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Iodine deficiency neonate

Most preterm babies are at high risk of iodine deficiency neonates, and especially preterm infants, are a very important population at risk of suffering the consequences of both iodine deficiency and excess, because of the impact of neonatal hypothyroxinemia on brain development. [Pg.484]

N. Kochupillai, M.M. Godbole, C.S. Pandav, A. Mithal and M.M.S. Ahuja, Environmental iodine deficiency, neonatal chemical hypothyroidism (NCH) and iodized oil prophylaxis, 331 "Iodine nutrition, thyroxine and brain development", N. Kochupillai, M.G. Karmakar and V. Ramalingaswami eds., Tata McGraw-Hill Publ., New Dehli (1986), pp. 87-93. [Pg.229]

We have investigated the possibility that this hypersensitivity is due at least partly to a less efficient mechanism of adaptation to iodine deficiency, namely to a reduction of the iodine content of the thyroid in iodine deficient neonates. [Pg.203]

TSH is produced in response to decreased iodine intake and diminished thyroid hormone production and is used as a measure of iodine status. TSH is best measured in neonates—in the developed world for surveillance against congenital hypothyroidism, and in endemic countries to estimate the magnitude of iodine deficiency. Neonatal TSH has been a useful advocacy tool to demonstrate to policy makers... [Pg.241]

A. Brain damage caused by maternal/fetal/neonatal iodine deficiency A. Brain damage caused by maternal hypothyroidism ... [Pg.451]

Iodine deficiency is still a major pubfic health problem worldwide, although substantial progress has been made towards its eradication in many countries. It is of particular importance in the pregnant woman, because of the sequelae that may be observed in the fetus and the neonate (Table 49.1). Epidemiological demonstration of the association... [Pg.469]

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]

Neonates, and especially preterm infants, are a population at risk of suffering the consequences of iodine deficiency because of the impact of neonatal hypothyroxinemia on brain development. We evaluate the possible association between mental development scores at different ages and iodine intake during the neonatal period. Sixty-seven preterm infants were subdivided into GA groups for data analysis. The mental development scores reported here are those of the Brunet-Lezine scale index for children (0-24 months of age). The children were tested at 6, 9, 12, 18 and 24 months of postnatal age, and results were corrected for their GA. The test assesses P, motor abilities and postural... [Pg.481]

Pregnant and lactating women and neonates are the main targets of the effects of iodine deficiency, because of the impact of maternal, fetal and neonatal hypothyroxinemia on... [Pg.482]

Early correction of hypothyroidism due to congenital defects in neonates has now become a standard practice in most developed countries in order to prevent longterm brain damage (Dussault and Glorieux, 1989). The more severe the fetal hypothyroidism, as indicated by bone retardation, the more Hkely are residual effects (Dussault and Glorieux, 1989). Such considerations indicate the urgent need for a preventive approach to the correction of iodine deficiency for developing countries, because treatment of individual cases is not usually possible. [Pg.601]

Neonatal TSH levels of 5mU/l or higher, especially in an iodine-deficient area, such as ours, are associated with a lower neurodevelopment score in 3-year-old children. [Pg.614]

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 Effects of Hypothyroidism Due to Iodine Deficiency in Neonatal Brain The Changes in Brain Metabolites Detected by Magnetic Resonance Spectroscopy... [Pg.625]

Brain MRS Findings in Neonates with Hypothyroidism due to Intrauterine Iodine Deficiency ... [Pg.630]

As stated above, MRS provides a noninvasive diagnostic tool for the biochemical characterization of pathophysiological processes in the brain. Therefore, in a recent study by Akinci et al. (2006), MRS was used to detect the changes in brain metabolites of neonates with hypothyroidism, born to mothers living in iodine-deficient areas before and after thyroxine replacement therapy. [Pg.630]

In that study, NAA, Cho and Cr were measured in frontal white matter (FWM), parietal white mater (PWM) and the thalamus of the eight full-term neonates with hypothyroidism. They were 5-7 days of age, and were born to mothers living in iodine-deficient areas. Their mothers had not received iodine supplementation in the pregestational or gestational period. A repeat MRS examination was performed after 8 weeks of thyroxine therapy. Metabolite levels of these patients were compared to levels obtained from eight full-term age-matched healthy neonates of mothers who had been using iodine-supplemented salt since the pregestational period. [Pg.630]

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]

Cho level does not significantly differ among healthy neonates and in neonates with congenital hypothyroidism due to iodine deficiency. [Pg.633]

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]

Note The fetus and neonate are both at risk of developing iodine-induced hypothyroidism. Many cases of hypothyroidism in newborns have been reported, especially in iodine-deficient regions of Europe, but also in iodine-sufficient areas. [Pg.929]

Iodine is readily absorbed when PVP-I is applied to the skin of a newborn infant, because of high cutaneous permeability, and neonates are very sensitive to iodine overload, as described previously. Topical PVP-I therapy is associated with a significant risk of hypothyroidism in neonates, especially very-low-weight babies (Smerdely et ai, 1989). Many cases of hypothyroidism induced by topical use of PVP-I have been reported in newborn infants, mainly from iodine-deficient regions (Markou et ai, 2001). However, a case of severe hypothyroidism in a neonate was also reported from North America, an iodine-sufficient region (Khashu et al. 2005). A premature infant developed severe hypothyroidism that required L-thyroxine replacement therapy after application of PVP-I for 20 days. [Pg.930]


See other pages where Iodine deficiency neonate is mentioned: [Pg.205]    [Pg.205]    [Pg.764]    [Pg.43]    [Pg.406]    [Pg.231]    [Pg.66]    [Pg.372]    [Pg.462]    [Pg.472]    [Pg.473]    [Pg.473]    [Pg.474]    [Pg.474]    [Pg.477]    [Pg.480]    [Pg.482]    [Pg.488]    [Pg.625]    [Pg.626]    [Pg.626]    [Pg.626]    [Pg.627]    [Pg.632]    [Pg.633]    [Pg.719]    [Pg.815]    [Pg.860]    [Pg.930]   
See also in sourсe #XX -- [ Pg.230 ]




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