血小板交叉配型对肿瘤化疗患者血小板输注效果的影响

目的探讨血小板交叉配型对肿瘤化疗患者血小板输注效果的影响。方法选取2016年2月至2017年2月在我院治疗的恶性肿瘤患者87例,采用随机数字表法将患者随机分为观察组(n=43)和对照组(n=44),观察组给予血小板交叉配型后输注,对照组给予直接血小板输注,两组患者均采用固相凝集法检测血小板抗体。结果 87例患者中,抗体阳性率为58.62%;随着血小板输注次数增加,抗体阳性率有增加的趋势(P0.05);对照组抗体阳性患者输注有效率为28.57%,明显低于对照组抗体阴性患者以及观察组抗体阴性和阳性患者(P0.05);对照组抗体阳性患者输注1h、24h CCI分别为(4.20±1.62)×109和(2.43±1.20)×109,明显低于对照组抗体阴性患者以及观察组抗体阴性和阳性患者(P0.05)。结论血小板抗体检测以及配型,能明显提高血小板输注效果,减少无效输注,值得临床推广使用。     

血小板输注患者血小板抗体筛检及血小板交叉配型情况调查分析

目的调查本地区血小板输注患者血小板抗体阳性率及临床血小板交叉不合实际发生率。方法采用固相凝集法分别比较160名有输血史的随机血小板输注患者(作为实验组)和160名无输血史的随机住院患者(作为对照组)的血小板抗体阳性率以及实验组中血小板抗体阳体患者和血小板抗体性阴性患者的临床血小板交叉不合实际发生率。结果实验组和对照组血小板抗体阳性率分别为44.4%(71/160)和16.3%(26/160),组间差异有统计学意义(P<0.05);实验组临床血小板交叉不合总体发生率为5.0%(8/160),其中血小板抗体阳性患者和血小板抗体阴性患者临床血小板交叉不合发生率分别为9.0%(7/71)和0(0/89),组间比较差异有统计学意义(P<0.01);实验组中输血次数<5次和输血次数≥5次的患者血小板抗体阳性率分别为29.0%(18/62)和54.1%(53/98)。结论本地区血小板输注患者血小板交叉不合临床实际发生率并不低,血小板抗体阳性患者的血小板交叉配型工作需要引起大家的重视。     

多次输血的恶性肿瘤患者不同配型方法输注血小板时的有效率比较分析

目的探讨多次输血的恶性肿瘤患者采用不同配型方法进行血小板输注的临床效果。方法有多次输血史、需输注血小板的恶性肿瘤患者173例,随机分为观察组87例和对照组86例,采用固相凝集法检测2组血小板抗体,统计血小板抗体阳性率。对照组随机选择ABO血型同型供者血小板进行输注;观察组均进行血小板交叉配型试验,依据试验结果选择相合的血小板进行输注。分别于血小板输注前、后24h采集前臂静脉血检测血小板计数,计算血小板计数增高指数(corrected count increment,CCI),评价血小板输注效果。结果 173例中血小板抗体阳性68例,其中观察组36例,对照组32例;观察组血小板抗体阳性者CCI[(6.15±2.18)×109/L]高于对照组[(2.34±1.27)×109/L](P0.05),血小板抗体阴性者CCI[(8.35±2.74)×109/L]与对照组[(7.93±2.51)×109/L]比较差异无统计学意义(P0.05);观察组血小板抗体阳性者血小板输注有效率(27.59%)高于对照组(3.49%),差异有统计学意义(P0.05)。结论多次输血恶性肿瘤患者输注血小板前检测血小板抗体,依据血小板交叉配型试验结果选择交叉配型相合的血小板进行输注,可提高血小板的输注效果。     

血小板抗体检测及配型对血小板输注无效的临床意义研究

对我院97例血小板输注无效患者应用固相凝集法检测患者的血小板抗体,应用CCI评估阳性和阴性患者的血小板输注效果,分析血小板抗体检测结果和输注效果的关系。血小板抗体阳性率是34.02%;阳性组患者1h与24h CCI值要明显小于阴性组(P0.05);阳性组无效输注率(75.75%)要显著大于阴性组(21.88%);配型组输注无效率(11.76%)要明显小于未配型组(100%)。血小板输注前有效检测血小板抗体并予以交叉配型对血小板输注临床效果的改善具有重要意义。     

多次输血患者血小板抗体检测与血小板输注疗效相关性研究

目的回顾性分析本院多次输血患者的血小板抗体阳性发生率和抗体强度以及血小板交叉配型三者的相关性。方法选取174例有3次以上输血史的临床患者作为实验对象进行分组研究,采用固相凝集法检测血小板抗体,记录血小板抗体强度,对血小板抗体阳性标本进行血小板交叉配型,计算血小板配型相合率。结果输血小板次数!3次组、3~5次组和"5次组的血小板抗体阳性产生率分别为19.23%、35.48%、63.33%,组间差异有统计学意义(P!0.05);多次输血患者血小板抗体阳性率为40.23%,与100例无输血史患者(6%)相比较,差异有统计学意义(P!0.05);不同血小板抗体强度(1+、2+、3+、4+)的血小板交叉配型相合率分别为78.57%、47.37%、26.32%、11.11%,组间比较差异有统计学意义(P!0.05);抗体阳性的血小板随机1次配型相合率为38.57%,5次配型相合率为75.71%,与抗体阴性(100%)相比较差异有统计学意义(P!0.05)。血小板配型相合组与不合组输注血小板后,24 h CCI相比较,差异有统计学意义(P!0.05)。结论多次输血的临床患者其同种免疫性血小板抗体的产生与输血次数呈正相关,输血次数越多抗体强度越高,相应的血小板交叉配型相合率越低。对多次输血的患者进行血小板抗体检测和交叉配型,可提高血小板输注疗效,保证临床治疗效果。     

血小板输注无效患者的血小板抗体筛查以及配合性输注措施分析

目的探讨血小板抗体筛查及配合性输注措施应用于血小板输注无效(PTR)患者的临床价值。方法选取2016年8月至2017年8月,在我院多次输血的患者255例,对输血前后的血小板计数值进行监测,对1h、24h血小板增高指数(CCI)值进行计算,对于判断为PTR者,进行血小板抗体筛查并行交叉配型,分析配合性输注效果。结果 255例多次输血患者中发现PTR者共82例(32.2%)。82例患者中血小板相关抗体阳性者62例(75.6%),血小板抗体阳性率与输血次数间存在明显相关性(r=0.552,P0.05);62例患者进行交叉配血,33例成功配合,28例输注有效,另外29例患者因配合未成功采用随机输注ABO同型血小板。配合性输注后及随机输注1h、24h后CCI值比较差异均具有统计学意义(P0.05)。结论血小板配合性输注能使血小板输注效果显著提高,而血小板抗体的产生是导致PTR的主要原因。     

交叉配合试验在肿瘤患者血小板输注中的临床应用

目的探讨血小板交叉配合试验对肿瘤患者血小板输注效果的临床价值。方法选择39例血小板相关抗体阳性的肿瘤患者,分为随机输注组与交叉配合输注组,计算输注后1h和24h血小板增加校正指数(CCI),判断血小板输注效果并进行比较分析。结果随机输注组与交叉配合输注组的1、24hCCI分别为(6.34±1.82)、(3.05±1.42)×109/L与(15.58±3.12)、(8.13±2.55)×109/L,差异有统计学意义(P0.05);血小板输注有效率分别为23.81%、83.33%与14.29%、72.22%,差异有统计学意义(P0.05)。结论对血小板相关抗体阳性的肿瘤患者进行输注前交叉配型可显著提高血小板输注的有效性。     

血小板配型输注效果及影响因素分析

目的比较血小板配型相合与随机输注的效果,并分析相关影响因素,探求提高血小板输注效果的方法。方法通过分析该院2013年7月至2014年6月申请血小板输注的住院患者进行血小板抗体筛查及特殊配型试验结果,比较不同影响因素对输注效果的影响,并评估血小板输注效果。分析性别、输血史、怀孕史对血小板抗体产生的影响。分析性别、输血次数、怀孕次数、输注类型、保存天数及联合其他成分输注对输注效果的影响。应用该院临床输血智能管理与评估系统评估血小板输注效果。结果 812例患者进行血小板抗体筛查试验,随机抽取抗体筛查阳性的87例患者,共1 247U血小板输注,抗筛阳性输注特殊配型血小板、抗筛阳性随机输注血小板、抗体筛查阴性随机输注血小板3种方式输注效果比较,差异有统计学意义(P0.05)。应用多因素Logistics回归分析,发现有输血史是血小板抗体产生的独立危险因素(P0.05,OR=13.104,95%CI:7.784~22.061)。性别(P0.05,OR=1.629,95%CI:1.236~2.148)、输血史、输注血小板类型(机采、去白、辐照)、血小板保存天数、同时输注红细胞(P0.05,OR=2.464,95%CI:1.053~5.765)、输注方式(特配)(P0.05,OR=0.576,95%CI:0.389~0.854)是血小板输注效果的危险因素。结论血小板抗体筛查阳性时,需配型输注,提高有效率;输血史影响抗体的产生;性别、输血次数、输注类型、保存天数、联合其他成分输注、血小板配型输注均影响血小板输注效果。     

血小板相关抗体检测在临床上对血小板输注效果的影响

目的探讨酶联免疫竞争的临床应用效果及血小板交叉配型对血小板输注效果的影响。方法采用ELISA法对临床确认的特发性血小板减少(ITP)104例、系统性红斑狼疮(SLE)27例、甲状腺功能亢进症43例、非免疫性血小板减少症(NATP)23例及正常对照80例进行检测,同时检测104例ITP和80例正常对照的网织血小板(RP);采用简易致敏红细胞血小板血清学技术(SEPSA)对部分血小板相关抗体阳性病例进行血小板交叉配型。结果各种免疫性血小板减少症患者血小板相关抗体(PALg)阳性率较高,与正常对照相比差异有统计学意义(P0.05),非免疫性血小板减少组与免疫性血小板减少组相少症相比,前者阳性率及各项指标增高不明显,104例ITP患者和正常对照组的RP分别为(13.6±5.2)%、(3.8±1.1)%,差异有统计学意义(P0.05)。对30例血小板相关抗体阳性且输注无效的患者进行血小板配型输注,其中25例相合,有效率为83%。结论血小板相关抗体检测具有一定的临床诊断价值,血小板配型可有效提高临床输注效果。     

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。     

Blood platelet kinetics and platelet transfusion

The discovery of citrate anticoagulant in the 1920s and the development of plastic packs for blood collection in the 1960s laid the groundwork for platelet transfusion therapy on a scale not previously possible. A major limitation, however, was the finding that platelet concentrates prepared from blood anticoagulated with citrate were unsuitable for transfusion because of platelet clumping. We found that this could be prevented by simply reducing the pH of platelet-rich plasma to about 6.5 prior to centrifugation. We used this approach to characterize platelet kinetics and sites of platelet sequestration in normal and pathologic states and to define the influence of variables such as anticoagulant and ABO incompatibility on post-transfusion platelet recovery. The “acidification” approach enabled much wider use of platelet transfusion therapy until alternative means of producing concentrates suitable for transfusion became available.The identification of platelets as a distinct cellular element of blood with a critical role in hemostasis in the late 1800s (1) inevitably led to speculation about platelet transfusion as a treatment for bleeding in patients with thrombocytopenia. The realization of this goal was delayed for many years by technical barriers. Development of citrate-based anticoagulants in the 1920s and flexible plastic blood containers in the 1950s–1960s made it feasible to collect blood in a plastic pack containing standard acid-citrate-dextrose (ACD) anticoagulant, centrifuge it slowly, and express the supernatant platelet-rich plasma (PRP) into a plastic side-pack for convenient transfusion. Early studies showed that platelets from multiple units of blood were needed to achieve a therapeutic effect in a bleeding patient. To prevent volume overload, this required that platelets be concentrated before being transfused. The obvious way to accomplish this was to centrifuge PRP at high speed, remove the supernatant plasma, and suspend the pelleted platelets in a small volume by gently massaging the plastic pack. It soon became apparent that concentrates prepared in this way almost invariably contained large and small platelet aggregates and few single platelets. Not surprisingly, clinicians were reluctant to transfuse these preparations. It was known at this time that platelets isolated from blood that had been anticoagulated with EDTA could be pelleted from PRP by centrifugation and dispersed without difficulty. To meet the growing demand for platelet transfusions, the Fenwal Company developed the “EDTA Platelet Pack,” consisting of a plastic collection bag containing EDTA and an attached satellite bag into which PRP could be expressed, concentrated by centrifugation into a pellet, and suspended in a small volume of plasma. Red cells were returned to the donor to enable repeated platelet donations. Despite the obvious limitations of this approach, thousands of pooled EDTA platelet concentrates were transfused in the late 1950s and the 1960s. This procedure was labor intensive, and its application was restricted to relatively few, critically ill patients.In 1961, Gardner and associates conducted seminal studies to define the pathophysiology of various thrombocytopenic disorders (2, 3). They labeled EDTA platelets with NaCr⁵¹O₄ to follow the cells after transfusion. In these studies, very few labeled platelets were detected in the peripheral blood during the first few hours after transfusion. After this time, a variable number of cells reentered circulation. The immediate sequestration of a large fraction of the transfused cells, possibly in the liver and lung (4), followed by the eventual return of some platelets into circulation was considered to be a consequence of the labeling procedure. At this time, working at the Thorndike Memorial Laboratory of the Boston City Hospital, we were similarly interested in studying platelet kinetics, and we confirmed the findings of Gardner and coworkers about the circulation kinetics of EDTA platelets. We examined PRP prepared from EDTA and ACD whole blood under phase microscopy and noted that platelet morphology was quite different in the two preparations. In ACD preparations, platelets were discoid in shape, but in EDTA preparations, they assumed an irregular, almost spherical configuration. Another striking difference was the appearance of PRP examined in a light beam while being gently agitated: ACD platelets shimmered and swirled, whereas an EDTA platelet suspension was uniform in appearance throughout. We wondered whether structural changes induced in platelets by EDTA explained the failure of most of these platelets to circulate after transfusion and carried out studies to determine whether platelet clumping in concentrates from ACD-prepared PRP could be prevented. Evaluation of several variables revealed that when the pH of ACD PRP was reduced from its starting value of about 7.2 to about 6.5 before centrifugation, the pelleted platelets could readily be dispersed, yet retained their normal discoid shape. In whole blood or in PRP, this degree of “acidification” could be achieved by simply adding an extra quantity of ACD, the anticoagulant then used routinely for blood collection. The apparent benefit of acidification persisted through repeated centrifugations and made it possible to characterize recovery and survival of ACD platelets in normal subjects (5). Our studies revealed that about 75% of the labeled ACD platelets were recovered in the recipient immediately after transfusion (Figure ​(Figure1).1). After the initial transfusion, the presence of labeled platelets in the blood steadily declined over nine days. In contrast, labeled EDTA platelets peaked in the blood around one day after transfusion and steadily declined afterward (Figure ​(Figure1).1). Scanning of body organs with a directional scintillation counter revealed that most of the radioactivity from ACD platelets not recovered in the blood was initially present in the spleen; however, transfused EDTA platelets mainly concentrated in the liver. As ACD platelets were cleared from the circulation, Cr⁵¹ accumulated in the liver and spleen, indicating that these organs are the major sites of platelet deposition. The linear clearance pattern suggested that under normal circumstances, platelets die as a consequence of “senescence,” rather than being randomly utilized (5). Open in a separate windowFigure 1Survival of autologous “citrate platelets” after transfusion to a normal subject.Approximately 75% of labeled platelets were recovered in the circulation immediately after being transfused. The red area denotes the range of blood platelet radioactivity after the injection of Cr⁵¹-labeled “EDTA platelets” on 10 occasions in 7 normal subjects. Adapted from ref. 5. Freireich and his colleagues at the National Cancer Institute soon confirmed the superiority of platelet concentrates prepared from acidified ACD blood in producing sustained platelet increases in thrombocytopenic patients (6). Over the next few years, this simple maneuver facilitated much wider use of platelet transfusions, especially in patients being treated for hematologic malignancies. We used the new methodology to characterize platelet clearance and sites of sequestration in normal individuals (5, 7) and in patients with platelet destruction mediated by alloantibodies (8) and autoantibodies (9), as well as to more fully define the role of anticoagulants and ABO incompatibility on recovery and survival of transfused platelets (10). We also demonstrated that “hypersplenic” thrombocytopenia is largely caused by pooling of a significant fraction of the total circulating platelet mass in an enlarged spleen, rather than being a consequence of suppressed platelet production or premature platelet destruction (11). Although acidifying citrated blood or PRP to prepare platelet concentrates for transfusion represented a significant improvement over what was previously possible, other advances soon followed. Mourad found that platelet concentrates prepared from nonacidified ACD blood could be manually suspended with little clumping, provided the platelet pellet was allowed to rest for some time at room temperature before manipulation (12). Other key developments were the finding by Murphy et al. that platelet viability is best maintained by storage at room temperature (13) and the evolution of pheresis systems for isolating large quantities of platelets from single donors. To my knowledge, reversible aggregation of platelets pelleted from citrated PRP is still not fully understood, but it seems almost certain that fibrinogen binding to partially activated α_IIbβ₃ integrin (GPIIb/IIIa) is involved, since fibrinogen-dependent platelet aggregation is markedly inhibited at pH 6.5 (6, 14). The EDTA-induced structural changes in platelets were well characterized by White (15). The “swirling” of platelets was shown to be a consequence of their normal discoid shape and to correlate fairly well with post-transfusion viability (16).     

Apheresis donors and platelet function: inherent platelet responsiveness influences platelet quality

BACKGROUND: Process-induced platelet (PLT) activation occurs with all production methods, including apheresis. Recent studies have highlighted the range and consistence of interindividual variation in the PLT response, but little is known about the contribution of a donors' inherent PLT responsiveness to the activation state of the apheresis PLTs or the effect of frequent apheresis on donors' PLTs. STUDY DESIGN AND METHODS: The relationship between the donors' PLT response on the apheresis PLTs was studied in 47 individuals selected as having PLTs with inherently low, intermediate, or high responsiveness. Whole-blood flow cytometry was used to measure PLT activation (levels of bound fibrinogen) before donation and in the apheresis PLTs. The effects of regular apheresis on the activation status of donors' PLTs were studied by comparing the in vivo activation status of PLTs from apheresis (n = 349) and whole-blood donors (n = 157), before donation. The effect of apheresis per se on PLT activation was measured in 10 apheresis donors before and after donation. RESULTS: The level of PLT activation in the apheresis packs was generally higher than in the donor, and the most activated PLTs were from high-responder donors. There was no significant difference in PLT activation before donation between the apheresis and whole-blood donors (p = 0.697), and there was no consistent evidence of activation in the donors immediately after apheresis. CONCLUSION: The most activated apheresis PLTs were obtained from donors with more responsive PLTs. Regular apheresis, however, does not lead to PLT activation in the donors.     

Status of platelet collection and platelet transfusion.

Platelet product derived from single donor plateletpheresis is required to reduce the risks of adverse reactions by blood transfusion. The objectives of this study are to evaluate the status of platelet collection and its efficacy by various kinds of plateletpheresis equipment and to assess the achievement of platelet transfusion by platelet product derived from a single donor. Since the blood centers have introduced some kinds of efficient plateletpheresis equipment, large units of platelet products have been supplied mainly for the patients. Amicus and CCS might be preferable plateletpheresis machines because of their collection efficiencies and wider indication for donors. The average number of donors of platelet product per patient has recently reached nearly 1.0, and around 90% of patients have received platelet product derived from a single donor in the recent several years. However, platelet transfusion derived from a single donor has not yet been completely achieved. Each regional blood center should seriously consider the efficacy of each plateletpheresis equipment and arrange the equipment to collect platelets more effectively to achieve platelet transfusion from a single donor.     

血小板抗体检测及配型对血小板输注无效的临床意义

目的 通过对比血小板配型前后血小板的输注效果,评估血小板抗体检测及配型对血小板输注无效的临床意义.方法 以出血症状改善情况、血小板计数增高指数(CCI)、血小板恢复百分率(PPR)为标准,对比配型前后血小板的输注效果.结果 25例血小板输注无效患者的血小板抗体筛查阳性9例; 9例血小板抗体阳性患者血小板交叉配型前后血小板输注有效率差异有统计学意义(P<0.01),配型后输注的 1 h和24 h CCI、PPR数值明显高于配型前输注的.结论 血小板抗体检测及血小板配型输注可以为患者选择适用的血小板,提高单采血小板的输注有效率,避免滥用血小板.     

Comparison of platelet count and platelet protein methods for determination of platelet MAO activity.

Platelet monoamine oxidase (MAO) activity in 10 normal volunteers was studied as a function of platelet protein or electronically-determined platelet counts. Comparisons of the two methods were made for samples assayed on the same day as well as one week later. The MAO activities resulting from both methods were significantly correlated and reproducible but the results of the platelet count method were, in most instances, slightly but significantly more reliable than the platelet protein method. The relevance of these results to the controversy concerning platelet MAO activity in schizophrenia is discussed.     

Endogenous glutathione and platelet function in platelet concentrates stored in plasma or platelet additive solution

Platelet function was studied in platelet concentrates by assay of the thrombin-induced release of endogenous serotonin and presence of the swirling phenomenon in relation to endogenous glutathione (GSH) and cysteine. In platelets stored in plasma, addition of cysteamine resulted in only a moderate fall in GSH after 5 days of storage, from an average of 14.91 to 11.46 nmol per 109 platelets. Exogenously added GSH had no effect, and addition of buthionine sulfoximine (BSO) resulted in almost complete depletion of GSH, to an average of 0.65 nmol per 109 platelets. Addition of cysteamine or GSH resulted in increased endogenous cysteine whereas BSO had no effect. In platelets stored in a platelet additive solution (T-sol), complete depletion of GSH was found in the presence of cysteamine, GSH and BSO. Endogenous serotonin was unchanged during storage both in plasma and in additive solution (2.8 nmol per 109 platelets). Despite almost total depletion of endogenous GSH, the thrombin-induced release of serotonin after 5 days' storage was significantly affected only in the presence of BSO in platelets stored in additive solution (mean values 72.3% vs. 63.3% of endogeneous serotonin, P < 0.05). Similarly, addition of cysteamine or GSH had no significant effect on swirling but BSO reduced the swirling score after 5 days' storage in platelet additive solution compared with plasma. After 10 days' storage, there was a significant reduction in swirling in the concentrates where BSO was added (P < 0.05).