Bechtold H, Lorenz J, Weilemann L S, Meinertz T, Trenk D, Andrassy K, Jähnchen E
Klin Wochenschr. 1984 Sep 17;62(18):885-6. doi: 10.1007/BF01712009.
In three patients treated with cephalosporins (one patient with latamoxef, two patients with cefazedone) vitamin K1 was injected to investigate whether this was followed by an increase in vitamin K1 2,3-epoxide plasma concentrations as compared to controls. Such a rise in K1-epoxide concentrations in the plasma can be demonstrated following treatment with coumarins. This reflects an inhibition of the vitamin K1-epoxide reductase in the liver. Coumarins are thought to induce hypoprothrombinaemia by such a mechanism. In all three patients we found a considerable increase in the vitamin K1-epoxide plasma concentrations following injection of 10 mg vitamin K1, whereas in normal subjects only traces of K1-epoxide could be detected (less than 0.030 micrograms/ml). The K1-epoxide concentrations found in our three patients treated with cephalosporins were 0.12, 0.16 and 0.19 micrograms/ml, respectively. This indicates that latamoxef or cefazedone might reduce clotting factor synthesis by a coumarin-like mechanism of action in these patients. Although the effect of cephalosporins in enhancing vitamin K1-epoxide plasma concentrations is less than that of coumarins, it might cause severe hypoprothrombinaemia in the presence of latent vitamin K deficiency.
在3例接受头孢菌素治疗的患者中（1例接受拉氧头孢治疗，2例接受头孢替唑治疗），注射维生素K1以研究与对照组相比，这是否会导致血浆中维生素K1 2,3-环氧化物浓度升高。香豆素治疗后可证实血浆中K1-环氧化物浓度会出现这种升高。这反映了肝脏中维生素K1-环氧化物还原酶受到抑制。据认为香豆素通过这种机制诱发低凝血酶原血症。在所有3例患者中，我们发现注射10 mg维生素K1后血浆中维生素K1-环氧化物浓度显著升高，而在正常受试者中仅能检测到微量的K1-环氧化物（低于0.030微克/毫升）。我们治疗的3例接受头孢菌素治疗的患者中检测到的K1-环氧化物浓度分别为0.12、0.16和0.19微克/毫升。这表明拉氧头孢或头孢替唑可能通过类似香豆素的作用机制降低这些患者的凝血因子合成。尽管头孢菌素提高血浆中维生素K1-环氧化物浓度的作用小于香豆素，但在存在潜在维生素K缺乏的情况下，它可能导致严重的低凝血酶原血症。
