Cornelissen M, Steegers-Theunissen R, Kollée L, Eskes T, Vogels-Mentink G, Motohara K, De Abreu R, Monnens L
Department of Pediatrics, University Hospital Nijmegen, The Netherlands.
Am J Obstet Gynecol. 1993 Mar;168(3 Pt 1):923-8. doi: 10.1016/s0002-9378(12)90846-7.
The null hypothesis of our study is that the incidence of vitamin K deficiency in mother-infant pairs exposed to anticonvulsant drugs is not higher than in controls.
In this multicenter observational case-control study, 25 pregnant women receiving anticonvulsant therapy and 25 pregnant controls were studied for PIVKA-II (protein induced by vitamin K absence of factor II) and vitamin K1 concentrations at 32 weeks' gestation and at delivery.
PIVKA-II was detectable in 54% of cord samples of the anticonvulsant group and in 20% of controls (chi 2, p = 0.01). In both groups vitamin K1 cord blood levels were predominantly below the detection limit. Maternal vitamin K1 concentrations were lower in women with epilepsy than in controls (Wilcoxon's rank sum test, p < 0.05), but PIVKA-II was rarely present.
The incidence of vitamin K deficiency is increased in neonates exposed to anticonvulsant drugs prenatally. Their mothers, however, are rarely vitamin K deficient.
本研究的无效假设是，暴露于抗惊厥药物的母婴对中维生素K缺乏症的发生率不高于对照组。
在这项多中心观察性病例对照研究中，对25名接受抗惊厥治疗的孕妇和25名对照孕妇在妊娠32周和分娩时的异常凝血酶原（维生素K缺乏诱导蛋白II）和维生素K1浓度进行了研究。
抗惊厥组54%的脐带样本中可检测到异常凝血酶原，而对照组为20%（卡方检验，p = 0.01）。两组脐带血中维生素K1水平大多低于检测限。癫痫女性的母体维生素K1浓度低于对照组（Wilcoxon秩和检验，p < 0.05），但很少出现异常凝血酶原。
产前暴露于抗惊厥药物的新生儿中维生素K缺乏症的发生率增加。然而，他们的母亲很少缺乏维生素K。
