Van Steenbergen W, Vermylen J
Department of Internal Medicine, University Hospital Gasthuisberg, Leuven, Belgium.
Am J Gastroenterol. 1995 Sep;90(9):1526-8.
A patient with primary biliary cirrhosis (PBC) developed marked hypoprothrombinemia with decreased concentrations of the vitamin K-dependent coagulation factors VII, IX, and X during treatment with rifampicin. The coagulation abnormalities were easily corrected by administration of vitamin K. Different mechanisms may be involved, such as a decreased production of menaquinones by intestinal bacteria, a warfarin-like effect by inhibition of the vitamin K epoxide reductase, or an increased oxidative degradation of vitamin K as a result of hepatic microsomal enzyme stimulation. Whatever the mechanism involved, the appearance of this complication in a patient with PBC probably points to the importance of a pre-existing poor vitamin K status. Patients with PBC, treated with rifampicin, should have a regular monitoring of their vitamin K status. Adequate vitamin substitution should be administered, if necessary.
一名原发性胆汁性肝硬化(PBC)患者在使用利福平治疗期间出现明显的低凝血酶原血症,维生素K依赖的凝血因子VII、IX和X浓度降低。通过给予维生素K,凝血异常很容易得到纠正。可能涉及不同的机制,如肠道细菌产生甲萘醌减少、抑制维生素K环氧化物还原酶产生类似华法林的作用,或由于肝微粒体酶刺激导致维生素K氧化降解增加。无论涉及何种机制,PBC患者出现这种并发症可能表明预先存在的维生素K状态不佳很重要。接受利福平治疗的PBC患者应定期监测其维生素K状态。如有必要,应给予充足的维生素替代治疗。