Mackie I J, Walshe K, Cohen H, McCarthy P, Shearer M, Scott S D, Karran S J, Machin S J
J Clin Pathol. 1986 Nov;39(11):1245-9. doi: 10.1136/jcp.39.11.1245.
Two patients with low random serum vitamin K1 concentrations but with normal prothrombin times and normal biological assays of the vitamin K dependent coagulation proteins were treated with an N-methyl-thiotetrazole cephalosporin (cefotetan) postoperatively. Four to six days later both patients developed a prolonged prothrombin time and a noticeable and specific lowering of the clotting activities of factors II, VII, IX and X, though the serum vitamin K1 concentrations remained unchanged. Crossed immunoelectrophoresis of prothrombin showed the appearance of a second peak corresponding to descarboxyprothrombin (PIVKA II). These abnormalities corrected after vitamin K administration. These data are consistent with the hypothesis that cephalosporins with an N-methyl-thiotetrazole side chain inhibit the hepatic utilisation of vitamin K but that this only causes hypoprothrombinaemia when liver reserves of vitamin K are low.
两名随机血清维生素K1浓度较低但凝血酶原时间正常且维生素K依赖凝血蛋白生物学检测正常的患者术后接受了N-甲基硫代四氮唑头孢菌素（头孢替坦）治疗。4至6天后，两名患者均出现凝血酶原时间延长以及因子II、VII、IX和X的凝血活性显著且特异性降低，尽管血清维生素K1浓度保持不变。凝血酶原的交叉免疫电泳显示出现了一个对应于脱羧凝血酶原（PIVKA II）的第二个峰。维生素K给药后这些异常得以纠正。这些数据与以下假设一致：具有N-甲基硫代四氮唑侧链的头孢菌素会抑制肝脏对维生素K的利用，但只有当肝脏维生素K储备较低时才会导致低凝血酶原血症。
