Developmental outcome of children with early transient thyroid hormone imbalances (original) (raw)
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O F the Thyroid Gland in Infancy , Childhood and Adolescence
2017
Thyroid 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 70% of the babies worldwide are born in areas without an organized screening program. New insights about genetic causes, screening strategies and treatment of congenital hypothyroidism are reported. Hyperthyroidism in newborns is usually a transient consequence of transplacental pa...
The Growth and Development in Healthy Child
Contemporary Pediatrics, 2012
Child-our assurance for the future… A healthy society consists of healthy families and healthy children. Therefore, healthy growth of children is important for society and for families. A healthy child is defined as the one who does not show any illness syndromes, but a steady body growth, physiological maturity and cognitive development (Çetinkaya & Conk, 2009; Kavaklı, 1992; Neyzi & Koc, 1983). The term "growth" is used for defining a quantitative increase in the body or in some of its parts, whereas the "development" is used for functional changes including those which arouse from emotional and social interactions (Behrman & Kliegman, 1996; Beyazova, 1996). Growth is product of various factors, thus, a complex situation. In this complex, the answers to genetic factors, nutrition, metabolism, endocrine system, and peripheral tissue are of great significance, and required for such a sensitive coordination (Arcasoy et al, 1994; Kandemir & Yordam, 1995). Starvation and inadequate nutrition cause resistance against the growth hormone (Kandemir & Yordam, 1995). In small children, malnutrition has a dampening effect for motivation and curiosity, limiting their desire to play games and make observations. Due to the decreased level of interactions with surroundings, mental and cognitive development of children are adversely affected (Bellamy, 1998). The growth of head and brain tissues is closely associated with nutrition. This growth is accelerated particularly at the intrauterine period and within the 4-5 years after delivery. At the age of 5, the brain tissiues are grown up to the 90-95% of an adult person's brain tissue. This period is important for the development of brain, intelligence, and mental state. The remaining 5-10% of development is achieved by the ages of 18-20 (Bertan & Guler, 1995). For healthy and desired growth energy is required (Kandemir & Yordam, 1995). Hypothyroidism and hypopituitarism are of the most notable examples. Monitoring child's growth is essential for bringing up healthy generations. To this end, regular checkups of infants and their measure analysis should be made carefully, while problematic situations that might arise from environmental factors should be resolved (Arcasoy et al, 1994).
Thyroid hormones states and brain development interactions
The action of thyroid hormones (THs) in the brain is strictly regulated, since these hormones play a crucial role in the development and physiological functioning of the central nervous system (CNS). Disorders of the thyroid gland are among the most common endocrine maladies. Therefore, the objective of this study was to identify in broad terms the interactions between thyroid hormone states or actions and brain development. THs regulate the neuronal cytoarchitecture, neuronal growth and synaptogenesis, and their receptors are widely distributed in the CNS. Any deficiency or increase of them (hypo- or hyperthyroidism) during these periods may result in an irreversible impairment, morphological and cytoarchitecture abnormalities, disorganization, maldevelopment and physical retardation. This includes abnormal neuronal proliferation, migration, decreased dendritic densities and dendritic arborizations. This drastic effect may be responsible for the loss of neurons vital functions and may lead, in turn, to the biochemical dysfunctions. This could explain the physiological and behavioral changes observed in the animals or human during thyroid dysfunction. It can be hypothesized that the sensitive to the thyroid hormones is not only remarked in the neonatal period but also prior to birth, and THs change during the development may lead to the brain damage if not corrected shortly after the birth. Thus, the hypothesis that neurodevelopmental abnormalities might be related to the thyroid hormones is plausible. Taken together, the alterations of neurotransmitters and disturbance in the GABA, adenosine and pro/antioxidant systems in CNS due to the thyroid dysfunction may retard the neurogenesis and CNS growth and the reverse is true. In general, THs disorder during early life may lead to distortions rather than synchronized shifts in the relative development of several central transmitter systems that leads to a multitude of irreversible morphological and biochemical abnormalities (pathophysiology). Thus, further studies need to be done to emphasize this concept.
Journal of Neuroendocrinology, 2004
The original concept of the critical period of thyroid hormone (TH) action on brain development was proposed to identify the postnatal period during which TH supplement must be provided to a child with congenital hypothyroidism to prevent mental retardation. As neuropsychological tools have become more sensitive, it has become apparent that even mild TH insufficiency in humans can produce measurable deficits in very specific neuropsychological functions, and that the specific consequences of TH deficiency depends on the precise developmental timing of the deficiency. Models of maternal hypothyroidism, hypothyroxinaemia and congential hyperthyroidism have provided these insights. If the TH deficiency occurs early in pregnancy, the offspring display problems in visual attention, visual processing (i.e. acuity and strabismus) and gross motor skills. If it occurs later in pregnancy, children are at additional risk of subnormal visual (i.e. contrast sensitivity) and visuospatial skills, as well as slower response speeds and fine motor deficits. Finally, if TH insufficiency occurs after birth, language and memory skills are most predominantly affected. Although the experimental literature lags behind clinical studies in providing a mechanistic explanation for each of these observations, recent studies confirm that the specific action of TH on brain development depends upon developmental timing, and studies informing us about molecular mechanisms of TH action are generating hypotheses concerning possible mechanisms to account for these pleiotropic actions.
Neonatal thyroid-stimulating hormone concentration and psychomotor development at preschool age
Archives of Disease in Childhood, 2016
Objective Thyroid hormones are essential for normal brain development. The aim of this study is to assess if high concentration of thyroid stimulating hormone (TSH) that is below the clinical threshold (5-15 mIU/L) at neonatal screening is linked to psychomotor development impairments in the offspring at preschool age. Design A total of 284 Belgian preschool children 4-6 years old and their mothers were included in the study. The children were randomly selected from the total list of neonates screened in 2008, 2009 and 2010 by the Brussels newborn screening centre. The sampling was stratified by gender and TSH range (0.45-15 mIU/L). Infants with congenital hypothyroidism (>15 mIU/L), low birth weight and/or prematurity were excluded. Psychomotor development was assessed using the Charlop-Atwell scale of motor coordination. The iodine status of children was determined using median urinary iodine concentration. Socioeconomic, parental and child potential confounding factors were measured through a self-administered questionnaire. Results TSH level was not significantly associated with total motor score (average change in z-score per unit increase in TSH is 0.02 (−0.03, 0.07), p=0.351), objective motor score (p=0.794) and subjective motor score (p=0.124). No significant associations were found using multivariate regression model to control confounding factors. Conclusions Mild thyroid dysfunction in the newborn-reflected by an elevation of TSH that is below the clinical threshold (5-15 mIU/L)-was not associated with impaired psychomotor development at preschool age.
Intellectual outcome in children with fetal hypothyroidism
The Journal of Pediatrics, 1987
Intellectual outcome fetal hypothyroidism in children with Eighty children with congenital hypothyroidism detected by newborn screening were grouped for presence of fetal hypothyroidism using skeletal maturity at the time of diagnosis as the index. Forty-five children with bone age <36 weeks were assigned to the delayed group; 35 with bone age 37 weeks to term were assigned to the nondelayed group. Although most children with athyroSis were found in the delayed group, the groups did not differ in birth weight, hormone levels, or family background. Assessments of intellectual and behavioral characteristics at 1, 2, 3, 4, and 5 years of age revealed that, although children in the delayed group performed within the normal range, their scores were significantly lower than those of the nondelayed group from age 2 years on. Perceptual-motor, visuaspatial, and language areas were most affected. There were no differences in behavior or temperamental characteristics.
Maternal and Child's Thyroid Function and Child's Intellect and Scholastic Performance
Thyroid, 2015
Background: Maternal hypothyroidism and/or hypothyroxinemia have been associated with child's poor neuropsychological development, but the results have been inconsistent. Methods: The Northern Finland Birth Cohort 1986 included all expected births within a year (9362 women, 9479 children) from the two northernmost provinces of Finland. Maternal serum samples (n = 5791) were obtained in early pregnancy (M-SD = 10.7-2.8 weeks' gestation), and serum samples from their children were obtained at 16 years of age (n = 5829). All samples were analyzed for thyrotropin, free thyroxine (fT4), and thyroid peroxidase antibodies. The children's school performance was evaluated by their main teachers at eight years of age, as well as by the adolescents themselves at 16 years of age. Data on possible severe intellectual deficiency and mild cognitive limitation were collected from healthcare records and registries for all children. Logistic regression estimated the odds of poor school performance or severe intellectual deficiency/mild cognitive limitation associated with exposure to maternal thyroid dysfunction. The odds of poor school performance associated with the adolescents' own thyroid function at age 16 were also estimated. Results are presented as odds ratios (OR) with confidence intervals (CI), adjusted for maternal/family covariates and child's sex. Results: Girls of mothers with subclinical hypothyroidism had more self-evaluated difficulties in mathematics than did girls of euthyroid mothers (OR 1.62 [CI 1.06-2.49]). Boys of hypothyroxinemic mothers repeated a school class more often than did boys of euthyroid mothers (OR 5.46 [CI 1.19-25.06]). Adolescents of hyperthyroid mothers had increased odds of poor self-evaluated performance in mathematics (OR 1.61 [CI 1.01-2.49]). Maternal thyroid dysfunction did not increase the odds of a child having severe intellectual deficiency/mild cognitive limitation. At 16 years of age, girls with hyperthyroidism by laboratory measurements had more difficulties in Finnish language (OR 2.82 [CI 1.42-5.61]) than did euthyroid girls. Boys with hypothyroxinemia by laboratory measurement had higher odds of having difficulties in Finnish and/or mathematics (OR 2.13 [CI 1.26-3.62]) than did euthyroid boys. Conclusions: Maternal thyroid dysfunction during early pregnancy was associated with poorer scholastic performance of the adolescent. Additionally, adolescents' own thyroid dysfunction was associated with difficulties in school performance assessed by self-evaluation.
Thyroid, 2014
Background: Thyroid hormones are required for normal brain maturation, and neonatal plasma thyroid hormone concentrations are low in infants less than 28 weeks gestation. It is not known whether treatment of such infants with thyroid hormone improves neurodevelopmental outcome. Methods: At three years corrected age, mental, motor, and neurological development was assessed in infants born at less than 28 weeks gestational age who had participated in a phase 1 trial of differing doses and modes of administration of thyroid hormone. The trial's endpoints were thyroid hormone (thyroxine, T4) and thyotropin plasma concentrations in eight study arms: six treated with T4 [4, 8, and 16 lg/(kg$day)], bolus or continuous], one treated with iodine only, and one treated with placebo. Follow-up at three years was not part of the original study goals. Developmental index scores, rates of cerebral palsy (CP), and rates of adverse outcome (death or moderate to severe delay in development and/or disabling CP) were compared between the eight study groups and between groups combined by dosage level, and between infants with and without T4 supplementation. Results: Of 166 randomized infants, 32 (19%) died in the neonatal period. Of the 134 survivors, follow-up results were available for 89 children (66%). Mental and motor development and rates of cerebral palsy did not differ in any of the comparisons made. Conclusion: In this study, no differences in neurodevelopment were found in relation to thyroid hormone treatment, but power was insufficient to detect any but very large differences.
Thyroid Hormones and Brain Development
Annual Review of Physiology, 1987
Thyroid hormone is a major physiological regulator of mammalian brain development. Cell differentiation, migration and gene expression are altered as a consequence of thyroid hormone deficiency or excess. The physiological role of thyroid hormone can perhaps be defined so as to ensure the timed coordination of different developmental events through specific effects on the rate of cell differentiation and gene expression. All triiodothyronine (T3) receptor isoforms are expressed in the brain and their spatial and temporal patterns of expression suggest unique and complementary functions for the different isoforms. Cell biology studies suggest a role for T3 and its receptors in oligodendroglial and neuronal differentiation and the control of cell death. Some of the effects on neuronal differentiation might be due to an action of thyroid hormone on the production of neurotropins and their receptors. In recent years a number of T 3-dependent genes have been identified in the rat brain, such as myelin protein-encoding genes or specific neuronal genes, and thyroid hormone-responsive elements have been demonstrated in some of these genes. The identification of the gene network regulated by thyroid hormone during brain development, the elucidation of the mechanism of regulation and the clarification of the physiological roles of the regulated genes remain major goals for future studies.
Journal of thyroid research, 2011
Although evidence suggests that maternal hypothyroidism and mild hypothyroxinemia during the first half of pregnancy alters fetal neurodevelopment among euthyroid offspring, little data are available from later in gestation. In this study, we measured free T4 using direct equilibrium dialysis, as well as total T4 and TSH in 287 pregnant women at 27 weeks' gestation. We also assessed cognition, memory, language, motor functioning, and behavior in their children at 6, 12, 24, and 60 months of age. Increasing maternal TSH was related to better performance on tests of cognition and language at 12 months but not at later ages. At 60 months, there was inconsistent evidence that higher TSH was related to improved attention. We found no convincing evidence that maternal TH during the second half of pregnancy was related to impaired child neurodevelopment.