Neonatal hypothyroxinemia: effects of iodine intake and premature birth

9 pages, 7 figures, 3 tables.We have investigated the effects of iodine (I) intake on urinary I excretion in preterm (PT) babies up to 2 months after birth and its effect on serum T4, free T4 (FT4), T3, TSH, and thyroglobulin (Tg) levels compared to those in term (T) newborns. Very premature and very sick infants were in negative I balance for the first weeks after birth. Later, these same infants, as well as the other PT and T newborns, were in positive balance; 75- 80% of the ingested I was not accounted for in the urine. The urinary I levels of PT and T neonates cannot be equated to their I intakes. T4, FT4, and T3 levels in PT and T neonates increased with postmenstrual age, whereas Tg decreased and TSH did not change. Serum FT4, T3, Tg, and TSH levels in PT neonates were affected negatively, independently from age, by a low I intake. PT birth also affected T4, FT4, and Tg negatively, independently from I intake and postmenstrual age, for at least 6-8 weeks after birth. Care should be taken to avoid I deficiency in PT neonates. However, even when I intake is adequate, PT newborns are hypothyroxinemic compared to T babies during an important period of brain development. This suggests the possible convenience of interventions that might mimic the intrauterine hormone environment and accelerate maturation.This work was supported by the Heinz-Koch Foundation (Milupa, Spain) and the Fondo de Investigaciones Sanitarias (FIS Grant 92/0888 and Fellowship 92/5351 to S.A.).Peer reviewe

Iodine Deficiency in Pregnancy: The Effect on Neurodevelopment in the Child

Iodine is an integral part of the thyroid hormones, thyroxine (T4) and tri-iodothyronine (T3), necessary for normal growth and development. An adequate supply of cerebral T3, generated in the fetal brain from maternal free T4 (fT4), is needed by the fetus for thyroid hormone dependent neurodevelopment, which begins in the second half of the first trimester of pregnancy. Around the beginning of the second trimester the fetal thyroid also begins to produce hormones but the reserves of the fetal gland are low, thus maternal thyroid hormones contribute to total fetal thyroid hormone concentrations until birth. In order for pregnant women to produce enough thyroid hormones to meet both her own and her baby’s requirements, a 50% increase in iodine intake is recommended. A lack of iodine in the diet may result in the mother becoming iodine deficient, and subsequently the fetus. In iodine deficiency, hypothyroxinemia (i.e., low maternal fT4) results in damage to the developing brain, which is further aggravated by hypothyroidism in the fetus. The most serious consequence of iodine deficiency is cretinism, characterised by profound mental retardation. There is unequivocal evidence that severe iodine deficiency in pregnancy impairs brain development in the child. However, only two intervention trials have assessed neurodevelopment in children of moderately iodine deficient mothers finding improved neurodevelopment in children of mothers supplemented earlier rather than later in pregnancy; both studies were not randomised and were uncontrolled. Thus, there is a need for well-designed trials to determine the effect of iodine supplementation in moderate to mildly iodine deficient pregnant women on neurodevelopment in the child

Maternal nonthyroidal illness and fetal thyroid hormone status, as studied in the streptozotocin-induced diabetes mellitus rat model

11 pages, 9 figures, 1 table.We have used the streptozotocin-induced diabetes mellitus pregnant rat as a model of maternal nonthyroidal illness. We measured the effects of different degrees of diabetes mellitus on maternal body weight, the outcome of pregnancy, circulating glucose, insulin, T4, T3, rT3, and TSH in mother and fetus, T4 and T3 in maternal and fetal tissues, and iodothyronine deiodinases in liver, lung, and brain. All of the changes in thyroid hormone status typical of nonthyroidal illnesses were observed in the mothers and were related to the degree of the metabolic imbalances. Most were controlled with a daily insulin dose of 0.5 U/100 g BW. Normalization of maternal placental T4, however, required higher insulin doses than in other maternal tissues. The number and body weight of the fetuses, their pituitary GH contents, and their thyroid hormone status were severely affected. The total extrathyroidal T4 and T3 pools decreased to one third of normal fetal values. T4 and T3 concentrations in the fetal brain were lower than normal, and the expected increase in type II 5'deiodinase activity was not observed. The low cerebral T3 only improved with adequate insulin treatment of the dams. It is concluded that maternal diabetes mellitus, and possibly other nonthyroidal illnesses that impair the availability of intracellular energy stores, may affect fetal brain T3 when thyroid hormones are essential for normal development.This work was supported by Grant 92–08 88 from the Fondo de Investigaciones Sanitarias, Spain.Peer reviewe

Yodo y embarazo

Yodo y embarazo

Maternal diabetes mellitus, a rat model for nonthyroidal illness: Correction of hypothyroxinemia with thyroxine treatment does not improve fetal thyroid hormone status

Maintenance of normal maternal thyroxinemia prevents severe triiodothyronine (T3) deficiency of the fetus with primary thyroid failure (1). We have studied whether thyroxine (T4) would also protect the fetal brain when maternal hypothyroxinemia is caused by nonthyroidal illnesses. We have used the streptozotocin-induced diabetes mellitus pregnant rat as a model of maternal nonthyroidal illness. We measured the effects of diabetes mellitus, and of correction of the ensuing maternal hypothyroxinemia with T4 as compared to insulin, on maternal body weight, the outcome of pregnancy, glucose, insulin, T4, T3, reverse T3, and thyrotropin levels in the maternal and fetal circulation, as well as T4 and T3 concentrations in tissues, and iodothyronine deiodinases in liver, lung, and brain. The diabetic mothers showed changes in thyroid hormone status typical of nonthyroidal illnesses. Thyroid hormone status of the fetuses was severely affected: the total T4 and T3 pools decreased to one-third of normal values. T4 and T3 concentrations in the fetal brain were lower than normal and the expected increase in 5'-deiodinase activity was not observed. Although insulin treatment avoided or mitigated these changes, the low cerebral T3 did not improve with T4 treatment of the maternal hypothyroxinemia. Several findings indicated that treatment of the severely ill dams with T4 was actually harmful for the outcome of pregnancy. These negative effects were observed without the expected increase in the maternal or fetal T3 pools.This work was supported by Grant FISS (Fondo de Investigaciones Sanitarias) 92/0888, Spain.Peer Reviewe

Detection of thyroid hormones in human embryonic cavities during the first trimester of pregnancy

et al.Transfer of maternal thyroxine (T4) to the human fetus near term has recently been demonstrated. We investigated whether maternal thyroid hormone is available to the conceptus during the first trimester of pregnancy as well. Transvaginal ultrasound-guided puncture of the embryonic cavities was performed during the first trimester of pregnancy to obtain coelomic fluid between 6 and 11 weeks, and amniotic fluid between 8 and 11 weeks of pregnancy. T4 was found in coelomic fluid with mean values (+/- SEM) being 961 +/- 193 pmol T4/L (747 +/- 150 pg/mL). Concentrations increased both with gestational age and with rising maternal serum T4. Concentrations of 3,5,3'-triiodothyronine (T3) were at least 30 times lower, and those of 3,3',5'-triiodothyronine (rT3) four times higher, than coelomic fluid T4. Thyroxine and rT3 in amniotic fluid (8-11 weeks) were markedly lower than in the coelomic fluid, and T3 was undetectable. These results show that maternal thyroxine can cross the placental barrier as early as the second month of pregnancy. T4 from the coelomic fluid may reach the embryo via the yolk sac. This finding raises the possibility that the increase in maternal T4 occurring during the first trimester may be functionally important for the developing embryo, when its thyroid is not yet functioning.This work was supported by grant 92 / 0888 of Fondo de Investigaciones Sanitarias (Spain) and grant nº 3.4530.93. from the “Fends de la Recherche Scientifique Médicale> (FRSM, Belgium).Peer Reviewe

Iodine status of pregnant women and their progeny in the minho region of Portugal

[Background]: Iodine sufficiency is particularly necessary throughout pregnancy, given its recognized impact on psychomotor performance of the offspring. There are no recent reports about iodine status or supplementation in Portugal, a country that the International Council for Control of Iodine Deficiency Disorders considered, in 2004, to have probably reached iodine sufficiency. The objective of this study was to evaluate in the Minho region of Portugal the iodine status of women throughout pregnancy and after delivery, and of their offspring. [Methods]: Urinary iodine concentration (UI) was determined in 78 nonpregnant premenopausal women, in 140 pregnant women in the three trimesters of pregnancy and after delivery, and in their 142 offspring. Milk iodine concentration was determined at day 3 and 3 months after delivery. The thyroid volume was determined in women in the third trimester of pregnancy and 3 months after delivery and in infants at 3 months of age. [Results]: Based on the World Health Organization criteria, both nonpregnant and pregnant women had iodine deficiency (ID), as documented by median UI of <75 μg/L and milk iodine concentration of <100 μg/L. Goiter was observed in 14% of the pregnant women. Concordant with the mother's ID, median neonatal UI was low (71 and 97 μg/L at 3 days and 3 months of age). Conclusion: Portuguese women of the Minho region have an inadequate iodine intake, which may compromise the potential for full psychomotor development of their progeny. These observations suggest that iodine supplementation should be implemented throughout pregnancy and lactation in Portugal. © Copyright 2009, Mary Ann Liebert, Inc.This study was supported by the Portuguese Science Foundation (FCT)-FEDER Grant POCTI_PSI_60948_2004 and by the Integrated Actions for exchange of scientists ‘‘Portugal-Spain E-84=2006.’’Peer Reviewe

Consecuencias de la deprivación del iodo y hormonas tiroideas

Consecuencias de la deprivación del iodo y hormonas tiroideas