Randi M L, Mares M, Fabris F, Tison T, Barbone E, Girolami A
Institute of Medical Semeiotics, University of Padua Medical School, Italy.
Arzneimittelforschung. 1991 Apr;41(4):414-6.
Ticlopidine (Ticlodone: CAS 55142-85-3) is able to develop a positive effect on claudication in patients affected by peripheral atherosclerotic disease (PAD). It is also known that ticlopidine decreases fibrinogen levels in plasma. 15 PAD patients treated with ticlopidine for 3 months were studied, evaluating the drug's effect both on maximum walking distance and on fibrinogen. Plasma fibrinogen as coagulable protein, fibrinogen antigen (Partigen method), 125I-fibrinogen survival, euglobulin lysis time and plasminogen were determined with the aim of clarifying if the decrease of plasma fibrinogen induced by ticlopidine is due to an increased destruction of a decreased production of the molecule. The normal levels of all tests before and after therapy both in ticlopidine treated patients and in the control group (acetylsalicylic acid + dipyridamol) indicate that the two hypotheses are not true. It is proposed that ticlopidine developing the known effect in decreasing the binding of fibrinogen to platelets induces a decrease only of activated fibrinogen.
噻氯匹定（力抗栓：化学物质登记号55142 - 85 - 3）对患有外周动脉粥样硬化疾病（PAD）的患者的间歇性跛行有积极作用。还已知噻氯匹定可降低血浆纤维蛋白原水平。对15例接受噻氯匹定治疗3个月的PAD患者进行了研究，评估该药物对最大行走距离和纤维蛋白原的影响。测定了作为可凝固蛋白的血浆纤维蛋白原、纤维蛋白原抗原（帕替根法）、¹²⁵I - 纤维蛋白原存活情况、优球蛋白溶解时间和纤溶酶原，目的是弄清楚噻氯匹定诱导的血浆纤维蛋白原减少是由于该分子的破坏增加还是产生减少。噻氯匹定治疗患者和对照组（乙酰水杨酸 + 双嘧达莫）治疗前后所有检测的正常水平表明这两种假设均不成立。有人提出，噻氯匹定发挥降低纤维蛋白原与血小板结合的已知作用，仅诱导活化纤维蛋白原减少。
