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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper describes the clinical, hormonal and radiologic profiles in 282 children evaluated for hypothyroidism. Short stature, mental retardation or puberal disturbances were often the presenting features in the older age group, whereas in the 1-5 years age group medical opinion was usually sought for symptomatology suggestive of thyroid hypofunction. Children in the 0-1 year group were suspected on the basis of psychomotor dysfunction. Skeletal immaturity was found in 93.0% of patients with overt hypothyroidism and in 36.6% cases with normal thyroid profiles but associated with malnutrition. High TSH levels were noted in 70.9% of the cases studied. 4.9% and 7.3% patients with normal TSH had low T3, and T4 levels respectively. FSH, testosterone and PRL levels were also affected in some patients with overt hypothyroidism. Therapeutic responses based on at least 1 year follow up were available in 170 cases. The results are discussed.
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PMID:Hypothyroidism in children/adolescents. Clinical and hormonal profiles. 263 58

Thyroxine (T4), triiodothyronine (T3), and thyrotropin (TSH) concentrations were measured on cord sera of 21 preterm infants with idiopathic respiratory distress syndrome (IRDS) and were compared to the values obtained from 15 healthy preterm infants. When log T3, log T4, and log TSH were considered as the dependent variables in the multivariate test Hotelling-Lawley-Trace, there was an overall difference between the two groups: F = 3.94, p = 0.03. When log T3 and log T4 were considered separately in an analysis of covariance, there was a significant difference between the two groups for log T3 after adjusting for birth weight and gestational age (F = 7.98, p = 0.008). However, for log T4 and TSH, there was no difference between the IRDS and control infants. These findings exclude the possibility of antenatal thyroid dysfunction in babies with IRDS. An explanation for reduced cord blood T3 concentration in infants with IRDS is lacking at present. Extrathyroidal factors that predispose to IRDS may also affect peripheral T3 generation. Alternatively, one might postulate that there is relative immaturity of both peripheral T3 generating pathway and lung development in infants who develop IRDS.
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PMID:Prenatal thyroid function abnormalities in infants with idiopathic respiratory distress syndrome. 649 49

Iodide-induced hypothyroidism with high TSH and low T4 under long term potassium iodide medication was observed in a toddler suffering from chronic wheezy bronchitis -- in spite of intermittent application. The pathophysiology of iodide-induced hypothyroidism and the apparent immaturity of adaptation to high exogenous iodide in newborn and infants are discussed.
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PMID:[Hypothyroidism following intermittent administration of potassium iodide]. 669 43

Histological examination of cockerel testes revealed the overlapping effects of FSH and TSH. Within the dose-range studied (20-160 microgram FSH and 27.5-220 microgram TSH), both hormones increased the cell number in the seminiferous cords including the number of spermatogonia, primary spermatocytes and pre-Sertoli cells. They also enhanced the mitotic activity of spermatogonia and accelerated spermatogenesis. Peak effects were observed after treatment with 160 microgram FSH and 55 microgram TSH dose. Liquefaction of cords due to hormone treatment was indicative of an acceleration of testicular ontogeny. Cross-effects of the two hormones were explained by receptor immaturity i.e. in the early stage of ontogenesis the receptors can bind both hormones due to the similarities in their structure. The maximum effects of the hormones were different, that of FSH being more marked.
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PMID:Histological analysis of the overlapping effect of hypophyseal hormones on the cockerel's testes. 677 81

In newly hatched chicken testes the gonadotropin receptors due to their immaturity are not specific but still structurally versatile and so they can bind both FSH and TSH which have a chemically related structure. The functional overlapping effect of FSH and TSH on the ultrastructure of Sertoli and Leydig cells of immature chicken testes was investigated. The activity of Sertoli cells was increased by FSH treatment and this increase correlated well with the amount of SER and RER in cells and with their increased surface activity. The vacuolization and degeneration observed at the apical part of the cells may refer to the formation of testicular tubules. After TSH treatment cell activity increased and in addition a considerable increase in RER and lipid droplets was observed. Fenestrated cisternae were often found in the Sertoli cells of the treated animals. In the Leydig cells, both hormones increased lysosomal activity and the number of lipid droplets. After FSH treatment the amount of SER increased while after TSH treatment the Golgi activity.
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PMID:Overlapping effect of follicle stimulating hormone (FSH) and thyrotropin (TSH) on the ultrastructure of immature chicken testes. 680 56

In order to assess neonatal thyroid function in the endemic goitre areas of Greece, T4 and TSH have been measured. Previous studies had shown that in these endemic areas, adults had low T4 but normal TSH values, probably because of an increase in the serum T3 level. In this study, T4 and TSH were measured in dried blood spots from 259 neonates. The fifty-four full-term neonates from the Greek endemic villages had a lower T4 value (8.8 +/- 0.66 micrograms/dl SE) but a higher TSH (15.37 +/- 1.12 mu/l) than the seventy-three full-term neonates from the non-endemic villages (T4:10.0 +/- 0.33 micrograms/dl, TSH:11.93 +/- 0.59 mu/l) or the ninety-eight from Athens (T4:10.0 +/- 0.33 micrograms/dl, TSH:10.96 +/- 0.64 mu/l). Premature neonates, both from Athens and from the endemic areas, have significantly lower T4 and significantly lower TSH values than the full-term ones from the same areas, probably because of the immaturity of the pituitary-thyroidal axis. It is concluded from these observations that (a) Neonates suffer more from the consequences of iodine deficiency than adults. The biochemical hypothyroidism reported here may be relevant to the delayed skeletal maturation previously reported from children of these same areas. This emphasizes the need for correcting even moderate iodine deficiency. (b) The occurrence of non-toxic goitre with normal TSH levels in adults is best explained by assuming that increased TSH stimulation is necessary for goitre formation during neonatal life, but not for goitre maintainance during adulthood. (c) Newborn screening programmes in these areas should take into account the present findings.
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PMID:The effects of mild iodine deficiency on neonatal thyroid function. 726 15

Thyroid hormones influence fetal and neonatal lung growth and maturation. However, the effect of naturally occurring, genetically determined hypo- or hyperthyroidism on fetal or neonatal lung maturation has not been examined. In the hyt/hyt mouse, primary hypothyroidism, which is characterized by a high serum TSH concentration, is transmitted as an autosomal recessive trait. It occurs due to a mutational defect in the beta-subunit of the TSH receptor. We studied the lung ultrastructure of the fetal [18-d-gestation (term = approximately 19.5 d)] and neonatal (< 1-d-old) hyt/hyt mouse. In addition, disaturated phosphatidylcholine and total phospholipid contents of newborn hyt/hyt mouse lungs were determined. Male and female hyt/hyt mice with a high serum TSH concentration were made euthyroid by adding 3,5,3'-triiodothyronine to drinking water and then mated. Balb-c mice served as euthyroid controls. Fetal and neonatal hyt/hyt mice had a higher serum TSH concentration than the Balb-c controls. Fetal hyt/hyt mouse lungs showed a large amount of intracellular glycogen and fewer lamellar bodies in epithelial type II cells compared with Balb-c fetal mouse lungs. The neonatal hyt/hyt mouse also showed signs of lung immaturity such as persistent epithelial cell glycogen, few lamellar bodies, reduced disaturated phosphatidylcholine content, and absent tubular myelin. We conclude that fetal and neonatal lung maturation is delayed in the hyt/hyt mouse with primary hypothyroidism.
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PMID:Delayed ultrastructural lung maturation in the fetal and newborn hypothyroid (Hyt/Hyt) mouse. 780 36

It is not known how immaturity and disease influence postnatal thyroid function in infants <30 wk of gestational age. We performed serial measurements of plasma thyroxine (T4), free T4 (FT4), triiodothyronine (T3), reverse T3 (rT3), TSH, and T4-binding globulin (TBG) in 100 infants of <30 wk of gestation, during the first 8 postnatal weeks, to investigate the influences of disease and gestational age on the time course of thyroid hormones. One hundred infants were divided twice into two groups: 1) in a group of 25-28 and of 28-30 wk of gestation; and 2) in a sick and a healthy group, with similar gestational ages. The time course of T4, FT4, T3, TSH, and TBG, but not rT3 differed significantly (p < 0.005) between the gestational age groups. T4 and FT4 decreased to levels below the cord blood value with a deeper FT4 nadir on d 7 in the youngest group. Disease decreased T4, FT4, T3, TSH, and TBG concentrations especially during the 1st wk after birth (p < 0.005). However, the FT4 nadir on d 7 was similar in sick and healthy infants. After 3 wk, T4, FT4, T3, and TBG were higher in the sick group compared with the healthy group. rT3 levels were not increased in sick infants. We conclude that the extent of the FT4 decrease after birth in infants of <30 wk gestation is mainly influenced by gestational age and probably reflects a transient depletion of thyroidal hormone reserves. rT3 cannot be used as a marker of nonthyroidal illness in very preterm infants.
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PMID:Thyroid function in very preterm infants: influences of gestational age and disease. 935 31

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.
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PMID:Thyroid function in the preterm infant. 1003 80

Plasma levels were measured of T4, free T4, T3, TSH in 64 premature neonates and in 41 those born at right time during the time-related course of the neonatal period. The results secured permit regarding the thyroid hypohormonosis syndrome in premature neonates as a consequence of the hypothalamic-hypophyseal-thyroid axis deficiency and of immaturity of the thyreostatic receptors as well. On the one hand, this promotes hypometabolism and, correspondingly, favours more economic utilization of bodily energy resources but on the other hand, such adaptation is not infrequently results in its failure and persistent thyrodeficiency, especially in very low-birth weight infants, during the whole of the neonatal period.
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PMID:[Transient neonatal hypothyrosis in premature neonates]. 1678 55


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