Cornelissen M, Steegers-Theunissen R, Kollée L, Eskes T, Motohara K, Monnens L
Department of Pediatrics, University Hospital Nijmegen, The Netherlands.
Am J Obstet Gynecol. 1993 Mar;168(3 Pt 1):884-8. doi: 10.1016/s0002-9378(12)90839-x.
The null hypothesis of this study is that extra vitamin K administered to pregnant women on a regimen of enzyme-inducing anticonvulsant therapy will not decrease the frequency of symptoms of vitamin K deficiency in their neonates.
A multicenter case-control study was performed on 16 pregnant women on anticonvulsant therapy who received 10 mg of vitamin K1 daily from 36 weeks of pregnancy onward. Concentrations of PIVKA-II (protein induced by vitamin K absence for factor II) and of vitamin K1 were determined in cord blood and compared with those in 20 controls.
In none of 17 cord samples was PIVKA-II detectable, compared with 13 of 20 in controls (chi 2, p < 0.001). Median cord vitamin K1 level was 530 pg/ml compared with below detection limit in most controls.
Antenatal vitamin K1 treatment decreases the frequency of vitamin K deficiency in neonates of mothers on anticonvulsant therapy.
本研究的无效假设是，接受酶诱导抗惊厥治疗方案的孕妇额外补充维生素K不会降低其新生儿维生素K缺乏症状的发生频率。
对16名接受抗惊厥治疗的孕妇进行了一项多中心病例对照研究，这些孕妇从妊娠36周起每天接受10毫克维生素K1。测定脐血中无维生素K诱导的蛋白II（PIVKA-II）和维生素K1的浓度，并与20名对照组进行比较。
17份脐血样本中均未检测到PIVKA-II，而对照组20份样本中有13份检测到（卡方检验，p<0.001）。脐血维生素K1水平中位数为530 pg/ml，而大多数对照组低于检测限。
产前维生素K1治疗可降低接受抗惊厥治疗母亲的新生儿维生素K缺乏的发生频率。
