Rosenn B M, Miodovnik M
Department of Obstetrics and Gynecology, University of Cincinnati, Ohio, USA.
J Matern Fetal Med. 2000 Jan-Feb;9(1):29-34. doi: 10.1002/(SICI)1520-6661(200001/02)9:1<29::AID-MFM7>3.0.CO;2-Z.
Glucose is the principal nutrient that the mother supplies to the fetus through the placenta by way of concentration-dependent mechanisms. In the presence of maternal hypoglycemia, with limited glucose supply, fetal hypoglycemia and hypoinsulinism ensue. This may be viewed as an adaptive mechanism to increase the chances of fetal survival in the face of limited maternal supply, albeit of a growth-restricted fetus. Fetal nutrient deprivation and the resulting hypoinsulinism may have both short- and long-term consequences. Intrauterine growth failure is associated with higher rates of gestational age-specific neonatal mortality and with long-term cognitive deficits. Furthermore, epidemiologic data suggest that diabetes, coronary artery disease, and hypertension are more common among adults who were small for gestational age at birth. Thus, pancreatic failure in adulthood may be either a response to excessive exposure to glucose as a result of maternal hyperglycemia, or as a result of hypoglycemia where nutrient deprivation leads to fetal growth restriction and reduced islet cell proliferation. Because low mean concentrations of maternal glucose in gestational diabetes are associated with an increased risk of fetal growth restriction, overzealous glycemic control during pregnancy may raise concerns regarding the possible effects on the infant. In the mother with Type 1 diabetes, strict glycemic control is often associated with an increased incidence of severe hypoglycemia. Up to 40% of women report at least one episode of severe hypoglycemia during pregnancy, requiring assistance by another person or professional intervention. It is quite possible that in some patients striving to optimize pregnancy outcome by maintaining the best possible glycemic control jeopardizes the well-being of the mother and the fetus. Thus, with respect to tight glycemic control of pregnant women with diabetes, the question arises: How tight is too tight? Is there a threshold below which the trade-off in terms of maternal morbidity as well as fetal growth restriction and its consequences outweighs the benefits of preventing the effects of maternal hyperglycemia?
葡萄糖是母亲通过胎盘以浓度依赖机制供给胎儿的主要营养素。在母亲低血糖且葡萄糖供应有限的情况下，会出现胎儿低血糖和低胰岛素血症。这可被视为一种适应性机制，以增加胎儿在母亲供应有限的情况下存活的机会，尽管胎儿生长受限。胎儿营养剥夺及由此产生的低胰岛素血症可能会产生短期和长期后果。宫内生长受限与特定孕周新生儿死亡率较高以及长期认知缺陷有关。此外，流行病学数据表明，出生时小于孕周的成年人患糖尿病、冠状动脉疾病和高血压更为常见。因此，成年期胰腺功能衰竭可能是由于母亲高血糖导致过度暴露于葡萄糖的结果，或者是由于营养剥夺导致胎儿生长受限和胰岛细胞增殖减少的低血糖的结果。由于妊娠期糖尿病患者母亲的葡萄糖平均浓度较低与胎儿生长受限风险增加有关，孕期过度严格的血糖控制可能会引发对其对婴儿可能产生的影响的担忧。在患有1型糖尿病的母亲中，严格的血糖控制通常与严重低血糖发生率增加有关。高达40%的女性报告在孕期至少发生过一次严重低血糖，需要他人协助或专业干预。很有可能在一些为了通过维持尽可能好的血糖控制来优化妊娠结局的患者中，会危及母亲和胎儿的健康。因此，对于糖尿病孕妇的严格血糖控制，问题就来了：多严格才算过于严格？是否存在一个阈值，低于该阈值时，在母亲发病率以及胎儿生长受限及其后果方面的权衡会超过预防母亲高血糖影响的益处？
