T3 Deficiency Research Articles

274 PRENATAL THYROID ABNORMALITIES IN PREMATURE INFANTS WITH RESPIRATY DISTRESS SYNDROME (RDS)

An association between RDS and prenatal thyroid dysfunction has been previously described. To further investigate the abnormalities in thyroid function, cord blood from 49 neonates was obtained for measurements of T3, T4 and TSH by RIA. The results in the 5 groups identified according to gestational age and disease are summarized below:In both RDS groups T3 was comparable and significantly lower than control groups, P<0.001. T4 in RDS II was significantly higher than in RDS I (P<0.05) but comparable to control II. TSH was slightly higher in RDS II but there was no significant difference in any group. The data demonstrate: 1. a persistent prenatal abnormality in T3 of RDS babies, 2. normal increase in T4 concentration according to gestational age in RDS babies, 3. normal thyroid function in babies who develop non-RDS illness. Since T3 is primarily derived from extrathyroid sources, the observation of low T3 and normal T4 excludes thyroid as the primary sight of T3 deficiency. T3 deficiency, however, may adversely effect the maturation of surfactant producing enzyme apparatus.

Screening for Congenital Metabolic Disorders in the Newborn Infant: Congenital Deficiency of Thyroid Hormone and Hyperphenylalaninemia

The Committee on Genetics of the American Academy of Pediatrics was formed in 1976. The initial reports from the Committee are published in this supplement to Pediatrics: one on guidelines for screening the newborn infant for hyperphenylalaninemia (including phenylketonuria [PKU]) and the other on screening for congenital hypothyroidism. The first statement describes guidelines for screening for thyroid hormone deficiency in newborn infants; it concerns a traditional problem in pediatrics, the prevention of cretinism. A statement on "T4 screening" has already been issued by the American Thyroid Association.1 Why is there need for another (and longer) statement from the Academy? The Task Force on Genetic Screening recommended a special review of T4 screening, and that recommendation has been acted on quickly in the hope that most of the mistakes made in PKU screening will not be repeated in T4 screening. The American Thyroid Association statement adequately describes the status of testing for T4 deficiency; it does not cover other essential components of an effective screening program, namely, provision for serving patient retrieval, diagnosis, and treatment. The Committee urges pediatricians and endocrinologists who elect to push ahead with T4 testing to pause and examine the many issues of mass newborn infant screening before they act too hastily, perhaps to the detriment of their patients and newborn infant screening programs. Dr. Jean Dussault served as consultant to the Committee when it examined T4 screening; his personal experience extends to ¼ million screened subjects and emanates from a model program which has largely avoided many pitfalls of newborn infant screening.

Total and Free Thyroid Hormone Concentrations in the Neonatal Period

Radioimmunoassay measurements of serum concentrations of thyroxine (T4), triiodothyronine (T3), free T4 (FT4), free T3 (FT3), and thyroxine binding globulin (TBG) were conducted in full-term newborn infants between birth and 5 days of age. The mean concentrations of T4 and FT4 increased from cord blood levels of 11.9 µg/100 ml and 2.9 ng/100 ml to peak values of 16.2 µg/100 ml and 7 ng/100 ml by 24 to 48 hours of age. Mean serum total and free T3 concentrations increased from cord blood levels of 50.5 ng/100 ml and 146 pg/100 ml to peak values of 419 ng/100 ml and 1,260 pg/100 ml by 24 hours of age. Mean T3/T4 and FT3/FT4 ratios increased from 1/238 to 1/39 and from 1/20 to 1/6, respectively, during this period. By 72 to 126 hours, both the T4 and T3 concentrations had fallen somewhat. Mean serum TBG concentrations were unchanged and approximated 5.0 mg/100 ml during the first 5 days of life. These data confirm earlier reports that the normal newborn infant rapidly becomes chemically hyperthyroid in the neonatal period due to increased thyroid hormone secretion; this neonatal hyperthyroid state is due more to T3 than to T4. The data also confirm earlier reports that the fetus is T3 deficient due to a decreased capacity to monodeiodinate T4 to T3 in extrathyroidal tissues. The rapid increase in serum T3 after delivery at a time when the capacity to convert T4 to T3 is reduced suggests that the increment in serum T3 is due, predominantly, to increased T3 secretion from the thyroid gland stimulated by the neonatal TSH surge. Thus with parturition, the newborn infant is transformed from a state of chemical T3 deficiency to a state of chemical T3 thyrotoxicosis.

Serum and thyroid gland triiodothyronine in the human fetus.

Serum T3 concentrations are low (<15 ng/100 ml) before 24 weeks and increase progressively thereafter to term, but both T3 and free T3 (FT3) levels are lower than paired maternal concentrations. Moreover, throughout gestation T4/T3 and FT4/FT3 ratios consistently exceed paired maternal ratios. The mean T4/T3 content ratio of fetal thyroid glands (14.3) is similar to that (19.5) of adult glands. These data indicate that a state of relative fetal T3 deficiency exists in the human as in the sheep. This deficiency probably is not due to decreased T3 secretion.