Volpé R, Ehrlich R, Steiner G, Row V V
Am J Med. 1984 Sep;77(3):572-8. doi: 10.1016/0002-9343(84)90125-6.
Symptoms and signs of severe hypothyroidism developed in a young woman at age 15. These symptoms progressed for a year; at age 16, she was found to have a firm goiter, thyroid autoantibodies, very low serum thyroxine and high thyrotropin values, indicating autoimmune thyroiditis with hypothyroidism. She received L-thyroxine, 0.20 mg per day, and was well until age 24 when she became pregnant. In the first trimester, manifestations indicative of hyperthyroidism developed; these were only ultimately recognized immediately after delivery of a 32-week still-born goitrous baby. Despite the discontinuation of thyroxine therapy, the hyperthyroidism persisted and was confirmed as Graves' disease by elevated thyroxine, triiodothyronine, and radioactive iodine uptake values, a diffuse scanning result, and the presence of thyroid-stimulating antibody. The patient was treated with propylthiouracil and became pregnant while receiving that regimen. Later, several months after delivery, the patient was treated with radioactive iodine, ultimately became hypothyroid, and has been treated ever since with thyroxine. She became pregnant again and, because of the continuing high titers of thyroid-stimulating antibody, received propylthiouracil, 100 mg daily, commencing in the third trimester of pregnancy, to avoid probable fetal hyperthyroidism due to the transplacental transfer of thyroid-stimulating antibody. In each of the last two pregnancies, when the infants were born, they seemed normal (because of the transplacental effect of propylthiouracil), but passive-transfer neonatal hyperthyroidism developed in each within 10 days after delivery, ultimately requiring treatment by conventional means. This case illustrates the following points: (1) Hyperthyroidism occasionally develops years after hypothyroidism. (2) In young women, high titers of thyroid-stimulating antibody may produce fetal and neonatal passive-transfer hyperthyroidism even at a time when the mother herself is no longer hyperthyroid; transplacental treatment of the fetus by maternal propylthiouracil ingestion may thus be necessary during the last trimester, but only when there is a high degree of probability that the fetus is at risk. (3) Because the infants had been protected in utero by the placental transfer of propylthiouracil, neonatal hyperthyroidism did not develop until several days after delivery.(ABSTRACT TRUNCATED AT 400 WORDS)
一名年轻女性在15岁时出现严重甲状腺功能减退的症状和体征。这些症状持续了一年；16岁时，她被发现有一个质地坚硬的甲状腺肿、甲状腺自身抗体、极低的血清甲状腺素和高促甲状腺素值，提示自身免疫性甲状腺炎伴甲状腺功能减退。她开始每天服用0.20毫克左甲状腺素，情况良好，直到24岁怀孕。在孕早期，出现了提示甲状腺功能亢进的表现；这些表现直到一个32周大的甲状腺肿死产婴儿出生后才被最终确认。尽管停止了甲状腺素治疗，但甲状腺功能亢进仍持续存在，甲状腺素、三碘甲状腺原氨酸和放射性碘摄取值升高、弥漫性扫描结果以及甲状腺刺激抗体的存在证实为格雷夫斯病。患者接受丙硫氧嘧啶治疗，并在该治疗方案期间再次怀孕。后来，分娩后几个月，患者接受放射性碘治疗，最终出现甲状腺功能减退，此后一直用甲状腺素治疗。她再次怀孕，由于甲状腺刺激抗体滴度持续升高，从妊娠晚期开始每天服用100毫克丙硫氧嘧啶，以避免由于甲状腺刺激抗体经胎盘转移导致胎儿可能出现甲状腺功能亢进。在最后两次怀孕中，婴儿出生时看起来正常（由于丙硫氧嘧啶的胎盘效应），但在出生后10天内均出现了被动转移型新生儿甲状腺功能亢进，最终需要采用传统方法治疗。该病例说明了以下几点：（1）甲状腺功能亢进偶尔会在甲状腺功能减退数年之后出现。（2）在年轻女性中，即使母亲自身不再患有甲状腺功能亢进，高滴度的甲状腺刺激抗体也可能导致胎儿和新生儿出现被动转移型甲状腺功能亢进；因此，在妊娠晚期可能需要通过母亲摄入丙硫氧嘧啶对胎儿进行经胎盘治疗，但前提是胎儿有很高的风险。（3）由于婴儿在子宫内受到丙硫氧嘧啶胎盘转移的保护，新生儿甲状腺功能亢进直到分娩后几天才出现。（摘要截取自400字）
