Decreased reverse T3 levels in neonates with central hypothyroidism.

Concern arises when a sick infant is found to have a low serum T4, normal thyroid hormone binding, and a nonelevated thyroid-stimulating hormone. Hypothyroxinemia in this situation can result from either euthyroid sick syndrome or central hypothyroidism. To help distinguish between these diagnostic possibilities, we have measured reverse T3 and other thyroid function chemistries in six neonates who have central hypothyroidism in association with hypopituitarism. We found that these infants all had reverse T3 levels that were much lower than reported normal levels for premature and term neonates. This finding suggests that low reverse T3 levels can help to distinguish infants with central hypothyroidism from sick and well infants who tend to have relatively elevated reverse T3 levels.

Adrenal responsiveness in very-low-birth-weight infants treated with dexamethasone.

This study was designed to investigate the effect of steroid administration in ill premature neonates. Twenty high-risk very-low-birth-weight (VLBW) infants [birth weight (BW) < or = 1,300 g] with a mean BW 948 +/- 220 g, gestational age (GA) 27 +/- 1.7 weeks underwent 1-hour ACTH (Cortrosyn) stimulation tests and determination of 17-hydroxyprogesterone (17OHP)/dehydroepiandrosterone sulfate (DHEAS) at 23.6 +/- 15.9 days poststeroid treatment for bronchopulmonary dysplasia (BPD)/airway obstruction. Metyrapone tests were also obtained in 18 infants. Baseline (nonsteroid-exposed) values for pre-/post-ACTH cortisol, 17OHP, DHEAS, and pre-/post-metyrapone compound S values were obtained in 5 infants. Eight of 18 (44%) infants had evidence of secondary (hypothalamic-pituitary) adrenal suppression based on abnormal metyrapone tests. No difference was found in BW, GA, time on O2 or AV, steroid dose/kg, or neonatal/postneonatal mortality between the suppressed and nonsuppressed groups. Two of 4 infants with borderline ACTH tests had subnormal compound S levels postmetyrapone. No relationship was found between steroid dose/kg and cortisol response post-ACTH. Additionally, corrected GA was not related to change in cortisol, 17OHP, and DHEAS pre-/post-ACTH. Two infants exhibited recovery of adrenal suppression documented by repeated metyrapone testing at 63 and 186 days poststeroid treatment. In conclusion, this study documents the apparent high incidence of secondary adrenal suppression in VLBW infants treated with dexamethasone. Clinical significance of these findings deserves further investigation.

Defective pancreatic alpha and beta cell secretion in thyrotoxicosis.

Pancreatic alpha and beta cell hormone secretion was studied in 11 patients with thyrotoxicosis before and in 7 patients after thyroid function was normalized with either prophylthiouracil or methimazole and propranolol (R). All had IV arginine and IV glucose infusions. Forty control subjects had IV arginine; 21 had IV glucose tests. After arginine, untreated patient had blunted serum insulin at both 15 and 30 minutes (p less than 0.05, p less than 0.001) compared to control subjects, blunted glucagon at 30 minutes (p less than 0.05) and blunted glucose at both 15 and 30 minutes (p less than 0.001, p less than 0.01) compared to control subjects. After glucose, untreated patients had lower nadir glucagon than in the studies with both arginine and glucose infusions. These data document blunted glucagon, suppressed glucose and insulin peaks after arginine in thyrotoxicosis, indicate that both alpha and beta cell hormone secretion may be abnormal, and that the preferential abnormality follows protein rather than carbohydrate loading.