Yamamoto K, Sekiguchi E, Takatani O
Thromb Haemost. 1984 Dec 29;52(3):292-6.
Platelet aggregation was studied in 18 patients with myeloproliferative disorders, including 14 patients with chronic myelogenous leukemia, 2 with polycythemia vera, 1 with myelofibrosis and 1 with thrombocythemia. Fourteen patients (78%) were abnormal in epinephrine-induced platelet aggregation, while 3 (17%) and 4 (22%) cases showed impaired ADP or collagen induced platelet aggregation, respectively. A significant decrease of total ADP content in resting unstimulated platelets and of the amount released to the medium after aggregation was found in all six patients who were evaluated. ATP and AMP in resting platelets tended to be slightly higher in patients compared with the control group. Released ATP was also significantly less, and the percentage release of ADP and ATP was significantly decreased in patients. A storage pool deficiency of adenine nucleotides was considered to be responsible for abnormal platelet function in patients with myeloproliferative disorders.
对18例骨髓增殖性疾病患者的血小板聚集情况进行了研究,其中包括14例慢性粒细胞白血病患者、2例真性红细胞增多症患者、1例骨髓纤维化患者和1例血小板增多症患者。14例患者(78%)肾上腺素诱导的血小板聚集异常,而分别有3例(17%)和4例(22%)显示二磷酸腺苷(ADP)或胶原诱导的血小板聚集受损。在接受评估的所有6例患者中,发现静息未受刺激血小板中的总ADP含量以及聚集后释放到培养基中的量均显著降低。与对照组相比,患者静息血小板中的三磷酸腺苷(ATP)和一磷酸腺苷(AMP)往往略高。释放的ATP也显著减少,患者中ADP和ATP的释放百分比显著降低。腺嘌呤核苷酸储存池缺乏被认为是骨髓增殖性疾病患者血小板功能异常的原因。