An error occurred while setting your user cookie. Please set your. browser to accept cookies to continue. This cookie stores just a. ID; no other information is captured. Accepting the NEJM cookie is. ![]() ![]() Disorders of the Thyroid Gland in Infancy, Childhood and Adolescence. This chapter is, in part, based on the previous version written by Prof. Rosalind Brown. ABSTRACTThyroid disorders in infancy, childhood and adolescence represent common and usually treatable endocrine disorders. Thyroid hormones are essential for normal development and growth of many target tissues, including the brain and the skeleton. Thyroid hormone action on critical genes for neurodevelopment is limited to specific time window, and even a short period of deficiency of TH can cause irreversible brain damage. During the first trimester of pregnancy fetal brain development is totally dependent on maternal thyroid function. Congenital hypothyroidism is one of the most preventable causes of mental retardation, but early diagnosis is needed in order to prevent irreversible SNC damage. Today more than 7. New insights about genetic causes, screening strategies and treatment of congenital hypothyroidism are reported. Hyperthyroidism in newborns is usually a transient consequence of transplacental passage of TSH receptor stimulating antibodies. Hypothyroidism can be detected in infants born to hyperthyroid mothers, due to transplacental passage of TSH receptor antibodies or hypothalamic- pituitary suppression. In childhood and adolescence autoimmune thyroid disease (AITD) as chronic lymphocytic thyroiditis and Graves’ disease account for the main cause of hypothyroidism and hyperthyroidism, respectively. Incidence of AITD increase from infancy to adolescence. Other autoimmune disorders are frequently associated. An increased risk of thyroid nodules and cancer is suggested. ![]() ![]() Differentiated thyroid cancer and medullary thyroid carcinoma in childhood and adolescence require specific expertise. Follow up programs are advised for high risk patients as long term survivors of childhood cancer. For complete coverage of this and related areas of Endocrinology, please visit our free online textbook, WWW. ENDOTEXT. ORG. As a result, abnormalities of thyroid gland function in infancy and childhood result not only in the metabolic consequences of thyroid dysfunction seen in adult patients, but in unique effects on the growth and /or maturation of these thyroid hormone- dependent tissues as well. In most instances, there are critical windows of time for thyroid hormone- dependent development and so the specific clinical consequence of thyroid dysfunction depends on the age of the infant or child. For example, newborn infants with congenital hypothyroidism frequently have hyperbilirubinemia, and delayed skeletal maturation, reflecting immaturity of liver and bone, respectively, and they are at risk of permanent mental retardation if thyroid hormone therapy is delayed or inadequate; their size at birth, however, is normal. In contrast, hypothyroidism that develops after the age of three years (when most thyroid hormone- dependent brain development is complete) is characterized predominantly by a deceleration in linear growth and skeletal maturation but there is no permanent effect on cognitive development. In general, infants with severe defects in thyroid gland development or inborn errors of thyroid hormonogenesis present in infancy whereas babies with less severe defects or acquired abnormalities, particularly autoimmune thyroid disease, present later in childhood and adolescence. In the newborn infant, thyroid function is influenced not only by the neonate ’ s own thyroid gland but by the transplacental passage from the mother of factors that affect the fetal thyroid gland. In the last several decades, there have been exciting advances in our understanding of fetal and neonatal thyroid physiology, and screening for congenital hypothyroidism has enabled the virtual eradication of the devastating effects of mental retardation due to sporadic congenital hypothyroidism in most developed countries of the world. In addition, advances in molecular biology have led to new insights regarding the early events in thyroid gland embryogenesis and mechanisms of thyroid action in the brain. At the same time, the molecular basis for many of the inborn errors of thyroid hormonogenesis and thyroid hormone action is being unraveled. However, new questions and new challenges arise. In particular, the survival of increasingly small and premature fetuses has resulted in a growing number of neonates with abnormalities in thyroid function and a continuing controversy as to which of these infants require therapy. This chapter will focus on current concepts regarding the ontogenesis of thyroid function in the fetus and will review the major disorders of thyroid gland function in infants and children. ONTOGENESIS OF THYROID FUNCTION IN THE FETUS AND INFANTThe ontogeny of mature thyroid function involves the organogenesis and maturation of the hypothalamus, pituitary, and thyroid glands as well as the maturation of thyroid hormone metabolism and thyroid hormone action. The placenta also plays a key role in the transfer of hormones and factors other than T4 that impact on thyroid function. In the first half of pregnancy, maternal T4 provides an important source of hormone for the developing fetus. Much of our knowledge derives from work in animal models, particularly sheep and rat. In interpreting these data, it is important to remember potential limitations in these models because of differences both in the structure of the placenta and timing of maturation. For example, the rat thyroid gland is much less mature at birth than its human counterpart and significant maturation of the thyroid gland and of the hypothalamic- pituitary- thyroid axis in this species occurs in the first 2 or 3 weeks after birth in the absence of placental or maternal influence, as compared with the third trimester in human infants. Thyroid Gland Embryogenesis. Thyroid gland development is extensively reviewed in an earlier chapter and is shown diagrammatically in Figure 1. In brief, the thyroid gland is derived from the fusion of a medial outpouching from the floor of the primitive pharynx, the precursor of the thyroxine (T4)- producing follicular cells, and bilateral evaginations of the fourth pharyngeal pouch, which gives rise to the parafollicular, or calcitonin (C) secreting cells. Commitment towards a thyroid- specific phenotype as well as the growth and descent of the thyroid anlage into the neck results from the coordinate action of a number of transcription factors, including thyroid transcription factor 1 (TTF1, now called NKX2 (1), TTF2 (now called FOXE1) and PAX8 (1,2). ![]() Because these transcription factors are also expressed in a limited number of other cell types, it appears to be the specific combination of transcription factors and possibly non- DNA binding cofactors acting coordinately that determine the phenotype of the cell. Other transcription factors and growth factors that play a role in early thyroid gland organogenesis include HHEX1, HOXA3 (3) and members of the fibroblast growth factor family, i. FGF1. 0, but the initial inductive signal is unknown. ![]() ![]() A role of the neighboring heart primordium in the specification of the thyroid anlage has been postulated. Studies of cadherin expression suggest that the caudal translocation of the thyroid anlage may also arise indirectly, as a result of the growth and expansion of adjacent tissues, including the major blood vessels (4). In late organogenesis, the sonic hedgehog (SHH) gene and its downstream target TBX1 appear to play an important role in the symmetric bilobation of the thyroid (5); SHH also suppresses the ectopic expression of thyroid follicular cells (6). During caudal migration the pharyngeal region of the thyroid anlage contracts to form a narrow stalk, known as the thyroglossal duct, which subsequently atrophies. ![]() Usually no lumen is left in the tract of its descent but, occasionally, an ectopic thyroid and/or persistent thyroglossal duct or cyst form if thyroid descent is abnormal. Figure 1. 5- 1. Approximate timing of thyroid gland maturation in the human fetus. In the human, embryogenesis is largely complete by 1. At this stage, tiny follicle precursors can be seen, iodine binding can be identified and thyroglobulin (Tg) detected in follicular spaces (7,8) . Thyroid hormones are detectable in fetal serum by gestational age 1. T4) and triiodothyronine (T3) being measurable. However, as discussed in further detail below, it is likely that a fraction of the hormones detectable at this early stage is contributed by the mother through transplacental transfer. Background The role of bracing in patients with adolescent idiopathic scoliosis who are at risk for curve progression and eventual surgery is controversial. Sasse Surgical Associates offers weight loss surgery to Reno and Carson City, Nevada patients. Contact bariatric surgeon Dr. Thyroid hormones continue to increase gradually over the entire period of gestation as does serum thyroxine- binding globulin (TBG) (9,1. TBG is present at levels of 1. L (5 mg/L) at gestational age 1. L (2. 5 mg/L). The serum TBG concentrations are higher in the infant then in adult humans as a consequence of placental estrogen effects on the fetal liver. In addition to the increase in total T4 there is also a progressive increase of the free T4 concentration indicating a maturation of the hypothalamic- pituitary- thyroid axis. The increased total T4 / thyrotropin (TSH) and free T4 /TSH ratios also indicate an increased ability of the thyroid gland to respond to TSH due to upregulation of the TSH receptor (1. Whereas the TBG and total T4 levels rise throughout gestation, the concentrations of free T4, and TSH rise until 3. We performed a multicenter, randomized, double-blind, placebo-controlled trial in which participants with one or two painful osteoporotic vertebral fractures that. Low-grade glioma: supratentorial astrocytoma, oligodendroglioma, and oligoastrocytoma in adults. Curr Neurol Neurosci Rep 2004; 4(3): 211-7.Medline. ![]() Best brand: kids best brand: new & hot brand: women: Rohrich is Dallas plastic surgeon and Professor of Plastic Surgery at the Department of Plastic Surgery at UT Southwestern Medical Center. Beyoncé Reminds Us Why the Grand Canyon Is One of America’s Best Travel Destinations. Mark Brinkley considers the logical impact behind an extra pane in triple glazing, and looks at whether triple glazing makes sense for your home. This chapter is, in part, based on the previous version written by Prof. Thyroid disorders in infancy, childhood and adolescence represent. Campylobacter is considered to be the most common cause of bacterial gastroenteritis worldwide, the single most common inciting agent for Guillain-Barre Syndrome, and. Tg can be identified in the fetal thyroid as early as the 5th week, and is certainly present in follicular spaces by 1. Tg secretion takes much longer and it is not known when circulating Tg first appears in the fetal serum (not shown). By the time of gestational age 2. ![]() Tg levels average approximately 1. L, much higher than in the adult and they remain approximately stable until the time of birth (1. Iodide concentrating capacity can be detected in the thyroid of the 1. Wolff- Chaikoff effect (reduction of iodide trapping in response to excess iodide) does not appear until 3.
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