Fisher D A
Corning Nichols Institute, San Juan Capistrano, California 92690, USA.
Clin Obstet Gynecol. 1997 Mar;40(1):16-31. doi: 10.1097/00003081-199703000-00005.
The fetal hypothalamic-pituitary-thyroid axis develops independently of the maternal axis, but it is dependent on the maternal-placental system for adequate supply of iodide substrate. This iodide is supplied by direct transfer of maternal plasma iodide and by placental deiodination of T4. In addition, although placental transport of iodothyronines is limited, significant maternal-fetal transfer of T4 occurs, accounting for approximately 30% of the average 10 ug/dL serum-T4 concentration in fetal-cord blood at term. Current information suggests that this maternal contribution to the fetal-T4 levels is important for normal fetal maturation, particularly of the central nervous system. Combined maternal-fetal hypothyroxinemia can lead to irreversible fetal central nervous system damage. The timing of this fetal T4 dependency is not clear. It may be important in the first half of gestation, before the fetal thyroid gland is capable of T4 production, as well as the latter half of gestation when thyroid hormone effects on multiple organ systems are developing. Management of fetal thyroid dysfunction requires normalization of maternal serum T4 concentrations, avoidance or careful monitoring of potentially goitrogenic drug effects in the fetus, and in some instances, direct or indirect fetal therapy. In most cases fetal hypothyroidism is sporadic and undetected, and prognosis for normal growth and development is excellent if the mother is euthyroid and the hypothyroid state is detected and adequately treated at birth. Fetal treatment by intraamniotic thyroxine injection has been provided in cases of inadvertent maternal radioiodine treatment of Graves' disease between 10 and 20 weeks gestation and for fetal goiter detected by ultrasound. Effective treatment of fetal hyperthyroidism in pregnant women with high titers of thyroid stimulating autoantibody is possible by judicious administration of antithyroid drugs to the mother. Management of the hyperthyroid state in the neonate also is essential.
胎儿下丘脑 - 垂体 - 甲状腺轴独立于母体轴发育，但碘底物的充足供应依赖于母体 - 胎盘系统。这种碘通过母体血浆碘的直接转运以及胎盘对T4的脱碘作用来提供。此外，虽然甲状腺素的胎盘转运有限，但T4会发生显著的母胎转运，足月时胎儿脐血中平均10μg/dL血清T4浓度的约30%来自母体。目前的信息表明，母体对胎儿T4水平的这种贡献对胎儿正常成熟很重要，尤其是对中枢神经系统。母婴联合甲状腺素血症可导致胎儿中枢神经系统不可逆损伤。胎儿对T4的这种依赖时间尚不清楚。在妊娠前半期，胎儿甲状腺尚不能产生T4时，以及在妊娠后半期，甲状腺激素对多个器官系统产生影响时，这可能都很重要。胎儿甲状腺功能障碍的管理需要使母体血清T4浓度正常化，避免或仔细监测胎儿潜在的致甲状腺肿药物作用，在某些情况下，还需要进行直接或间接的胎儿治疗。在大多数情况下，胎儿甲状腺功能减退是散发性的且未被检测到，如果母亲甲状腺功能正常，且在出生时检测到甲状腺功能减退状态并得到充分治疗，正常生长发育的预后良好。对于妊娠10至20周期间因母体意外接受放射性碘治疗格雷夫斯病以及超声检测到胎儿甲状腺肿的情况，已采用羊膜腔内注射甲状腺素进行胎儿治疗。通过明智地给母亲使用抗甲状腺药物，可以有效治疗甲状腺刺激自身抗体滴度高的孕妇的胎儿甲状腺功能亢进。新生儿甲状腺功能亢进状态的管理也至关重要。
