Hoyseth K S, Jones P J
Division of Human Nutrition, School of Family and Nutritional Sciences, University of British Columbia, Vancouver.
Life Sci. 1989;44(10):643-9. doi: 10.1016/0024-3205(89)90468-2.
Extensive research has been aimed at characterising FAS and FAE. Whereas the symptomology for FAS has been established, that of FAE remains to be fully characterized. Various mechanisms of ethanol induced teratogenesis have been proposed however it remains to be defined how these mechanisms combine to produce the entire constellation of teratogenic characteristics observed. At present, impaired placental transport, abnormal muscle organogenesis and fetal hypoxia have limitations in explaining the entire spectrum of defects in FAS. The role of prostaglandins and hormones requires further research. Also, other as yet unidentified mechanisms may exist. Even if the composite mechanism can be established, ethanol effects in utero will likely not be preventable by any approach other than consumption modification. In light of this notion, future research into identifying high-risk pregnant drinkers for clinical intervention is emphasized. Intervention leading to abstinence or, if this is not possible, removing the infant as early as possible from an intrauterine environment that is causing growth retardation and fetal distress, are the only solutions available at present.
大量研究旨在对胎儿酒精综合征(FAS)和酒精相关出生缺陷(FAE)进行特征描述。虽然FAS的症状学已经明确,但FAE的症状学仍有待全面描述。已经提出了乙醇诱导致畸的各种机制,但这些机制如何结合产生所观察到的全部致畸特征仍有待确定。目前,胎盘转运受损、肌肉器官发育异常和胎儿缺氧在解释FAS的全部缺陷范围方面存在局限性。前列腺素和激素的作用需要进一步研究。此外,可能还存在其他尚未确定的机制。即使能够建立综合机制,除了改变饮酒习惯外,任何方法都可能无法预防子宫内的乙醇影响。鉴于这一观点,强调未来要进行研究以识别高危饮酒孕妇以便进行临床干预。导致戒酒的干预措施,或者如果无法戒酒,则尽早将婴儿从导致生长发育迟缓及胎儿窘迫的子宫内环境中移出,是目前仅有的解决办法。