Zavagli G, Taddeo U, Bolelli G, Orlandi M, Bartolini G, Tomasi V
Prostaglandins Leukot Med. 1985 Sep;19(3):241-50. doi: 10.1016/0262-1746(85)90137-4.
It has been reported that a long term treatment with cimetidine may give rise to thrombotic complications and may cause reversible damage to blood cells. In 57 patients on long term cimetidine treatment, platelet aggregates, platelet aggregation in vitro, plasma 6-keto-PGF1 alpha/thromboxane B2 ratio and platelet cyclic AMP levels were assessed. In 52% of the patients, platelet aggregate ratios were abnormal and collagen and ADP-hypersensitive platelets were observed. Such alterations began occurring after the first month of therapy and were shown to worsen progressively during the administration. Four of these patients, who developed unexpected thrombotic compliances after about 7 months of therapy, showed higher than normal plasma thromboxane B2, lower plasma 6-keto-PGF1 alpha and two of them, lower platelet cyclic AMP concentrations. It is suggested that cimetidine, through an unknown mechanism which probably involves activation of endogenous cyclic AMP phosphodiesterase, may favour the action of platelet aggregating agents.
据报道,长期使用西咪替丁治疗可能会引发血栓形成并发症,并可能对血细胞造成可逆性损伤。对57例接受长期西咪替丁治疗的患者进行了血小板聚集物、体外血小板聚集、血浆6-酮-前列环素F1α/血栓素B2比值以及血小板环磷酸腺苷水平的评估。在52%的患者中,血小板聚集率异常,并且观察到对胶原和二磷酸腺苷敏感的血小板。这些改变在治疗的第一个月后开始出现,并在给药期间逐渐恶化。其中4例患者在治疗约7个月后出现意外的血栓形成并发症,其血浆血栓素B2高于正常水平,血浆6-酮-前列环素F1α低于正常水平,其中2例患者的血小板环磷酸腺苷浓度较低。有人认为,西咪替丁可能通过一种未知机制(可能涉及内源性环磷酸腺苷磷酸二酯酶的激活)促进血小板聚集剂的作用。