Short-Term Hyperthyroidism Followed by Transient Pituitary Hypothyroidism in a Very Low Birth Weight Infant Born to a Mother With Uncontrolled Graves' Disease

  • Ryuzo Higuchi
    1 From the Department of Perinatal Medicine, Wakayama Medical College, Wakayama City, 641-0012, Japan.
  • Takeshi Kumagai
    1 From the Department of Perinatal Medicine, Wakayama Medical College, Wakayama City, 641-0012, Japan.
  • Masakazu Kobayashi
    1 From the Department of Perinatal Medicine, Wakayama Medical College, Wakayama City, 641-0012, Japan.
  • Takaomi Minami
    1 From the Department of Perinatal Medicine, Wakayama Medical College, Wakayama City, 641-0012, Japan.
  • Hirofumi Koyama
    1 From the Department of Perinatal Medicine, Wakayama Medical College, Wakayama City, 641-0012, Japan.
  • Yuki Ishii
    1 From the Department of Perinatal Medicine, Wakayama Medical College, Wakayama City, 641-0012, Japan.

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<jats:p>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.</jats:p><jats:p>The maternal thyroid function was free triiodothyronine (FT3), 21.1 pg/mL; free thyroxine (FT4), 8.1 ng/dL; TSH, &lt;0.03 μU/mL; thyroid-stimulating hormone receptor antibody, 52% (normal: &lt;15%); thyroid-stimulating antibody, 294% (normal: &lt;180%); and thyroid-stimulation blocking antibody, 9% (normal: &lt;25%) on the day of delivery. A nonstress test revealed fetal tachycardia &gt;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 FT4 and FT3 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, FT4and FT3 were 1.1 ng/dL and 2.9 pg/mL, respectively, and we stopped propylthiouracil administration. Although FT4decreased 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-μ/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.</jats:p><jats:p>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.</jats:p>

収録刊行物

  • Pediatrics

    Pediatrics 107 (4), e57-e57, 2001-04-01

    American Academy of Pediatrics (AAP)

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