Abstract:

Note: mu = 0.000001 and is expressed in gram.

T4, T3, actualally means "T sub 3, or 4" mathematically.

Thus, 0.000001gT4/T3=........

Thyrod function wsa evaluated in cord serum of healthy full-term newborns and compared to that of mothers immediately after deficiency, however with a marginal iodine supply (<100 mu g/day in 80% of women).

The aim of the study was to delineate the interrelationships between the thyroid statuses of mother and child at birth. Maternal thyroid function was characterized at delivery by relative hypothyroxinemia; increased T3/T4 ratios, indicating preferential T3 secretion; slightly increased TSH levels within the normal range in 97% of women; increased serum thyroglobulin (TG) values which were above normal in 60% of women; and also goiter formation in almost 10% of women.

The findings indicated glandular stimulation and confirmed earlier reports that pregnancy constitutes a stress for the maternal thyroid economy, enhanced by the limited ability of iodine in the diet. By contrast, newborns showed a strikinly distinct pattern: there were no relative hypothyroxinemia and free T4 levels were significantly higher than in the respective mothers (19.4 vs.14.7 pmol/L;P<0.001).

In spite of these differences, however, mean neonatal TSH and TG vs. 1.9 mU/L for TSH(P<0.001)and 70 vs. 40 mu g/L for TG (P<0.001). Furthermore, neonatal TG and TSH levels increased in parallel and were highly correlated with maternal data, suggseting a regulatory link between both thyroid economies. The results suggested that the common regulatory link is the limited availability of the iodine supply.

In conclusion, the study demonstrates that even in conditions with a marginally low iodine intake, pregnancy constitutes a stimulus for both the maternal and newborn thyroids. Changes in both groups are associated and the abnormalities in TSH and TG are amplified in the newborns.

The TSH and TG alterations at birth in full-term healthy newborns, associated with similar alterations in maternal thyroid function, provide evidence for a common stimulatory factor, relative iodine deficiency. The data emphasize the hypersensitivity of neonatal thyroid function to marginal iodine deficiency and point to the need to increase the iodine supply in groupes at risk, such as women during pregnancy, and also nweborns in the perinatal period.

Thyroid function in the neonatal perid has been stuided extensively for more than fifteen years, since the introduction of systematic screening for congenital hypothyroidism. Healthy full-term infants are born with normal free T4 levels and a low T3 syndrome due to the immaturity of T4 deiodination systems.

TSH at birth is most often normal or slightly elevated; during the first twenty-four hours of life, a marked TSH surge occurs, followed by a rapid rise of T3 and subsequently of T4 levels. And because of the high maternal estrogen impregnation during gestation, newborns have increased serum T4-binding globulin (TBG)levels.

Maternal and fetal thyroid functions are essentially autonomously regulated, except when grugs given to the mother cross the placenta to interfere with fetal thyroid function. Nevertheless, in conditions with severe iodine deficiency, thyroid function parameters of mother and neonate are clearly correlated:they both exibit low T4 and high TSH levels.

In addition, thyroid function is usually more critically altered in neonates compared with mothers, and the alterations can be prevented by adequate iodine supplementation given to mothers during gestation.

In an area with a limited iodine intake ( les than 100 mu g/day in 80% of women) and hence without overt iodine deficiency, it was recently shown that pregnancy constitute a stress for the maternal thyroid, both in healthy women, and in patients with mild underlying thyroid abnormalities.

Thyroid function was characterized in a significant of pregnant women by relative hypothyroxinemia, preferential T3 secretion, slightly elevated, albeit normal, TSH levels, and abnormal serum thyroglobulin (TG)levels in a majority of women at delivery. The pattern clearly suggested excessive glandular stimulation. The aim of of the work was to delineate, as a part of this prospective cohort study, whether the thyroid status of mothers and their newborns was correlated, and in particular whether alterations of thyroid function were also present in the offspring at birth.

Methods And Subjects

Seven hundred and thirty-two consecutive pregnant women were originally enrolled in the study. Thirty-four patients were excluded; they did not complete gestation because of a miscarriage (n = 31) or had overt thyroid dysfunction at initial presentation (n = 3). The cohort hence encompassed a total of 698 euthyroid women who gave informed concent to the study at initial presentation.

The protocol of the investigation had been accepted by the Ethical Committee of the Faculty of Medicine. Based on clinical and laboratory information available from the evaluation carried out at initial presentation, all women were euthyroid.

Parameters of thyroid function evaluated sequentially during gestation, and the results were reported in detail.

Five hundred-fifty women gave birth in an institution and maternal thyroid function was assessed 1-3 days after delivery. In 452 cases, cord blood was obtained at delivery and centrifuged within twelve hours and serum was kept frozen at -20 degrees C, until further use.

Comparative analyses of maternal and noenatal thyroid functions were carried out in two hundred and twenty (220) paired sets of available data, including only healthy full-term babies with gestational age at delivery greater than or equal to thirty-seven weeks born after uncomplicated deliveries, with an Apgar score at 5 min greater than or equal to eight (8).

The following parameters were determined: total T4 and T3, free T4, TG, TBG, and TSH. The molar T3/T4 and T4/TBG ratios; example, the TGB saturation level were computed, the method employed have been recorded.

Total T4, T3, TBG, and TG were measured by conventional RIAs. Free T4 was determined using the two-step Gamma-Coat [125I]free T4 (Clinical Assays, Baxter, Cambridge, MA). Serum TSH was determined using a sensitive immunoradiometric assay (RIAbead II, Abbott, North Chicago, IL). Urinary iodine concentration was assessed using a fully automated Technicon Autoanalizer, employing the Sandell-Kolthoff reaction.

Statistical analyses were carried out using the SPSS program(Statistical Package for Social Sciences, SPSS Inc., Chicago, IL), employing parametric and noneparametric tests as appropriate, on a PC-compatible Elite-AT computer (Compuline, Brussel, Belguim).

Results

Parameters of thyroid function at birth in cord serum of neonates and mothers after delivery were recorded;(in a table which cannot be technically documented here). Nevertheless, in the newborns, the mean total T4 was slightly however significantly higher compared with that of mothers (154 vs. 143 nmol/L; P < 0.001), despite having a 30% lower mean serum TBG (365 vs. 511nmol/L; P < 0.001).

In addition, total T4 levels in the newborns were appropriate for TBG values, hence yielding normal saturation levels of TBG by T4, between 30% and 55% in 96% of babies. In contrast, the mean TBG saturation level was markedly reduced in mothers, compared with that of newborns (28.5 vs. 42.4%, P < 0.001).

The mean free T4 concentration was also significantly higher in newborns, compared with that of mothers (19.4 vs. 14.7 pmol/L; P < 0.001). The neonates exibited a lower T3 syndrome characteristic of thyroid function at birth: more than 90% had T3 levels below 1.4 nmol/L, with a mean T3 level of 0.9 nmol/L, compared with 3.4 nmol/L (P < 0.001) in mothers.

As a consequence of low T3, the molar T3/T4 ratio was extremely low in the newborns, with a mean value of 0.006, compared with 0.024 in mothers (P<0.001).