Blockmans D, Bounameaux H, Vermylen J, Verstraete M
Thromb Haemost. 1986 Feb 28;55(1):90-3.
One case of heparin-induced thrombocytopenia is reported. Aggregation was observed in the platelet-rich plasma of this patient in the presence of two commercial standard heparin preparations (from a final concentration of 0.025 IU/ml upwards), of two semi-synthetic heparin analogues (0.1 APTT U/ml) and of three low-molecular weight heparin (LMWH) fractions (0.1 anti-Xa U/ml) but not in the presence of five other LMWH fractions. The patient's isolated platelets no longer aggregated in the The patient's isolated platelets no longer aggregated in the presence of heparin but the phenomenon recurred after addition of the patient's platelet poor plasma (PPP). Furthermore, addition of patient's PPP to control platelets led to heparin-induced aggregation. The phenomenon was associated with thromboxane generation and could be blocked by in vitro addition of aspirin, PGI2, and PGD2 whereas the lag phase was dose-dependently prolonged by adenosine. It is concluded that platelet aggregation may be induced in some patients by standard heparin and by certain LMWH fractions or semi-synthetic analogues, independently of their molecular weight and anticoagulant activity.
报告了1例肝素诱导的血小板减少症。在该患者富含血小板的血浆中,观察到两种商业标准肝素制剂(终浓度从0.025 IU/ml起)、两种半合成肝素类似物(0.1 APTT U/ml)和三种低分子肝素(LMWH)组分(0.1抗Xa U/ml)存在时发生聚集,但在其他五种LMWH组分存在时未发生聚集。患者的分离血小板在肝素存在时不再聚集,但加入患者的血小板贫浆(PPP)后该现象复发。此外,将患者的PPP加入对照血小板会导致肝素诱导的聚集。该现象与血栓素生成有关,体外添加阿司匹林、前列环素(PGI2)和前列腺素D2(PGD2)可阻断该现象,而腺苷可剂量依赖性地延长延迟期。结论是,标准肝素以及某些LMWH组分或半合成类似物可能在一些患者中诱导血小板聚集,这与其分子量和抗凝活性无关。