Hambidge M, Hackshaw A, Wald N
Department of Paediatrics, University of Colorado Health Services Centre, Denver.
Br J Obstet Gynaecol. 1993 Aug;100(8):746-9. doi: 10.1111/j.1471-0528.1993.tb14266.x.
To investigate the relationship of zinc in the causation of neural tube defects and so explore the possible role as a cause of these defects.
Stored serum samples collected as part of the Medical Research Council's multicentre randomised trial section of vitamin supplementation in the prevention of neural tube defects were retrieved in respect of women who had had an affected pregnancy together with four matched unaffected controls per case. One control was selected from each of the four randomisation groups: 1. no extra vitamins; 2. folic acid supplementation alone; 3. folic acid and other vitamin supplementation; and 4. other vitamin supplementation, such that it was matched with an NTD case by study centre, maternal age (the year of birth differed at most by one year) and duration of storage of the serum sample (in most instances to within the same year).
A prospective case-control study using serum samples stored at -40 degrees C. The serum samples were collected from women at entry to the trial, immediately before the women became pregnant and at about 12 weeks of pregnancy.
Twenty-seven women with a pregnancy associated with a neural tube defect and 108 matched controls with unaffected pregnancies.
There was no association between serum zinc levels and neural tube defects; the mean values in microgram/dl were: 82 and 85 in cases and controls, respectively, at entry to the study; 86 and 87 micrograms/dl just before pregnancy; and 76 and 80 micrograms/dl in the first trimester of pregnancy. Folic acid supplementation did not have an effect on serum zinc levels.
Within the range of serum zinc levels observed among women in our study, serum zinc is not a cause of neural tube defects, and periconceptional folic acid supplements do not compromise the zinc status of the mother or the embryo with respect to zinc intake.
研究锌与神经管缺陷病因之间的关系,从而探索锌作为这些缺陷病因的可能作用。
从医学研究委员会预防神经管缺陷维生素补充多中心随机试验部分收集的储存血清样本中,选取有神经管缺陷妊娠的女性及其每例匹配的4名未受影响的对照。从四个随机分组中各选一名对照:1. 不额外补充维生素;2. 仅补充叶酸;3. 补充叶酸和其他维生素;4. 补充其他维生素,使其在研究中心、母亲年龄(出生年份相差最多1年)和血清样本储存时间(大多数情况下在同一年)与神经管缺陷病例相匹配。
一项前瞻性病例对照研究,使用储存在-40摄氏度的血清样本。血清样本在妇女进入试验时、即将怀孕前和怀孕约12周时采集。
27名有神经管缺陷妊娠的妇女和108名匹配的未受影响妊娠的对照。
血清锌水平与神经管缺陷之间无关联;研究开始时,病例组和对照组的平均水平(微克/分升)分别为82和85;怀孕前分别为86和87微克/分升;怀孕头三个月分别为76和80微克/分升。补充叶酸对血清锌水平无影响。
在我们研究中观察到的女性血清锌水平范围内,血清锌不是神经管缺陷的病因,孕前补充叶酸在锌摄入方面不会损害母亲或胚胎的锌状态。