title: The incidence of gestational hyperthyroidism and postpartum thyroiditis in treated patients with Graves' disease.
abstract: Graves' disease (GD) is one of the most common thyroid diseases that cause hyperthyroidism. Gestational transient thyrotoxicosis (GTT) is nonautoimmune hyperthyroidism that occurs in women with a normal pregnancy. Postpartum transient thyroiditis (PTT) is a destructive thyroiditis induced by autoimmune mechanism in the postpartum period. Hyperthyroidism due to GD usually tends to improve during the course of gestation and exacerbate after delivery. When the patient with treated GD presents with thyrotoxicosis in the early pregnancy or in the postpartum period, differential diagnosis of exacerbation of GD with GTT or PTT is important because the latter disorders are fundamentally transient. To evaluate the incidence of GTT and PTT in a GD population, we investigated the thyroid functions, thyrotropin receptor antibodies (TRAb), and human chorionic gonadotropin (hCG) during pregnancy and for 1 year after delivery for 39 pregnancies in 34 women with GD. The incidence of GTT was 26% (10/39) of pregnancies. The peak value of hCG in the GTT group ([23.7 +/- 14.5] x 10(4) IU/mL, n = 9) was significantly higher than that in the non-GTT group ([13.3 +/- 4.7] x 10(4) IU/mL, n = 19). The incidence of PTT was 44% (17/39) of deliveries. The free triiodothyronine (FT(3))/free thyroxine (FT(4)) ratio of the exacerbation group of GD (3.1 +/- 1.0, n = 10) at the time of thyrotoxicosis after delivery was significantly higher than that of the PTT group (2.5 +/- 0.4, n = 16). The peak TRAb value of the exacerbation group of GD (72.5 +/- 121.7 IU/L, n = 10) at the time of thyrotoxicosis after delivery was also significantly higher than that of the PTT group (1.4 +/- 0.8 IU/L, n = 16). In conclusion, the high peak value of hCG is valuable for suspecting GTT, and the high FT(3)/FT(4) ratio is valuable for suspecting recurrence in the patients with GD. In both situations, changes of TRAb were also valuable in differentiating the recurrence of GD from GTT or PTT.
authors.affiliation: Clinical Research Institute, Division of Endocrinology and Metabolism, Kyoto Medical Center, National Hospital Organization, Kyoto 612-8555, Japan. ttagami@kyotolan.hosp.go.jp
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Tagami
authors.forename: Hanae
authors.initials: H
authors.lastname: Hagiwara
authors.forename: Takashi
authors.initials: T
authors.lastname: Kimura
authors.forename: Takeshi
authors.initials: T
authors.lastname: Usui
authors.forename: Akira
authors.initials: A
authors.lastname: Shimatsu
authors.forename: Mitsuhide
authors.initials: M
authors.lastname: Naruse
mesh_terms: D000328:Adult; D013956:Antithyroid Agents / Q000627:therapeutic use; D001323:Autoantibodies / Q000097:blood; D003937:Diagnosis, Differential; D005260:Female; D006111:Graves Disease / Q000175:diagnosis* / Q000188:drug therapy / Q000453:epidemiology* / Q000276:immunology; D006801:Humans; D015994:Incidence; D049590:Postpartum Period; D011247:Pregnancy; D011248:Pregnancy Complications / Q000175:diagnosis* / Q000453:epidemiology* / Q000276:immunology; D015995:Prevalence; D012008:Recurrence; D013960:Thyroid Function Tests; D013966:Thyroiditis / Q000175:diagnosis* / Q000453:epidemiology* / Q000276:immunology; D013971:Thyrotoxicosis / Q000175:diagnosis / Q000453:epidemiology / Q000276:immunology; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D013956:Antithyroid Agents; D001323:Autoantibodies; D014284:Triiodothyronine; D013974:Thyroxine