Kimura M, Amino N, Tamaki H, Ito E, Mitsuda N, Miyai K, Tanizawa O
Department of Laboratory Medicine, Osaka University Medical School, Japan.
Clin Endocrinol (Oxf). 1993 Apr;38(4):345-50. doi: 10.1111/j.1365-2265.1993.tb00512.x.
The thyroid gland is physiologically stimulated in normal early pregnancy. However, clinical thyrotoxicosis in normal pregnancy has not been well described. In order to clarify this we examined thyroid function and thyrotoxic symptoms in relation to emesis in normal pregnancy. We also investigated the possible mechanism of gestational thyrotoxicosis.
Thyroid function was evaluated in view of the clinical thyrotoxic symptoms and the severity of gestational emesis in early pregnancy of 51 normal women. Two pregnant women who showed clinical thyrotoxicosis were followed serially during and after pregnancy.
Serum free T4, free T3 and TSH were measured by radioimmunoassay and hCG by fluoroimmunoassay. Thyroid-stimulating activity of pregnancy sera was measured by cAMP increase in cultured FRTL-5 cells.
Fifty-one pregnant women were divided into three groups: those without emesis (n = 24), with emesis (n = 19) and with hyperemesis (n = 8). Serum free T4 and free T3 were higher in the hyperemesis group (P < 0.01) and the emesis group (P < 0.01), and serum TSH was suppressed to less than 0.1 mU/l in both groups, while serum hCG was not significantly different among these three groups. However, serum thyroid-stimulating activity was remarkably high in the hyperemesis group (P < 0.01). Thus the ratio of thyroid-stimulating activity to hCG was higher in the hyperemesis group (P < 0.05) and the emesis group (P < 0.05) compared with that in the group without emesis. These thyroid-stimulating activities were abolished by treatment of the serum with anti-hCG antibody. Two of eight women with hyperemesis, who had the highest free T4 and thyroid-stimulating activity/hCG ratio, showed overt clinical symptoms of thyrotoxicosis; all the symptoms disappeared in association with a fall in thyroid-stimulating activity and free T4.
Clinical thyrotoxicosis is caused by circulating hCG with higher biological activity in pregnant women with hyperemesis. A new clinical entity of 'gestational thyrotoxicosis' is proposed and tentative characteristics are discussed.
在正常妊娠早期，甲状腺会受到生理性刺激。然而，正常妊娠期间的临床甲状腺毒症尚未得到充分描述。为了阐明这一点，我们研究了正常妊娠中甲状腺功能和甲状腺毒症症状与呕吐的关系。我们还研究了妊娠甲状腺毒症的可能机制。
对51名正常孕妇妊娠早期的临床甲状腺毒症症状和妊娠呕吐严重程度进行评估，以评价甲状腺功能。对两名出现临床甲状腺毒症的孕妇在孕期及产后进行连续跟踪。
采用放射免疫分析法测定血清游离T4、游离T3和促甲状腺激素（TSH），采用荧光免疫分析法测定人绒毛膜促性腺激素（hCG）。通过培养的FRTL-5细胞中cAMP的增加来测量妊娠血清的促甲状腺活性。
51名孕妇分为三组：无呕吐组（n = 24）、呕吐组（n = 19）和妊娠剧吐组（n = 8）。妊娠剧吐组和呕吐组的血清游离T4和游离T3较高（P < 0.01），两组血清TSH均被抑制至低于0.1 mU/l，而三组血清hCG无显著差异。然而，妊娠剧吐组的血清促甲状腺活性显著较高（P < 0.01）。因此，与无呕吐组相比，妊娠剧吐组和呕吐组的促甲状腺活性与hCG的比值更高（P < 0.05）。用抗hCG抗体处理血清后，这些促甲状腺活性被消除。8名妊娠剧吐女性中有2名，其游离T4和促甲状腺活性/hCG比值最高，表现出明显的甲状腺毒症临床症状；随着促甲状腺活性和游离T4下降，所有症状消失。
妊娠剧吐孕妇的临床甲状腺毒症是由具有较高生物活性的循环hCG引起的。提出了“妊娠甲状腺毒症”这一新的临床实体，并讨论了其初步特征。
