Holoprosencephaly as a possible embryonic alcohol effect.
Holoprosencephaly as a possible embryonic alcohol effect.
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前脑无裂畸形可能是胚胎酒精效应所致。
DOI：
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发表时间：
1991
期刊：
影响因子：
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通讯作者：
Wayne L. Andrews
中科院分区：
文献类型：
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作者：
Gabriel M. Ronen;Wayne L. Andrews
三名患有前脑畸形婴儿的母亲在怀孕期间大量饮酒。我们假设早期酒精暴露可能是他们畸形的一个原因。这三位母亲仅在妊娠早期饮酒，但第一位母亲在整个妊娠期间继续服用氯二氮环氧化物和丙咪嗪。她的婴儿患有脑前叶全裂畸形，并伴有中唇裂、眼内斜视和鼻梁扁平。其余患儿为半叶前脑全裂和脑积水。后2例婴儿没有表现出胎儿酒精综合征的特征。所有3例婴儿的g带染色体检查均正常。人类怀孕期间酒精暴露与前脑畸形的关系仅被简要提及，尽管这种畸形在动物中是由酒精引起的。这3名婴儿可能支持这样的假设，即妊娠早期急性或亚急性重度酒精暴露可导致前脑全裂，而无需长期酒精暴露，也不必引起胎儿酒精综合征的典型面部表现。
Three mothers of infants with holoprosencephaly consumed alcohol heavily in pregnancy. We postulate that early alcohol exposure is a possible cause of their malformation. The 3 mothers consumed alcohol only in the first trimester but the first mother continued to take chlordiazepoxide and imipramine throughout the pregnancy. Her infant had an alobar holoprosencephaly associated with a median cleft lip, ocular hypotelorism, and a flat nose. The other infants had semilobar holoprosencephaly and hydrocephalus. These latter 2 infants did not show the characteristic facies of the fetal alcohol syndrome. G-band chromosome studies were normal in all 3 infants. The association of holoprosencephaly with alcohol exposure during pregnancy in humans has been mentioned only briefly, although this malformation has been induced by alcohol in animals. These 3 infants may support the hypothesis that acute or subacute heavy alcohol exposure early in pregnancy could lead to holoprosencephaly without the necessity of a chronic alcohol exposure and without necessarily causing the typical facial findings of the fetal alcohol syndrome.
遗传对因发育接触酒精而引起的大脑生长受限的影响。
影响因子：
3.4
作者：
Goodlett,CR;Gilliam,DM;Nichols,JM;West,JR
通讯作者：
West,JR