diseased vessel wall. Haemodynamic forces enrich platelets in a fluid boundary layer adjacent to the vessel wall where they flow along the endothelium scanning it for defects. Once the platelets detect an injury they immediately adhere--a process beginning with initial deceleration and attachment via glykoprotein (GP) Ibalpha receptor-binding to immobilized von Willebrand factor (VWF). The GPIb receptor requires no stimulation. This is in contrast to subsequently interacting receptors such as integrin alphaIIbbeta3 (GPIIb/IIIa), integrin alpha2beta1, and GP VI, which are activated via outside-in and inside-out signalling. The latter receptors bind to their respective ligands: VWF, fibrinogen, collagen and other subendothelial proteins. Upon the first layer of adherent platelets additional accrual of platelets is transient when mediated by VWF, but is then stabilized by fibrinogen bridging integrin alphaIIbbeta3 receptors on neighboring platelets. Such aggregates present a large mass of procoagulant membranes, the surface of which serves for complexation and activation of clotting factors. Thereby fibrin polymerization is accelerated manyfold. In addition, platelets contain mRNA for fast production of tissue factor, the most effective trigger of extrinsic coagulation. The formed fibrin fibers stabilize the platelet aggregates against detachment by shear forces. A shortened clotting time probably due to activated membranes was also found with microparticles generated at high shear rates through GPIb-VWF-interaction. Thus, platelets and platelet derived microparticles seem to play an important role not only in focussing the haemostatic response to the region of injury but also in initiating and accelerating the subsequent clotting reaction.     

The release of prion protein from platelets during storage of apheresis platelets

BACKGROUND: Recent studies using a time-resolved fluoroimmunoassay method (dissociation-enhanced lanthanide fluoroimmunoassay) showed that platelets and plasma are the main reservoir of the normal isoform of cell-associated prion protein (PrPc) in human blood. The aims of the present study were to monitor PrPc levels in various fractions of apheresis platelets during storage by using the DELFIA method and to assess the association of this release with alpha-granule protein ss-thrombo-globulin and cytoplasmic LDH. STUDY DESIGN AND METHODS: Units of apheresis platelets (n = 6) were obtained from volunteer donors by the use of a cell separator and stored up to 10 days. Samples (7-9 mL) were aseptically collected from each unit on storage Days 1, 2, 3, 4, 5, 8, and 10. Platelet-poor plasma and apheresis platelets were prepared and the former split into two fractions, one centrifuged at 40,000 x g for 2 hours at 4 degrees C to remove microparticles. The spun microparticles, apheresis platelets and platelet samples, platelet-poor plasma, and high-spun plasma fractions were stored in a frozen state until they were tested. RESULTS: The results showed that the mean overall levels of PrPc throughout storage remained within 15 percent of Day 1 levels. In contrast, the mean cellular levels in platelets significantly decreased to 46 percent of Day 1 levels by Day 10 of storage (p<0.01), while the corresponding levels in plasma significantly rose as much as 329 percent (p<0.01). Moreover, although microparticle-bound PrPc was released during storage, it was increasingly superseded by soluble protein. PrPc and ss-thrombo-globulin release exhibited very similar patterns (p<0.01). In contrast, LDH showed a significant increase in high-spun plasma only toward the end of the storage period (p<0.01). CONCLUSION: These results indicate that PrPc is released from platelets during the storage of apheresis platelets and that this release is probably due mainly to platelet activation and alpha-granule release in the first few days of storage. Moreover, the released PrPc is increasingly composed of soluble proteins, as the storage period exceeds 5 days.     

血小板的临床应用

目的　探讨合理、有效应用血小板。方法回顾性调查 1 993～ 1 999年本院血小板应用的输血资料并进行总结。结果临床各科的血小板减少所致出血性疾病 ,已广泛应用血小板输血治疗 ,全部有效 ;手术成功率显著提高。结论血小板输血疗效确切 ;血小板输注的指征及剂量尚需结合临床实际情况而定。     

Preparation of IgA-deficient platelets

The IgA-deficient patient presents a difficult transfusion problem, particularly if he or she has previously been immunized and has formed IgA antibodies. Blood components from IgA-deficient donors may be used safely but are often not accessible to transfusion facilities. A satisfactory red cell component may be obtained by standard freezing and washing methods. There is no comparable platelet concentrate that uniformly affords protection against anti-IgA-mediated reactions. A method has been developed for the preparation of an IgA-deficient platelet concentrate by washing with citrate-buffered saline. Platelets prepared in this manner were transfused successfully to an IgA-deficient patient with a history of anaphylaxis related to transfusion. It was further demonstrated that the removal of IgA is enhanced if platelets are washed within 48 hours of collection. When platelets were stored for more than 48 hours, similar washing techniques resulted in significantly higher levels of IgA in the platelets washed with either buffered (p = 0.004) or unbuffered (p = 0.0002) saline. Platelets washed with unbuffered saline (pH 4.5-5.5) contained substantially more IgA than did platelets washed in a similar manner with citrate-buffered saline (pH 6.5-6.8) (p = 0.001).