III.

In 14 stroke patients showing angiographic recanalization of the occluded internal carotid artery or middle cerebral arterial axis, the postrecanalized angiograms demonstrated several findings that have been considered to be generally rare in cerebral infarction. These findings principally consisted of narrowing of arterial caliber in six cases (43 percent), mass effect in eight cases (57 percent) and capillary blush in five cases (36 percent).

Early diagnosis and β-blocker therapy for high-risk patients with LQTS are important for prevention of cardiac events during pregnancy and the postpartum period, and β-blocker therapy may be tolerated for babies in LQT-P cases.

ABSTRACT. 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 U/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 thyroidstimulating 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-/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. Pediatrics 2001;107(4). URL: http://www. pediatrics.org/cgi/content/full/107/4/e57; pituitary hypothyroidism, Graves' disease, thyroxine, triiodothyronine, placental transfer.ABBREVIATIONS. FT 3, free triiodothyronine; FT 4, free thyroxine; TSH, thyroid-stimulating hormone; TRAb, thyroid-stimulating hormone receptor antibody; TSAb, thyroid-stimulating antibody; TRH, thyrotropin-releasing hormone; T 4 , thyroxine; T 3, triiodothyronine. CASE REPORTA male infant was born at 27 weeks 2 days of gestational age to a 27-year-old G2P0 mother who was diagnosed at age 13 years with thyrotoxicosis attributable to Graves' disease. She was noncompliant with medication and had an elective abortion at age 26 years because of thyrotoxicosis. Premature rupture of the membranes occurred at 27 weeks 2 days of the second gestation and a nonstress test revealed fetal tachycardia Ͼ200 beats per minute. The mother was transferred to our hospital because of threatened premature labor a...