traduce el siguiente texto: Euthyroid Sick Syndrome 
In acutely ill patients, thyroid function changes take place. It is hypothesized that alterations in thyroid hormone occur as an adaptive response to decreased basal metabolic rates in severely ill patients. The syndrome has been observed in sick infants and children.82 These patients may have acute or chronic nonthyroidal illnesses. There is a decrease in T3 activation in the periphery. The consistent finding is an abnormally low serum T3 level, an increase in the rT3 level, and a reduction in TSH secretion. Normal TSH secretion can also be observed during mild or moderate illnesses. However, the TSH is inappropriately low in the context of low serum T3 levels.75 T4 may be low or normal and FT4 may be normal, depending on the metabolic clearance rate of T4. In preterm infants, T4, FT4, and T3 levels are naturally lower than those in term infants, and rT3 is high.83 Therefore, thyroid tests in a preterm infant may be hard to interpret, especially when infants are sick from nonthyroidal diseases. The most common neonates with euthyroid sick syndrome are preterm infants with respiratory distress syndrome.83,84 In the pediatric population, nonthyroidal illnesses associated with this syndrome include severe gastroenteritis, acute leukemia, anorexia nervosa, renal disease, burns, and surgical stress. Euthyroid sick syndrome is found in patients with metabolic stress (e.g., diabetic ketoacidosis), in pediatric patients who underwent cardiac surgery, and in pediatric patients with cancer.85 There is a sharp rise in rT3 and a less dramatic fall in T3 by 2 hours after cardiac surgery. Reverse T3 returns to normal before T3. The changes in thyroid function tests are a continuum.75 There is an inverse relationship between the severity of illness and the T3 level. In euthyroid sick syndrome, abnormal thyroid function gradually reverts to normal function as the patient’s primary illness improves.37 During recovery, TSH may be transiently elevated (up to 15 mU/L). Treatment with thyroid hormone is not indicated in these patients. 
Transient Hypothyroxinemia of Prematurity 
In preterm infants, postnatal thyroid hormone concentrations may differ from those in term infants. The thyroid hormone concentrations vary based on the degree of prematurity. There are multiple etiologies such as loss of maternal transfer of T4 86; immaturity of hypothalamic-pituitary-thyroid axis87 and peripheral metabolism of iodothyronines,88 iodine deficiency,89 nonthyroidal illness;83 and decreased TBG concentrations secondary to undernutrition or hepatic dysfunction.90 Thyroid metabolism can be affected by other factors: exogenous sources of iodine, dopamine infusions, blood transfusion, and glucocorticoid treatment. In preterm infants, hypothalamic-pituitary-thyroid immaturity is characterized by a limited neonatal TSH surge, decline in T4 in the first week of life, limited TSH response to hypothyroxinemia, and a prolonged TSH response to TRH. Impairment of T4 to T3 and increases in D3 activity may also influence thyroid function tests.31 Only in the third trimester does hypothalamic TRH begin to increase markedly.31,91 In transient hypothyroxinemia in premature infants (before 30 to 32 weeks’ gestation), thyroid function tests show low T4 and FT4 levels with normal or low TSH levels. Thyroid hormone replacement has not been consistently effective in improving neurologic outcomes or reducing morbidity.92,93 Research efforts continue to investigate this question. At the current time, therapy is only recommended when low T4 is accompanied by TSH elevation. 83,92 Abnormalities in thyroid levels in preterm infants can be difficult to interpret when the infants are ill from nonthyroidal diseases. Preterm infants at risk should be monitored by serial determinations of FT4 and TSH. T4 treatment should be initiated if the illness state is expected to be persistent and TSH remains elevated for a month or longer. A dosage of 4 to 5 μg/kg of oral levothyroxine was suggested in earlier dosage studies.94,95 
Low Triiodothyronine Syndrome in Premature Infants 
Changes in thyroid function tests during neonatal adaptation are qualitatively similar to those in term infants but occur at lower concentrations in premature infants. The neonatal surge and T4 and T3 peak responses diminish with decreasing gestational age.31 Premature infants have increased susceptibility to neonatal morbidity, including birth trauma, acidosis, hypoxia, hypoglycemia, hypocalcemia, and infection, all superimposed on feeding disorders and relative malnutrition. All of these factors tend to inhibit peripheral T4 to T3 conversion. This action leads to the characteristically low T3 state seen in premature infants. Serum T3 values may remain low in these infants for 1 to 2 months. Other features of the low T3 syndrome in premature infants are variable but usually include elevated serum rT3 levels and normal or low total serum T4 concentrations. Free T4 levels usually are in the range of healthy premature infants or matched gestation age and weight.31 TSH values are low in these infants. Treatment with thyroid hormone is not warranted.92,93 
Iodine Deficiency 
Severe iodine deficiency is associated with cretinism. Iodine deficiency is a rare cause of transient hypothyroidism in North America but may occur in dieting women who are not eating bread or using salt. Many countries have initiated salt iodination. Iodine is a critical component of thyroid hormone synthesis; therefore, even mild to moderate forms of iodine deficiency can result in an adverse outcome for the fetus. Although the mother with iodine deficiency may be clinically euthyroid with normal T3 levels, maternal T4 concentration is low in iodine deficiency. An increase in type 2 DI activity is detected in the fetus in response to iodine deficiency. Because normal development of the fetal neocortex is dependent on maternal T4, which is the primary source of cerebral T3, low levels of maternal T4 place the infants at risk of neurologic cretinism. The fetus can experience several neurologic manifestations, such as deafness, motor deficits (spasticity, trunk rigidity, flexion dystonia, muscle wasting), and mental retardation. Therefore, it is imperative for the pregnant mother to receive an adequate supply of iodine early in pregnancy to avoid brain damage in the fetus.96,97 Vitamin supplements that contain at least 250 μg iodine should be used daily.20 Preterm infants are at increased risk of iodine deficiency. The premature separation from the maternal supply of iodine and thyroid hormone prevents the preterm infant from accumulating adequate amounts of intrathyroidal hormone. Therefore, the infant is unable to keep up with postnatal thyroid hormone demands. The biochemical profile of iodine deficiency in the newborn comprises low T4 and elevated TSH levels. Iodine deficiency can lead to a transient state of thyroid dysfunction. An infant is sensitive to maternal iodine nutrition during fetal development. The thyroid is also protected against iodide excess that might otherwise lead to hyperthyroidism. The sources of excess iodide are pharmaceutical: amiodarone, povidone–iodine, and radiographic dyes. The quantity of iodine organified to TG displays a biphasic response to increasing doses of iodide, at first increasing and then decreasing. The decreasing yield is termed the Wolff-Chaikoff effect. The inhibition of iodothyronine formation is reduced over time, the escape phenomenon. This does not occur in the thirdtrimester fetus, so long-term high iodine intake must be avoided because it will cause fetal hypothyroidism. 
Disorders of Thyroid Hormone Carrier Protein 
Thyroid hormone in the circulation travels bound to transport proteins (TBG, TBPA, and albumin). As discussed previously, these carrier proteins are produced by the liver. The gene for TBG, the primary transport protein, is located on the long arm of the X chromosome; thus, TBG defects are inherited in an X-linked manner. Given that TBG is the major transport protein, TBG deficiency causes significant thyroid changes in total thyroid hormone concentration. But given that free concentrations remain normal, these individuals are euthyroid. Treatment is not required. Primary T4 newborn screening methods may be misleading, and confirmation with fT4 levels is necessary before initiation of treatment. 
Thyroxine-Binding Globulin Deficiency 
The prevalence of thyroxine-binding globulin (TBG) deficiency varies from 1 in 2500 to 1 in 12,000 newborns.75,98,99 The frequency in males is much higher, 1 in 2400 to 1 in 2800 males, because it is an X-linked trait.99 The transmission of this trait is usually from affected males to female offspring.75 TBG deficiency has no clinical importance but leads to abnormal laboratory tests. Congenital central hypothyroidism can be detected on newborn screen programs that utilize T4-reflex thyroid-stimulating hormone (TSH) test method. Congenital central hypothyroidism must be distinguished from TBG deficiency. The diagnosis of congenital central hypothyroidism is made with low serum free T4 and can be supported by the presence of other pituitary hormone deficiencies. Serum TBG levels play an essential role in the diagnosis of TBG deficiency but do not play a role in the diagnosis of congenital central hypothyroidism.100 Serum TBG levels are very low in affected males and are approximately half of normal in carrier females. In about half of the families with this trait, the TBG level shown by radioimmunoassay is very low. In the other half, the defect is partial; serum T4 levels vary similarly. Affected persons are euthyroid, with normal serum TSH responses to exogenous TRH. Treatment is not indicated.98 As many as 26 different mutations have been reported in the TBG gene. These mutations have included a single amino acid substitution or deletion, leading to abnormal post-translational processing.75 Two novel mutations in the TBG gene identified most recently include a T insertion at the beginning of intron 1 between nucleotides 2 and 3 and a T deletion in exon 1 leading to a truncated protein. Both mutations fail to produce a functional TBG molecule.101 In partial TBG deficiency, the defects are associated with altered TBG binding of T4.75 Females tend to have partial TBG deficiency, whereas males generally have complete TBG deficiency. A partial deficiency comprises reduced TBG levels and normal TSH and FT4 with T4 values at the lower limit of normal. A complete deficiency comprises undetectable TBG levels with normal TSH, normal FT4, and low levels of T4. Another useful laboratory tool is T3RU, which is elevated with TBG deficiency.102 However, this is an indirect measure of TBG levels.