High dose gammaglobulin therapy in adults with idiopathic thrombocytopenic purpura (ITP) clinical effects

Summary This study of the effect of high-dose intravenous gammaglobulins with one or two courses of therapy in 18 adults with idiopathic thrombocytopenia purpura showed a platelet rise in thirteen patients. The highest response rates were seen in splenectomized adults. In chronic patients the response was transient only. If therapy was effective, increased values of platelet-associated IgG were reduced, while shortened platelet survival times were prolonged. There was no influence of high-dose gammaglobulins on platelet function. Different 7S-preparations such as -propiolactone modified Ig, pH 4 treated Ig and reduced and alkylated Ig have comparable effects.Supported by the Deutsche Forschungsgemeinschaft (Mu 277/9-4)     

心痛安颗粒剂对不稳定性心绞痛患者血小板功能及凝血系统的影响

目的 :观察心痛安颗粒剂对不稳定性心绞痛患者血小板和凝血系统的作用。方法 :6 0例不稳定性心绞痛患者随机分为心痛安组 (30例 ,常规西药加心痛安颗粒剂治疗 )与对照组 (30例 ,单用常规西药治疗 ) ,观察治疗前后血小板最大聚集率 (Ma% )血小板 α颗粒膜糖蛋白 (GMP- 140 )和 D-二聚体 (D- D)的变化。结果 :治疗后 ,心痛安颗粒组的 Ma% ,GMP- 140和 D- D经治疗后明显下降 ,下降幅度明显大于对照组。结论 :心痛安颗粒剂可能通过抑制血小板聚集、活化和纤维蛋白合成而发挥治疗不稳定性心绞痛的作用。     

15种理气中药体外对人血小板聚集的影响

目的观察15种理气中药对体外肾上腺素诱导的人血小板聚集的影响.方法试管内人血小板加中药孵育前后,比浊法测定血小板聚集.结果11种理气药具有抗血小板聚集作用(P＜0.05～0.001),其中枳实的抑制作用较阳性对照阿司匹林明显(P＜0.01),青皮、陈皮与阿司匹林无差异(P＜0.05).柿蒂、甘松、檀香、沉香对血小板聚集无明显作用(P＞0.05).结论多数理气药(11/15)在体外具有抗人血小板聚集作用,枳实、青皮、陈皮3种作用强于或与阿司匹林相当.     

整合素血小板膜糖蛋白IIb、IIIa在系膜增殖性肾炎中的表达

目的 :观察整合素血小板膜糖蛋白Ⅱb、Ⅲa(GPⅡb、GPⅢa)在人类系膜增殖肾炎 (MsPGN)中肾内表达 ,探讨GPⅡb Ⅲa在MsPGN的作用。方法 :18例肾活检标本均行光镜HE、PAS、PASM Masson染色 ,电镜及免疫荧光检查 ,以SABC法测定肾组织中GPⅡb、GPⅢa、P 选择素 (P 140 )、纤维连接蛋白 (FN)、粘连蛋白 (LN)表达与正常对照组分别比较 ,并行计算机图像分析。结果 :PAS阳性物 (PAS+ )、PASM阳性物 (PASM+ )及FN、LN明显增生 ;GPⅡb、GPⅢa、P 140表达上调 ;肾小球细胞数 (n)、平均肾小球体积 (AVG)及肾小球硬化指数显著增加 ;肾小管、间质轻度受损。结论 :GPⅡb、GPⅢa在肾小球及肾小管间质表达上调与系膜细胞基质增生、细胞浸润、肾小球硬化相关 ;可能与肾小球疾病中凝血功能紊乱、血小板在肾脏的致病作用相关     

降纤酶治疗急性脑梗塞后血液流变学指标的变化

目的　评定降纤酶治疗急性脑梗塞对血液凝血、纤溶系统及血小板的影响。方法　24例急性脑梗塞患者随机分为降纤酶组和常规治疗组,测定治疗前后血浆纤维蛋白原(Fg)、D-二聚体、凝血酶原时间(PT)、白陶土部分凝血活酶时间(KPTT)、血小板最大聚集率(P     

Diagnostic Utility of Platelet Count/Lymphocyte Count Ratio and Platelet Count/Mean Platelet Volume Ratio in Periprosthetic Joint Infection Following Total Knee Arthroplasty

BackgroundDiagnosing a periprosthetic joint infection (PJI) can be challenging and often requires a combination of clinical and laboratory findings. Monocyte/lymphocyte ratio, neutrophil/lymphocyte ratio, platelet/lymphocyte ratio (PLR), and platelet/mean platelet volume ratio (PVR) are simple predictors for inflammation that can be readily obtained from complete blood count. The aim of this study is to evaluate the diagnostic utility of these markers in predicting PJI in total knee arthroplasty (TKA) patients.MethodsA total of 538 patients who underwent revision TKA with calculable marker ratios prerevision in 2 groups were evaluated: (1) 206 patients with a preoperative diagnosis of PJI (group I) and (2) 332 patients treated for revision TKA for aseptic failures (group II). The diagnostic abilities of the markers were assessed via receiver operator characteristic curve analysis.ResultsThe optimal threshold of PVR at 30.82 had the highest sensitivity of 87.7%, while the optimal threshold of PLR at 234.13 had the highest specificity of 82.5%. Both PLR and PVR, when combined with Musculoskeletal Infection Society thresholds for erythrocyte sedimentation rate, C-reactive protein, synovial WBC, and PMN%, achieve significantly higher sensitivity and specificity rates for PJI at or above 97% (PLR: 99.03%; 98.80%; PVR: 98.54%;97.89%).ConclusionOur study demonstrates that PVR and PLR, which are readily available and inexpensive to obtain from complete blood counts, when combined with serum and synovial fluid markers have increased sensitivity and specificity comparable to that of alpha defensin. This suggests that PVR and PLR can be used together with other hematologic and aspirate markers to increase the accuracy of PJI diagnosis in TKA patients.     

内毒素所致DIC时血小板胞浆Ca^2＋浓度变化的研究

本实验观察内毒素在体外对兔血小板胞浆游离钙浓度[Ca~(2+)]i的作用以及用二次注射内毒素法复制DIC模型时对[Ca~(2+)]i的影响。结果表明静息血小板[Ca~(2+)]i为112±24 nM,内毒素可直接作用于血小板,使[Ca~(2+)]i呈剂量依赖性升高。内毒素致DIG时(Ca~(2+)]i可升高三倍。结果提示内毒素可能是通过升高血小板[Ca~(2+)]i而激活血小板。血小板的激活可能是导致DIC的重要发病机制之一。     

蛇毒抗栓酶对氧自由基致血小板变化的影响

次黄嘌呤／黄嘌呤氧化酶体系产生的氧自由基在体外能明显增加血中板膜微粘度，脂质过氧化代射产物丙二醛含量，血小板胞内游离钙浓度和血小板５－羟色胺的释放量。０．０３ｕ／ｍｌ的蛇毒抗栓酶明显抑制前二种效应，但促进血小板释放５－羟色胺，增加血小板胞内游离钙浓度，结果表明蛇毒抗栓酶对血小板膜有保护作用。     

Effects of taprostene,a stable prostacyclin analogue,on haemodynamics,platelet function and arachidonate metabolism in healthy volunteers

Summary In order to assess the effect of taprostene on haemodynamics, platelet function and arachidonate metabolism in 4 healthy volunteers an intravenous infusion of 25 ng · kg^–1 · min^–1 was given for 6 h.During the infusion period systolic blood pressure dropped from 130 to 111 mm Hg and diastolic blood pressure from 77 to 69 mm Hg. The heart rate rose from 77 to 84 beats/min.During the taprostene infusion the slope and height of the ADP and collagen induced platelet aggregation curves were significantly inhibited and the sensitivity of platelets to PGI₂ and PGE₁ was increased.Plasma and serum thromboxane B₂, conversion of exogenous radiolabelled arachidonic acid, WU-test, circulating endothelial cell count, concentration of platelet factor 4, -thromboglobulin, malondialdehyde and the PGI₂-synthesis stimulating plasma factor did not show any clear drug-related alteration.It is concluded that infusion of taprostene 25 ng · kg^–1 · min^–1 caused measurable inhibition of platelet function ex vivo.     

“In vitro” and “ex vivo” effects of picotamide,a combined thromboxane A2-synthase inhibitor and -receptor antagonist,on human platelets

Summary Picotamide (G 137), a new non prostanoid inhibitor of in vitro arachidonic acid induced platelet aggregation, has been further characterized in in vitro and ex vivo studies.When whole blood was activated with collagen in the presence of picotamide 5×10^–4 M, thromboxane B₂ production was decreased, and 6-keto-PGF₁ generation was significantly increased, suggesting a reorientation of platelet endoperoxide metabolism following blockade of thromboxane synthetase. Picotamide also inhibited platelet aggregation and clot retraction induced by the endoperoxide analogue U46619 in human platelets, indicating thromboxane A₂-receptor antagonism, possibly of competitive nature.A single oral dose of picotamide 1 g in 24 healthy volunteers produced a significant inhibition of collagen, arachidonic acid and U46619-induced platelet aggregation. Serum levels of thromboxane B₂ were also reduced.Chronic administration of picotamide 1.2 g/d to patients with vascular disease resulted in a prompt and persistent fall in their increased plasma levels of -thromboglobulin.The results indicate that picotamide is a combined thromboxane B₂-synthetase inhibitor and thromboxane A₂-receptor antagonist in human platelets, and that it may prove useful as an antithrombotic agent.