Papalambros Efstathios, Sigala Fragiska, Travlou Anthi, Bastounis Elias, Mirilas Petros
First Department of Surgery, Laiko Hospital, University of Athens Medical School, Athens, Greece.
J Am Coll Surg. 2004 Jul;199(1):69-77. doi: 10.1016/j.jamcollsurg.2004.02.027.
We investigated heparin influence on P-selectin (platelet adhesion molecule), and the association of P-selectin with antibodies against heparin-platelet factor 4, known mediators of heparin induced thrombocytopenia (HIT) occurring in about 5% of vascular patients.
This cohort study included 78 patients, 22 to 90 years old (mean age +/- SD, 66.5 +/- 12.2 years), suffering from arterial thromboembolism (n = 43), deep vein thrombosis (n = 21), and peripheral arterial occlusive disease (PAOD) (n = 14). Plasma P-selectin was tested by ELISA before heparin administration (day 1), and under heparin treatment (day 7). HIT antibodies on day 7 were assayed using a sandwich-type ELISA. Platelets and fibrinogen were measured on days 1 and 7. P-selectin was also examined in 30 healthy controls, 22 to 81 years old (49.8 +/- 16.4 years).
On day 7, patients with PAOD had increased P-selectin and HIT antibodies, and decreased platelets compared with patients with arterial thromboembolism or deep vein thrombosis, in whom P-selectin decreased, and HIT antibodies were mostly negative. Fibrinogen increased in all patients. HIT antibody titers and P-selectin were positively associated and were increased in nine patients who developed lower limb artery occlusion or bypass thrombosis, stroke, or myocardial infarction during hospitalization (days 5 to 24). Five of these patients suffered from PAOD and the majority had taken heparin in the past.
P-selectin and HIT antibodies could be useful markers of HIT syndrome-associated thromboses during hospitalization of vascular patients receiving heparin. In arterial thromboembolism or deep vein thrombosis, P-selectin decreases without HIT antibody development. In PAOD, their concomitant increase may alert the surgeon to forthcoming life-threatening complications.
我们研究了肝素对P-选择素（血小板黏附分子）的影响，以及P-选择素与抗肝素-血小板因子4抗体的关联，肝素-血小板因子4是肝素诱导的血小板减少症（HIT）的已知介质，约5%的血管疾病患者会发生HIT。
这项队列研究纳入了78例年龄在22至90岁（平均年龄±标准差，66.5±12.2岁）的患者，他们患有动脉血栓栓塞（n = 43）、深静脉血栓形成（n = 21）和外周动脉闭塞性疾病（PAOD）（n = 14）。在给予肝素前（第1天）和肝素治疗期间（第7天），通过酶联免疫吸附测定（ELISA）检测血浆P-选择素。在第7天使用夹心型ELISA检测HIT抗体。在第1天和第7天测量血小板和纤维蛋白原。还对30名年龄在22至81岁（49.8±16.4岁）的健康对照者进行了P-选择素检测。
在第7天，与动脉血栓栓塞或深静脉血栓形成患者相比，PAOD患者的P-选择素和HIT抗体增加，血小板减少，而动脉血栓栓塞或深静脉血栓形成患者的P-选择素减少，且HIT抗体大多为阴性。所有患者的纤维蛋白原均增加。HIT抗体滴度与P-选择素呈正相关，在住院期间（第5至24天）发生下肢动脉闭塞或搭桥血栓形成、中风或心肌梗死的9例患者中升高。其中5例患者患有PAOD，且大多数患者过去曾使用过肝素。
P-选择素和HIT抗体可能是接受肝素治疗的血管疾病患者住院期间HIT综合征相关血栓形成的有用标志物。在动脉血栓栓塞或深静脉血栓形成中，P-选择素降低且无HIT抗体产生。在PAOD中，它们的同时增加可能提醒外科医生即将出现危及生命的并发症。
