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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe iodine-induced hypothyroidism was recently diagnosed in several neonates raising the responsibility of the iodine antiseptic agents routinely used in these patients. Postnatal iodine overload due to cutaneous application of these agents (povidone iodine and fluorescinated alcoholic-iodine solution) was studied in 5 patients. Thyroid function studies were performed in iodine-overload neonates and in control neonates with comparable gestional age. Results indicated strong evidence of cutaneous absorption of iodine from the antiseptic agents used, leading to hypothyroidism in 12 of them. The frequency and the severity of thyroid dysfunction was closely related to the degree of prematurity. Full recovery was observed in all cases after withdrawal of the iodine-containing agents. It is therefore recommended to avoid any postnatal use of iodine preparations in neonates, mainly in preterm infants, and to use iodine antiseptic agents with great caution, when necessary during the neonatal period.
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PMID:[The thyroid gland of the newborn infant and postnatal iodine overload]. 49 28

During the period 1965-1976, 43 pregnancies in 42 thyrotoxic mothers were seen. Thirty-nine pregnancies in 38 patients were analyzed further. Twenty-six patients (27 pregnancies) were treated with antithyroid agents with (9) or without (17) supplemental thyroid hormone therapy and 5 were subjected to subtotal thyroidectomy. In these groups spontaneous abortion occurred in 4 patients (12.5%), prematurity in 3 (9.4%) and perinatal death in one whereas 25 pregnancies ended at term (78%). Two pairs of twins were born and the number of live children in these 32 pregnancies was 29. Hypothyroidism developed in one patient after operation. Thyroid crisis occurred at delivery in one patient in whom the antithyroid therapy was interrupted before labour. Seven patients were not treated with specific antithyroid therapy. In this group there was one twinbirth, one premature birth, one stillbirth and one child died shortly after birth. Thyroid crises developed at delivery in two mothers. The authors use subtotal thyroidectomy if usual indications for operation are present and antithyroid therapy when the thyroid gland is small and diffuse. Beta-receptor blocking agents are recommended only as adjuncts to the antithyroid therapy. A close surveillance of the patients and the free thyroid hormone level during therapy is important and after thyroidectomy treatment with thyroid hormone is recommended until after delivery.
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PMID:Thyrotoxicosis and pregnancy. An analysis of 43 pregnancies in 42 thyrotoxic mothers. 63 98

The neonatal changes in the plasma concentration thyrotropin, T3, T4 and cortisol were followed in six lambs born 7 days before term, after injection of oestrogen into the ewes, and in six full-term animals. The plasma T3 concentrations were significantly lower in the preterm animals 1 h, 8 h, 36 h, 44 h, 5 days, 15 days, 20 days and 30 days after birth. The plasma T4 concentrations were significantly higher in the preterm lambs than in the controls during the first 16 h of life. The T3/T4 ratios were constantly lower in the preterm animals during the first 20 days of life. The plasma cortisol concentrations were significantly lower in the preterm lambs over the first 8 h of life. In contrast to the full-term animals, the thyroid of the preterm ones did not respond to an increase in the plasma concentration of thyrotropin by a rise in the plasma concentration of the iodinated hormones. Thyroid function seems affected by prematurity during the first month of life. The T4 to T3 conversion may be impaired and the plasma T3 concentration is depressed. Since the thyroid seemed to be relatively insensitive to a thyrotropin surge induced, for instance, by cold, thermoregulation could be impaired in preterm lambs. The low concentration of T3 and cortisol observed at birth may also contribute to a reduction in the synthesis of the pulmonary surfactant. These results can therefore, at least in part, explain the high mortality rate observed in premature mammals.
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PMID:Neonatal changes in the concentrations of thyrotropin, triiodothyronine, thyroxine and cortisol in the plasma of pre-term and full-term lambs. 744 Sep 43

Hypothyroidism during pregnancy occurs in 1/1600-2000 deliveries, according to the most recent publications. The most common causes are chronic autoimmune thyroid disease, radiodine-131 treatment, or surgical removal. The diagnosis is difficult to make on clinical grounds alone, even in advanced cases, and a high index of suspicion is needed. Some women are at high risk of developing hypothyroidism, and they should be screened. These women may have had previous treatment for hyperthyroidism; high-dose neck irradiation, evidence of thyroid autoimmunity, amiodarone therapy, suspected hypopituitarism, and type I diabetics. The best laboratory test is the serum TSH, followed, if elevated, by a free T4 index and a TPO-ab titer. Thyroid antibodies have been associated with an increased (double) risk of miscarriage and postpartum thyroiditis. Frequent (22-44%) pregnancy-induced hypertension leading to preterm delivery, and prematurity is the main complication observed in those still hypothyroid near term. Proper therapy eliminates or reduces the risk. No congenital anomalies have been reported in the most recent studies, and the data available shows that both physical and mental development have been normal until children are 10 years old. However, one study reported lower IQs in children of euthyroid women with positive TPO-ab than in children of TPO-ab negative mothers. Levothyroxine is the treatment of choice. Euthyroidism must be reached and maintained in a timely fashion. Many women need more thyroxine during pregnancy, and surveillance of thyroid function is needed throughout gestation to make dose adjustments when needed. During the postpartum periods the thyroxine requirements decrease to preconception levels.
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PMID:Management of hypothyroidism during pregnancy. 910 50

Thyroid hormones are important for both perinatal adaptation and long-term psychomotor development; however, there is limited information on the effects of extreme prematurity and antenatal TSH-releasing hormone (TRH) treatment on pituitary-thyroid function. In this study we assayed plasma triiodothyronine (T3) and TSH in infants who were part of a collaborative trial of antenatal maternal TRH therapy. Within the control population (n = 166), infants of 24-28-wk and 28-32-wk gestational age had comparable levels of T3 (0.94 and 1.06 nmol/L, respectively) and TSH (5.7 and 7.2 mU/L) at birth, but the increases at 2 h and subsequent T3 levels were less in the 24-28 wk versus 28-32-wk gestation infants. In the TRH-treated group (n = 131), T3 was lower in the first day for infants delivered 7-72 h after antenatal TRH compared with control infants. TSH at birth was approximately 3.5-fold greater for infants delivered at 0-6 h after the last TRH dose compared with the control group and was suppressed in infants delivering at 7-36 h. T3 and TSH levels were not different between control and TRH-treated groups at 3-28 d of age. In TRH stimulation tests on d 28, control and TRH-treated groups had similar peak levels of TSH and incidence of exaggerated response (TSH > or = 35 mU/L). We conclude that extremely premature infants have a reduced postnatal surge in TSH and T3 and maintain lower T3 concentrations, probably reflecting tertiary hypothyroidism. The stimulatory and suppressive effects of antenatal TRH treatment observed at birth are transient and do not affect pituitary-thyroid responsiveness at 28 d of age.
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PMID:Plasma thyroid hormones in premature infants: effect of gestational age and antenatal thyrotropin-releasing hormone treatment. TRH Collaborative Trial Participants. 980 44

Neonatal hyperthyroidism has mostly been described in the context of maternal Graves' disease. It has been estimated that about 0.2% of pregnant women have Graves' disease; however only 1% of the children born to these women are described as having hyperthyroidism. In most of the cases, the disease is due to maternal antibodies transferred from the mother into the fetal compartment, which stimulate the fetal thyroid by binding to the thyrotropin (TSH) receptor. In this form of neonatal hyperthyroidism, thyrotoxicosis disappears with the clearance of the maternal antibodies and usually signs disappear during the first 4 months of life. Rare forms of persistent, nonimmune neonatal hyperthyroidism are explained by molecular abnormalities of the TSH receptor. Prematurity is frequent, as well as hypotrophia. Tachycardia, goiter, hyperexcitability, poor weight gain, hepatomegaly and/or splenomegaly, stare and/or eyelid retraction are among the most frequent neonatal thyrotoxicosis clinical signs. Diagnosis is based on the determination of the blood level of thyroxine (T4), triiodothyronine (T3), and TSH. Even if these levels are normal in the cord blood, tests should be repeated 3 to 10 days later to detect possible delayed appearance of the disorder. These parameters should be interpreted according to the age of the neonate. To confirm the immune nature of this hyperthyroidism, thyroid-stimulating immunoglobulins (TSI) should be determined. The TSI determination is crucial in identifying nonimmune causes of neonatal hyperthyroidism: in this neonatal hyperthyroidism, TSI are not detected, either by radioreceptor assay and/or by functional assay, and molecular studies are needed to identify the mutation. Mutation of the TSH receptor leading to its constitutive activation and to neonatal hyperthyroidism have been described. Germline mutations are found in hereditary hyperthyroidism; de novo germline mutations can cause sporadic congenital hyperthyroidism.
Thyroid 1998 Dec
PMID:Hyperthyroidism in early infancy: pathogenesis, clinical features and diagnosis with a focus on neonatal hyperthyroidism. 992 Mar 74

Thyroid gland function develops and matures during fetal life, with production of serum thyroxine (T4) concentrations beginning around 12 weeks gestation and increasing to term. Infants born prior to term have lower cord serum T4 concentrations that correlate with gestational age or birth weight. This is partially the result of lower thyroxine-binding globulin (TBG) concentrations. The cord serum free thyroxine (FT4) concentrations also correlate with gestational age, but they are not proportionately as low as the cord T4 concentration. Preterm infants have a postnatal thyrotropin (TSH) surge and rise in serum T4 and triiodothyronine (T3), which is qualitatively similar to, but quantitatively smaller than, term infants. In contrast to term infants, preterm infants often experience a fall in serum T4 and T3 in the first week of life to below birth levels. This drop appears to be the result of many factors, including nutritional problems and decreased hepatic TBG production, immaturity of hypothalamic-pituitary control of the thyroid gland, immaturity of the thyroid gland itself, and increased tissue utilization of T4. These changes are impacted by complications of prematurity, such as respiratory distress syndrome (RDS), which result in nonthyroidal illness-like changes. Again, serum FT4 seems less affected, and when measured by equilibrium dialysis may be in the normal range for age. Several studies have correlated different measures of morbidity and mortality in the preterm infant with lower serum T4 concentrations. However, as with adults, it may be that low serum T4 concentrations are a marker of the sickest preemies. Also, as with adults, this has led to speculation that T4 treatment might be beneficial in improving these complications of prematurity, in particular the neurological outcome. While some studies appear to show improvement in some facet of medical complications with T4 treatment, most show no effect. Regarding neurological outcome, the 2 best controlled trials do not show improvement in neuropsychiatric testing outcome assessed up to 2 years of age. One study, however, showed an IQ that was 18 points higher in the T4-treated subgroup less than 27 weeks gestational age. It may be that the most preterm infants, eg, those less than 27 weeks of age, are at a disadvantage compared with their intrauterine counterparts, in that they lack the maternal thyroid hormone contribution and are forced to adapt to extrauterine life before their hypothalamic-pituitary-thyroid axis is mature enough to deal with tissue thyroxine demands. Further controlled studies are needed to determine if this subgroup of infants indeed may benefit from transient thyroid hormone supplementation.
Thyroid 1999 Jan
PMID:Thyroid function in the preterm infant. 1003 80

Resistance to thyroid hormone (RTH), usually caused by an inherited defect of the thyroid hormone receptor, (TRbeta), results in a reduced responsiveness of target tissues to thyroid hormone. Until now, more than 600 cases with RTH have been identified. Although usually linked to the TRbeta gene, located on chromosome 3, RTH may also occur in the absence of mutations in the coding region of this gene. We report a 10-month-old boy who had laboratory findings typical of RTH. He was born prematurely on the 34th week of gestation and his thyrotropin (TSH) during neonatal screening was 121 microU/mL, a value very high for RTH or prematurity. Direct sequencing of the TRbeta gene from the patient's genomic DNA revealed a heterozygous substitution of the normal valine with a mutant methionine in codon 336 (V336M) that has not been previously reported. In vitro expression studies showed that this mutant TRbeta has an impaired triiodothyronine (T3)-dependent transactivation that reduces the activity of the wild-type TRbeta (dominant negative effect). While the functional impairment of V336M is not unusual compared to other TRbeta gene mutations, the very high TSH value in this prematurely born infant suggests that fetuses with RTH have altered maturation of the hypothalamo-pituitary-thyroid axis or actually may suffer from hypothyroidism.
Thyroid 1999 Oct
PMID:Resistance to thyroid hormone caused by a new mutation (V336M) in the thyroid hormone receptor beta gene. 1056 Sep 54

During the past four decades major advances in the management of premature infants have led to progressive reduction in mortality. During this period mortality in very low birth weight infants (VLBW, <1500 grams and <30 weeks gestation age) has decreased, and more than 50% of infants less than 24 weeks gestation age now survive, increasing the population of VLBW infants in intensive care nursery environments. Thyroid function in these infants is characterized by decreased TSH and T4 responses to parturition, low serum total T4 and TSH levels and variable free T4 concentrations during the first 2-4 postnatal weeks of life. These features reflect a state of transient hypothalamic-pituitary or central hypothyroidism. There is a high prevalence of morbidity in these infants, as well, often associated with further reductions in serum total T4, T3, TBG and TSH concentrations and variable levels of free T4 and reverse T3, resembling the non-thyroidal illness (NTI) syndrome in adults. The etiologic roles of thyroid system immaturity and NTI in the transient hypothyroxinemia of prematurity (THOP) and the impact of THOP on the subsequent neurological deficits in VLBW infants remains unclear. Several thyroxine supplementation trials have been conducted with inconclusive results. Further studies are planned or in progress.
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PMID:Thyroid function and dysfunction in premature infants. 1764 79

Thyroid problems are common in children. While serum thyroid function tests lead to an accurate diagnosis in most patients, unique patient situations can produce misleading results. Total T4 measurements can incorrectly suggest hypothyroidism in congenital thyroid binding globulin (TBG) deficiency and hyperthyroidism in TBG excess, as seen in high estrogen states. Free T4 (FT4) measurement techniques involve either physical separation of unbound thyroxine from serum binding proteins or estimation of FT4 levels in the presence of binding proteins. These estimation techniques are susceptible to under- or over-estimation of FT4 levels when binding proteins are low or high. Other complicating factors arise in the setting of prematurity or systemic non-thyroidal illness (NTI), simulating central hypothyroidism. Thyroid stimulating hormone (TSH) levels in children have a wider normal range than in adults and are affected by drugs and NTI. Additionally, heterophile and anti-T4 or anti-TSH antibodies can interfere with accurate T4 or TSH measurement.
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PMID:Pediatric thyroid testing issues. 1816 71


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