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Neonates thyroid deficiency

Brown, W.J., Verity, M.A., and Smith, R.L., 1976, Inhibition of cerebellar dendrite development in neonatal thyroid deficiency. Neuropath. apol, Neurobiol., 2 191. [Pg.87]

Table 1. The activity of enzymes, as markers of nerve cell types, in different regions of rat brain during neonatal thyroid deficiency and following long-term rehabilitation ... [Pg.141]

Extensive work has been performed to assess neonatal thyroid functional status in communities in iodine-deficient parts of the country. KochupiUai et al. (1986) showed that the incidence of neonatal hypothyroidism varied from 7.5% to 13.3% in the highly endemic sub-Himalayan districts of Gonda, Gorakhpur and Deoria. In comparison, the incidence of neonatal hypothyroidism in Delhi was 0.6%, while coastal Kerala, which was not endemic for goiter, had a neonatal hypothyroidism incidence of 0.12%, comparable with the congenital hypothyroidism rates of 0.02—0.05% reported in iodine-sufficient countries. [Pg.1274]

Although cretinism was already described by the turn of the century, the involvement of thyroid deficiency in this malady was not reported until the 1930 s (Kerley, 1936). Soon thereafter, animal studies were carried out which made clear the necessity of thyroid hormones for general somatic and neural development during the neonatal and early postnatal period in the rat, which is roughly equivalent to the first year of life in the human (Salmon, 1936 Scow and Simpson, 1945 Eayrs and Taylor, 1951 Eayrs and Horn, 1955 Hamburg and Vicari, 1957 Eayrs, 1961). [Pg.79]

Recently, data on iodine nutrition and neonatal thyroid function in Europe, confirm the continuing presence of severe iodine deficiency affecting neonatal thyroid function and hence a threat to early brain development. ... [Pg.30]

Few countries in Europe are severely iodine deficient, but many, perhaps a majority, have a marginal iodine intake varying from 50 to 100 pg/day. The first world conference on neonatal thyroid screening held in Quebec in 1979 showed that, although the incidence of permanent sporadic congenital hypothyroidism in the newborn was similar in North America and in Europe, i.e. around 1/4000 live births, the incidence of transient primary hypothyroidism was almost six times higher in Europe... [Pg.201]

One important aspect of the impact of iodine deficiency on thyroid function is thus the evidence, based essentially on neonatal thyroid screening programs that, both in conditions of severe and moderate iodine deficiency thyroid function is more severely affected in neonates than in adults. Therefore, it appears that neonates and especially preterms, are particularly sensitive to the effects of iodine defidaicy. [Pg.202]

M.C. Sorcini, A. Diodato, C. Fazzini et al.. Influence of environmental iodine deficiency on neonatal thyroid screening results, J Endocrinol Invest 11 309(1988). [Pg.216]

Neonatal thyroid screening is an important additional tool for evaluating the potential consequences of iodine deficiency on brain development and for monitoring iodine prophylaxis at the population level. Indeed, neonates, whose very low thyroidal iodine stores make them hypersensitive to iodine deficiaicy, frequently have altered thyroid function tests (elevated serum TSH, possibly low T4) even at moderate degrees of iodine deficiency that do not appear to affect thyroid function in the adults. Therefore, a shift towards higher neonatal TSH values has been proposed as a useful tool to detect and monitor iodine deficient newborn populations. However, such a shift can be interpreted validly if representative sampling of newborns is carried out (at least one hundred determinations in randomly selected populations), with the use of sensitive assays for TSH measurements. [Pg.474]

Data on iodine nutrition and neonatal thyroid function in Europe confirm the continuing presence of severe iodine deficiency. This affects neonatal thyroid function and hence represents a threat to early brain development. These data have raised great concern about iodine deficiency, which is also heightened by awareness of the hazard of nuclear radiation with carcinogenic effects following the Chernobyl disaster in the former Soviet Union (Table 1). [Pg.230]

Kreutler PA, Varbanov V, Goodman W, et al. 1978. Interactions of protein deficiency, cyanide, and thiocyanate on thyroid function in neonatal and adult rats. Am J Clin Nutr 31 282-289. [Pg.257]

Thyroid hormone is essential for normal growth and development during embryonic life. Thyroid hormone deficiency during fetal and neonatal development results in mental retardation. There is slowing of physical and mental activity, as well as of cardiovascular, gastrointestinal, and neuromuscular function. Depression may result from untreated hypothyroidism. ... [Pg.1381]

The realization that iodine deficiency in pregnancy has a pronounced effect on fetal, neonatal and childhood brain function has resulted in a large body of knowledge on the effects of thyroid hormone on brain and nervous-system development (see Grave, 1977 DeLong et ai, 1989 Stanbury, 1994 Bemal, 2002). [Pg.470]

The observations relating to iodine deficiency in pregnancy are firstly those concerned with maternal thyroid function and maternal goiter. Maternal urinary iodine (UI) excretion is the usual method of assessing iodine status in the population at risk or the individual, and is discussed below. Neonatal indicators of maternal iodine deficiency are goiter and neurointellectual impairment. [Pg.471]

After birth, plasma T4 increases in the newborn, mainly due to a new source of iodine provided by the mother through the milk (Escobar del Rey et al, 1987). Iodine is actively concentrated in the milk, which acts as a vehicle to improve the thyroidal status of the newborn. There are small increases in the plasma T4, as well as in brain T4 (Obregon et al, 1991), which together with a large increase in D2 activity in the brain are able to increase T3 in the brain of neonates up to normal levels (Figure 64.3). Therefore, the fetus is able to respond to iodine deficiency the same as the adult rat, but it is more sensitive to iodine deficiency due to its dependence on maternal T4. [Pg.618]

The median urinary iodine (MUI) concentration provided a measure of the current nutritional status of iodine. MUI was performed in spot urine samples obtained from all mothers and their neonates 5 days after delivery, by using the Sandell—Kolthoff reactions. Decreased MUI excretion of both neonates with hypothyroidism and their mothers was classified as mild-to-moderate iodine deficiency according to the WHO criteria. The mean total thyroid volume (TTvol) of the neonates and their mothers was increased on ultrasonography, whereas no palpable thyroid tissue was detected on physical examination (Table 65.3). [Pg.630]

Notes Laboratory parameters of mothers and their neonates in maternal subciinicai hypothyroidism maternai thyroid hormone ieveis were either siightiy increased (TSH and TT3) or near normai (TT4). Both mothers and their neonates had decreased MUi and increased TTvoi. These observations were the consequences of iodine deficiency (MUi median urinary iodine TSH thyroid-stimuiating hormone TT3 serum totai T3 TT4 serum totai T4 TTvoi totai thyroid voiume). [Pg.631]

Development of iodine-induced thyroid dysfunction is influenced by a person s prior iodine intake. Cases of thyrotoxicosis being induced by contrast media are mainly reported in Europe or Australia, where dietary iodine levels are low, as described by Fradkin and Wolff (1983). Except for cases due to amiodarone, the incidence of iodine-induced hyperthyroidism is very low in regions where dietary iodine is adequate (Roti and degfl Uberti, 2001). Neonates treated with PVP-I often develop hypothyroidism in iodine-insufficient regions of Europe, but rarely do so in iodine-sufficient regions of the United States, as described by Brown et al. (1997). Thus, persons who five in areas where iodine is deficient in the diet are at risk of developing thyroid dysfunction induced by iodine-containing pharmaceuticals. [Pg.929]

The fetus and neonate are both at risk of developing iodine-induced hypothyroidism (Table 96.3). Many cases of such hypothyroidism in fetuses and neonates have been reported, especially in iodine-deficient regions of Europe, but also in iodine-sufficient areas. Iodide goiter in neonates is usually a transient problem. However, tracheal obstruction due to such goiter can be fatal (Markou et al, 2001 Wolff, 1969). Transient hypothyroidism without elevation of thyroid-stimulating hormone (TSH) in extremely... [Pg.929]


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