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Hyperthyroidism neonatal

Some neonates born to mothers with Graves disease will be hyperthyroid at delivery. Antithyroid drug therapy (propylthiouracil 5-10 mg/kg per day or methimazole 0.5-1 mg/kg per day) may be required for up to 12 weeks. One drop per day of SSKI may be used in the first few days to rapidly reduce thyroid hormone synthesis and release. [Pg.680]

Developmentally, thyroid hormones interact with sex hormones such that hypothyroidism prolongs the critical period for testosterone-induced defeminization (see below) [3] in contrast, the hyperthyroid state prematurely terminates the sensitivity to testosterone [3]. Undoubtedly, an important link in these and other effects is synapse formation. Hypothyroidism increases synaptic density, at least transiently [3]. Interesting parallels with synapse formation are reported for learning behavior in rats neonatal hypothyroidism impairs learning ability, whereas hyperthyroidism accelerates learning initially, followed by a decline later in life [3]. [Pg.854]

Karpman BA, Rapoport B, Filetti S, Fisher DA. Treatment of neonatal hyperthyroidism due to Graves disease with sodium ipodate. J Clin Endocrinol Metab 1987 64(l) 119-23. [Pg.323]

Neonatal hypothyroidism has been reported after maternal use of antithyroid drugs (106,107). Transient neonatal hyperthyroidism in a female child born to a mother who had been treated with potassium iodide and carbimazole during pregnancy was followed by sexual precocity (108). [Pg.342]

Domenech E, Santisteban M, Moya M, Gonzalez C, Cortabarria C, Mendez A, Alvarez J, Rodriguez-Luis JC. Hipertiroidismo neonatal transitorio e hijo de madre hipertiroidea tratada. Posterior aparicion de precocidad sexual. [Transient neonatal hyperthyroidism in the child of a treated hyperthyroid mother. Subsequent appearance of sexual precocity.] An Esp Pediatr 1985 22(4) 281-7. [Pg.345]

The most significant of the abnormalities observed in a hypothyroid brain is a hypoplastic neuropile, i.e., a marked reduction in the number of connections between neurons [102], This has been observed both in the cerebrum and the cerebellum. For instance a permanent and dramatic reduction in the arborization of the dendritic tree of the Purkinje cell is observed in the hypothyroid cerebellum [103]. The length of the primary dendritic trunk is increased and a deficit in the number, density and branching of the dendritic spines is noticed. In contrast neonatal hyperthyroidism accelerates development of spines. Similar findings have been reported for the cerebrum, i.e., reduction in length and branching of pyramidal neurons, of the density of axonal terminals and of the number of spines [102],... [Pg.74]

Acute viral hepatitis Neonates/young infants Cirrhosis Hyperthyroidism... [Pg.3035]

Riboflavin is a nutritional supplement used during periods of deficiency known as ariboflavinosis. Riboflavin deficiency usually occurs in association with malabsorption, alcoholism, or protein-calorie deficiency, and is rarely the sole vitamin deficiency. Riboflavin needs are increased during chronic debilitative stress to the body such as malabsorption diseases of the small intestine, liver disease, hyperthyroidism, alcoholism, and during pregnancy and lactation. Neonates undergoing phototherapy for hyperbiliru-binema also have increased nutritional needs. [Pg.2285]

The fetal thyroid-pituitary axis functions independently from the mother s axis in most cases. However, if the mother has preexisting Graves disease (see Chapter 52), her autoantibodies can cross the placenta and stimulate the fetal thyroid gland. Thus the fetus can develop hyperthyroidism. Measurement of thyrotropin-binding inhibitory immmioglobu-lins (TBII) is useful for assessing risk of fetal or neonatal Graves disease. [Pg.2163]

Another important group, the National IDD Advisory Committee (NIDDAC) chaired by Professor Chen Zupei, has played a crucial role in the national program. Under the leadership of the MOH, NIDDAC provides scientific and technical guidefines, standards and recommendations. It also provides evidence for poficy development (IDD Newsletter, 1998). Since 1993 NIDDAC has re-evaluated and standardized the measmement of thyroid gland size by palpation and ultrasound standardized urinary iodine testing methods. It has also evaluated the technical aspects and the application of neonatal TSH in IDD monitoring, iodine excess and excessive dietary iodine-induced goiter, and the role of iodized oil in the prevention and control of IDD and iodine-induced hyperthyroidism (Chen, 2002). [Pg.828]

Povidone-Iodine Adverse Reactions Adverse reactions associated with povidone-iodine appHcation include unpleasant odor, skin irritation and allergic reactions. Systemic absorption through topical appHcation may result in metabohc acidosis, hypothyroidism (neonates), hyperthyroidism, electrolyte disturbances and kidney dysfunction (Wax, 2006). Several case reports by Marks (1982),... [Pg.924]

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 hippocampus, like the cerebellum, is a structure which undergoes a large part of its development postnatally. Therefore, this brain region has also been studied with regard to the effects of altered thyroid states during the neonatal period. There are both similarities and differences in the effects of neonatal hypo- and hyperthyroidism on the hippocampus compared to the cerebellum, which may reflect the specific differences in ongoing developmental processes and their regional specificities. [Pg.84]

Lauder, J.M., 1979, Granule cell migration in the developing rat cerebellum. Influence of neonatal hypo- and hyperthyroidism, Dev. Biol.. 70 105. [Pg.88]

Endocrine Prenatal, perinatal, or postnatal iodine overload can cause problems such as transient hyperthyrotropinemia, hypothyroidism, or hyperthyroidism in preterm and term infants [SED-15, 1896 SEDA-30, 279 SEDA-31, 411 SEDA-32, 440], Severe hypothyroidism in two term neonates resulted from iodine overload caused by postnatal use of an iodine-containing antiseptic [26 ]. One case was caused by excessive application of the antiseptic to the umbilicus and the other from maternal breast milk following the use of an iodine antiseptic by the mother for her episiotomy incision. [Pg.380]

Neonatal hyperthyroidism has, however, provided new arguments in favor of a pathogenic role of LATS in hyperthyroidism. Some children are bom with hyperthyroidism, including exophthalmos. The symptoms are transient and subside within a month after birth. The severity and duration of the symptoms are related to the levels of LATS in the mother s and infant s blood. [Pg.456]


See other pages where Hyperthyroidism neonatal is mentioned: [Pg.680]    [Pg.680]    [Pg.1312]    [Pg.283]    [Pg.354]    [Pg.73]    [Pg.762]    [Pg.1312]    [Pg.73]    [Pg.612]    [Pg.289]    [Pg.74]    [Pg.952]    [Pg.1863]    [Pg.2086]    [Pg.1380]    [Pg.1380]    [Pg.1389]    [Pg.83]    [Pg.13]    [Pg.488]    [Pg.856]    [Pg.859]    [Pg.927]    [Pg.94]    [Pg.373]    [Pg.638]    [Pg.80]    [Pg.81]   
See also in sourсe #XX -- [ Pg.680 ]




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