Lipsky J J
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
J Antimicrob Chemother. 1988 Mar;21(3):281-300. doi: 10.1093/jac/21.3.281.
Hypoprothrombinaemia is regarded as a serious adverse effect of antimicrobial therapy. This effect has commonly been attributed to the potential of these drugs to kill intestinal bacteria, a possible source of vitamin K, which is a necessary co-factor in the synthesis of four of the clotting factors. This review examines the evidence for and against this hypothesis, first in experimental animals, then in humans, and assesses the reports of antibiotic associated hypoprothrombinaemia in man, with particular attention to information about the mechanism. The hypothesis that it is the destruction of intestinal bacteria that ultimately results in hypoprothrombinaemia may not be justified. Certain antibiotics, which contain thiol-leaving groups, may produce hypoprothrombinaemia because the thiol group inhibits the vitamin K-dependent step in clotting factor synthesis.
低凝血酶原血症被视为抗菌治疗的一种严重不良反应。这种效应通常归因于这些药物杀死肠道细菌的可能性，而肠道细菌是维生素K的一个可能来源，维生素K是四种凝血因子合成中必需的辅助因子。本综述首先在实验动物中，然后在人类中检验了支持和反对这一假说的证据，并评估了人类中抗生素相关性低凝血酶原血症的报告，特别关注有关机制的信息。认为最终导致低凝血酶原血症的是肠道细菌的破坏这一假说可能并不成立。某些含有硫醇离去基团的抗生素可能会导致低凝血酶原血症，因为硫醇基团会抑制凝血因子合成中维生素K依赖的步骤。
