Short-term hyperthyroidism followed by transient pituitary hypothyroidism in a very low birth weight infant born to a mother with uncontrolled Graves' disease.
Transient hypothyroxinemia in infants born to mothers with poorly controlled Graves' disease was first reported in 1988. We report that short-term hyperthyroidism followed by hypothyroidism with low basal thyroid-stimulating hormone (TSH) levels developed in a very low birth weight infant born at 27 weeks of gestation to a noncompliant mother with thyrotoxicosis attributable to Graves' disease. We performed serial thyrotropin-releasing hormone (TRH) tests in this infant and demonstrated that TSH unresponsiveness to TRH disappeared at 6.5 months of age. The maternal thyroid function was free triiodothyronine (FT(3)), 21.1 pg/mL; free thyroxine (FT(4)), 8.1 ng/dL; TSH, <0.03 microU/mL; thyroid-stimulating hormone receptor antibody, 52% (normal: <15%); thyroid-stimulating antibody, 294% (normal: <180%); and thyroid-stimulation blocking antibody, 9% (normal: <25%) on the day of delivery. A nonstress test revealed fetal tachycardia >200 beats per minute, and a male infant weighing 1152 g was born by emergency cesarean section. Thyroid-stimulating hormone receptor antibody was 16% and thyroid-stimulating antibody was 370% in the cord blood. We administered 10 mg/kg per day of oral propylthiouracil from day 1. Tachycardia along with elevated FT(4) and FT(3) levels in the infant decreased from 200/minute to 170/minute, 4.7 ng/dL to 2.9 ng/dL, 7.0 pg/mL to 4.8 pg/mL, respectively, in the first 33 hours. At 5 days, FT(4) and FT(3) were 1.1 ng/dL and 2.9 pg/mL, respectively, and we stopped propylthiouracil administration. Although FT(4) decreased to 0.4 ng/dL, TSH was quite low and did not respond to intravenous TRH by 14 days of age. We began daily levothyroxine 5-micro/kg supplementation. The responsiveness of TSH to TRH did not become significant until 4 months old and normalized at 6.5 months old. At this time, levothyroxine was stopped. We conclude that placental transfer of thyroid hormones may cause hyperthyroidism in the fetal and early neonatal periods and lead to transient pituitary hypothyroidism in an infant born to a mother with uncontrolled Graves' disease.
Higuchi
R
R
Department of Perinatal Medicine, Wakayama Medical College, Wakayama City, 641-0012, Japan. rhiguchi@wakayama-med.ac.jp
Kumagai
T
T
Kobayashi
M
M
Minami
T
T
Koyama
H
H
Ishii
Y
Y
D000328:Adult; D005260:Female; D005865:Gestational Age; D006111:Graves Disease / Q000097:blood*; D006801:Humans; D006980:Hyperthyroidism / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D007037:Hypothyroidism / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D018828:Immunoglobulins, Thyroid-Stimulating / Q000097:blood; D007231:Infant, Newborn; D019102:Infant, Very Low Birth Weight / Q000097:blood*; D008297:Male; D008431:Maternal-Fetal Exchange; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood*; D013972:Thyrotropin / Q000097:blood / Q000502:physiology; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology; D013974:Thyroxine / Q000097:blood / Q000502:physiology
D018828:Immunoglobulins, Thyroid-Stimulating; C118905:thyroid stimulation-blocking antibody; D013973:Thyrotropin-Releasing Hormone; D013972:Thyrotropin; D013974:Thyroxine