Thyroid-stimulating hormone neonatal

Use of measurement of blood thyroxine or thyroid-stimulating hormone (TSH) in the neonatal diagnosis of congenital hypothyroidism. 

Li FX, Byrd DM, Deyhle GM, Sesser DE, Skeels MR, Katkowsky SR, Lamm SH (2000) Neonatal thyroid-stimulating hormone level and perchlorate in drinking water. Teratology... 

Of 26 fetuses with hydrops fetalis and supraventricular tachycardias, 25 received transplacental drug therapy prenatal conversion occurred in 15 (82). Nine fetuses were converted to sinus rhythm using either flecainide (n = 7) or amiodarone (n = 2) as first-line therapy, while digoxin either alone or in association with sotalol failed to restore sinus rhythm in all cases. After first-line therapy, supraventricular tachycardia persisted in 10 fetuses, nine of whom received amiodarone alone or in association with digoxin as second-line therapy, and five of whom converted to sinus rhythm. Of 11 neonates who received amiodarone in utero, two developed raised thyroid stimulating hormone concentrations on postnatal days 3-4 they received thyroid hormone and had normal outcomes. 

The indicator for this condition is neonatal serum thyroid-stimulating hormone (TSH). A prevalence of 1-10% of elevated TSH has been reported from various endemic diseases (Kochupillai et ai, 1986). There is evidence from India of an epidemiological correlation, with subsequent intellectual performance from India (Kochupillai et ai, 1986) and elsewhere (Delange, 1994). 

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... 

It is therefore important to assess the iodine intake levels of the population to identify iodine deficiency prior to the onset of more apparent manifestations. Together with investigations of the prevalence of goiter, epidemiological indicators, such as urinary excretion of iodine and neonatal levels of thyroid-stimulating hormone (TSH), have been used. Of these methods, ioduria is the most widely used biochemical marker, due to the low cost and the simplicity of the testing procedure (Esteves, 1997 Dunn etal., 1993). 

In the neonate, neural NE promotes nonshivering thermogenesis, i.e., heat production via stimulation of lipolysis and fatty acid oxidation in brown adipose tissue ( 63) with the support of thyroid hormone. Brown adipose tissue contains a high density of mitochondria with an uncoupling protein that allows the cells to oxidize fatty acids and generate heat as a major product NE released at nerve endings stimulates cAMP-mediated lipolysis in these cells and promotes thermogenesis by this y83-mechanism (Chapter 14). 

In the most simplistic physiological model, inadequate intake of iodine results in a reduction in thyroid hormone production, which stimulates increased TSH production. TSH acts directly on thyroid cells, and without the ability to increase hormone production, the gland becomes hyperplastic. In addition, iodine trapping becomes more efficient, as demonstrated by increased radioactive iodine uptake in deficient individuals. However, this simplistic model is complicated by complex adaptive mechanisms which vary depending on the age of the individual affected. In adults with mild deficiency, reduced intake causes a decrease in extrathyroidal iodine and reduced clearance, demonstrated by decreased urinary iodine excretion, but iodine concentration in the gland may remain within normal limits. With further reduction in intake, this adaptive mechanism is overwhelmed, and the iodine content of the thyroid decreases with alterations in iodination of thyroglobulin, in the ratio of DIT to MIT, and reduction in efficient thyroid hormone production. The ability to adapt appears to decrease with decreasing age, and in children the iodine pool in the thyroid is smaller, and the dynamics of iodine metabolism and peripheral use more rapid. In neonates, the effects of iodine deficiency are more directly reflected in increased TSH. Diminished thyroid iodine content and increased turnover make neonates the most vulnerable to the effects of iodine deficiency and decreased hormone production, even with mild deficiency. 

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