Hypothyroxinemia Of Prematurity Research Articles

Patterns of Endocrine Disorders in a Neonatal Intensive Care Unit: A Single-Center Retrospective and Descriptive Study

Background: Endocrine disorders in infants in neonatal intensive care units (NICU) represent a significant clinical concern. Understanding the frequency and variety of these disorders is crucial for effective patient management. Objectives: This single-center retrospective study was conducted to examine the frequency and patterns of endocrine disorders among neonates in the NICU. Methods: We performed a retrospective review of 1 845 patient records over five years from the NICU at Çanakkale Onsekiz Mart University Health Practice and Research Hospital. The study included patients admitted between January 1, 2016, and March 31, 2021, who were diagnosed with endocrine disorders according to the international classification of diseases (ICD). Diagnostic criteria were used to identify and categorize endocrine disorders, primarily focusing on hypoglycemia, congenital hypothyroidism, hypothyroxinemia of prematurity, neonatal hyperthyrotropinemia (HTT), and disorders of calcium and magnesium metabolism. Data analysis was conducted using descriptive statistics. Results: Endocrine disorders were identified in 14.6% (CI: 13.15 - 16.38) of the neonates. The most prevalent were thyroid disorders (5.15%, CI: 4.23 - 6.25), disorders of calcium metabolism (3.68%, CI: 2.92 - 4.64), and disorders of glucose homeostasis (3.63%, CI: 2.87 - 4.58). Notably, neonatal HTT was more frequent than previously reported. The majority of endocrine issues occurred in premature infants. Hypoglycemia was the most frequent glucose homeostasis disorder, affecting 24.7% (CI: 19.9 - 30.2) of those diagnosed with endocrine issues. Among the cases with calcium metabolism disorders, hypocalcemia was predominant (79.4%, CI: 68.3 - 87.3), with the majority (89%, CI: 80.1 - 95.9) being classified as early neonatal hypocalcemia. Conclusions: Endocrine disorders, particularly those related to thyroid, calcium, and glucose homeostasis, remain prevalent issues in the NICU. Prematurity significantly contributes to these complications. The frequency and variety of endocrine disorders are likely to evolve with improvements in laboratory techniques and diagnostic methods. Future larger-scale studies could provide more comprehensive insights into these disorders.

Hypothyroxinemia and weight velocity in preterm infants.

Hypothyroxinemia of prematurity (HOP) is characterized by low free thyroxine (FT4) associated with low or normal thyroid stimulating hormone (TSH). The objective of this study is to define FT4 and TSH values in very preterm infants (<32 weeks postmenstrual age, PMA) and correlate hypothyroxinemia and levothyroxine treatment with growth velocity at 28 days and 36 weeks PMA. Preterm neonates <32 weeks PMA admitted to the regional neonatal intensive care unit (NICU) at the Children's Hospital of Georgia (USA) between January 2010 and July 2022 were routinely screened for hypothyroxinemia. FT4 and TSH values were obtained on 589 eligible neonates between day of life (DOL) 4 and 14. Growth velocity (g/kg/day) from DOL 14 to DOL 28 and 36-weeks PMA were calculated for each neonate and potential explanatory variables (PMA, sex, and race) were incorporated into multivariate regression models to identify associations between HOP and growth velocity. In 589 preterm infants, PMA at birth was strongly associated inversely with FT4 (R=0.5845) and modestly with TSH (R=0.2740). Both FT4 and gestational age, but not TSH or levothyroxine treatment, were associated with growth velocity at 28 days of life and at 36 weeks PMA. We provide a large data set for identifying FT4 and TSH measurements and identify hypothyroxinemia of prematurity as a potential mediator of slow postnatal growth in very preterm infants.

Thyroid Function in 509 Premature Newborns Below 31 Weeks of Gestational Age: Evaluation and Follow-up

Preterm and low birth weight (LBW) neonates may present with thyroid dysfunction during a critical period for neurodevelopment. These alterations can be missed on routine congenital hypothyroidism (CH) screening which only measures thyroid stimulating hormone (TSH). The objective of this study was to evaluate a protocol for thyroid function screening (TFS) six years after national implementation. Serum TSH and free thyroxine (fT4) were measured during the second week of life in neonates below 31 weeks. Patients with abnormal TFS (fT4 <0.8 ng/dL and/or TSH >5 mU/L) were followed up with repeated tests until normal levels were reported. Patients who were still on levothyroxine (LT4) at three years of age were re-evaluated. Five-hundred and nine neonates were included. Thyroid dysfunction was detected in 170 neonates (33%); CH n=20 (3.9%) including typical CH n=1; delayed TSH elevation CH n=19; hypothyroxinemia of prematurity (HOP) n=15 (2.9%); and transient hyperthyrotropinemia n=135 (26.5%). Twenty-one neonates (4.1%) were treated (20 for CH and 1 for HOP). At 3-year follow-up only three patients were diagnosed with permanent CH and still need treatment. LBW infants tended to have TSH levels higher than those with adequate weight. This protocol was able to detect thyroid dysfunction in preterm neonates who were not identified by the current program based on TSH determination in whole-blood. This thyroid dysfunction seems to resolve spontaneously in a few months in the great majority of neonates, but in some cases LT4 could be needed. There is a critical need for specific guidelines regarding the follow-up and re-evaluation of transient CH in preterm neonates.

Hypothyroxinemia of prematurity – Is it really transient and benign?

Hypothyroxinemia of prematurity – Is it really transient and benign?

Effect of levothyroxine supplementation in extremely low birth weight infants with transient hypothyroxinemia of prematurity

This study aimed to determine the short- and/or long-term outcomes of levothyroxine replacement therapy in extremely low birth weight (ELBW) infants with transient hypothyroxinemia of prematurity (THOP). The medical records of 335 ELBW infants with THOP were reviewed retrospectively to identify whether levothyroxine treatment affects short- and/or long-term outcomes at a corrected age of 2 years. The infants were arbitrarily grouped based on thyroxine (T4) (free T4 [fT4]) levels into group 1 (n = 142), which included infants with T4 (fT4) levels < 2.5 (0.5) ng/dl, and group 2 (n = 193), which included those with T4 (fT4) levels ranging from ≥ 2.5 (0.5) ng/dl to < 4.5 (0.9) ng/dl. Levothyroxine replacement therapy was not associated with beneficial short- or long-term outcomes in ELBW infants with THOP. Short-term outcomes, such as mortality and composite morbidities, and long-term outcomes, such as failure to achieve catch-up height at a corrected age of 2 years, were significantly higher in group 1 than in group 2, regardless of levothyroxine treatment status. Levothyroxine replacement therapy is not associated with short-or long-term advantages in ELBW infants with THOP. This study suggests that the severity of THOP may be the major determinant of adverse outcomes in ELBW infants with THOP, rather than levothyroxine treatment.

Congenital Hypothyroidism in Preterm Newborns - The Challenges of Diagnostics and Treatment: A Review.

Preterm newborns are forced to adapt to harsh extrauterine conditions and endure numerous adversities despite their incomplete growth and maturity. The inadequate thyroid hormones secretion as well as the impaired regulation of hypothalamus-pituitary-thyroid axis may lead to hypothyroxinemia. Two first weeks after birth are pivotal for brain neurons development, synaptogenesis and gliogenesis. The decreased level of thyroxine regardless of cause may lead to delayed mental development. Congenital hypothyroidism (CH) is a disorder highly prevalent in premature neonates and it originates from maternal factors, perinatal and labor complications, genetic abnormalities, thyroid malformations as well as side effects of medications and therapeutic actions. Because of that, the prevention is not fully attainable. CH manifests clinically in a few distinctive forms: primary, permanent or transient, and secondary. Their etiologies and implications bear little resemblance. Therefore, the exact diagnosis and differentiation between the subtypes of CH are crucial in order to plan an effective treatment. Hypothyroxinemia of prematurity indicates dynamic changes in thyroid hormone levels dependent on neonatal postmenstrual age, which directly affects patient’s maintenance and wellbeing. The basis of a successful treatment relies on an early and accurate diagnosis. Neonatal screening is a recommended method of detecting CH in preterm newborns. The preferred approach involves testing serum TSH and fT4 concentrations and assessing their levels according to the cut-off values. The possible benefits also include the evaluation of CH subtype. Nevertheless, the reference range of thyroid hormones varies all around the world and impedes the introduction of universal testing recommendations. Unification of the methodology in neonatal screening would be advantageous for prevention and management of CH. Current guidelines recommend levothyroxine treatment of CH in preterm infants only when the diagnose is confirmed. Moreover, they underline the importance of the re-evaluation among preterm born infants due to the frequency of transient forms of hypothyroidism. However, results from multiple clinical trials are mixed and depend on the newborn’s gestational age at birth. Some benefits of treatment are seen especially in the preterm infants born <29 weeks’ gestation. The discrepancies among trials and guidelines create an urgent need to conduct more large sample size studies that could provide further analyses and consensus. This review summarizes the current state of knowledge on congenital hypothyroidism in preterm infants. We discuss screening and treatment options and demonstrate present challenges and controversies.

Thyroid Function in Preterm/Low Birth Weight Infants: Impact on Diagnosis and Management of Thyroid Dysfunction.

Maternal thyroid hormone crosses the placenta to the fetus beginning in the first trimester, likely playing an important role in fetal development. The fetal thyroid gland begins to produce thyroid hormone in the second trimester, with fetal serum T4 levels gradually rising to term. Full maturation of the hypothalamic-pituitary-thyroid (HPT) axis does not occur until term gestation or the early neonatal period. Postnatal thyroid function in preterm babies is qualitatively similar to term infants, but the TSH surge is reduced, with a corresponding decrease in the rise in T4 and T3 levels. Serum T4 levels are reduced in proportion to the degree of prematurity, representing both loss of the maternal contribution and immaturity of the HPT axis. Other factors, such as neonatal drugs, e.g., dopamine, and non-thyroidal illness syndrome (NTIS) related to co-morbidities contribute to the “hypothyroxinemia of prematurity”. Iodine, both deficiency and excess, may impact thyroid function in infants born preterm. Overall, the incidence of permanent congenital hypothyroidism in preterm infants appears to be similar to term infants. However, in newborn screening (NBS) that employ a total T4-reflex TSH test approach, a higher proportion of preterm babies will have a T4 below the cutoff, associated with a non-elevated TSH level. In NBS programs with a primary TSH test combined with serial testing, there is a relatively high incidence of “delayed TSH elevation” in preterm neonates. On follow-up, the majority of these cases have transient hypothyroidism. Preterm/LBW infants have many clinical manifestations that might be ascribed to hypothyroidism. The question then arises whether the hypothyroxinemia of prematurity, with thyroid function tests compatible with either non-thyroidal illness syndrome or central hypothyroidism, is a physiologic or pathologic process. In particular, does hypothyroxinemia contribute to the neurodevelopmental impairment common to preterm infants? Results from multiple studies are mixed, with some randomized controlled trials in the most preterm infants born <28 weeks gestation appearing to show benefit. This review will summarize fetal and neonatal thyroid physiology, thyroid disorders specific to preterm/LBW infants and their impact on NBS for congenital hypothyroidism, examine treatment studies, and finish with comments on unresolved questions and areas of controversy.

Serial Thyroid Function Test in Very Low Birth Weight Neonates

AbstractThyroid dysfunction is more common in preterm and low birth weight infants, and may be missed if thyroid function test (TFT) is not repeated. Thus, we attempted to study the pattern of thyroid function among very low birth weight (VLBW) infants with birth weight less than 1,500 g by serial TFTs. Serum free thyroxine (FT4) and thyrotropin (thyroid-stimulating hormone [TSH]) levels of VLBW infants were tested on fifth to seventh days of life and repeated after 4 weeks of age. Based on serial FT4 and TSH results, abnormal TFT was classified into four groups—transient hypothyroxinemia of prematurity (THOP), transient hyperthyrotropinemia (THT), delayed TSH rise, and overt congenital hypothyroidism (CH). Stata 15.1 (Stata Corp, Texas, United States) was used for analysis. Ninety-six VLBW infants were enrolled with mean gestational age of 30.5 ± 2.7 weeks and median (interquartile range) birth weight of 1,200 (317) g. Out of 96 cases, 30 (31.2%) infants had abnormal TFT. Ten (10.4%) infants had THOP, 7 (7.3%) infants had THT, 11 (11.5%) infants had delayed TSH rise, and 2 (2.1%) infants had overt CH. There were no significant differences in demographic profile and clinical characteristics between neonates with normal and abnormal TFTs. Five infants required levothyroxine supplementation (two infants with overt CH and three infants with delayed TSH rise). VLBW neonates have higher incidence of CH and delayed rise of TSH in this study. In resource-limited settings, repeating TFTs at least once after 4 weeks of age may be suggested to identify delayed rise of TSH which may need intervention.

Lack of association between hypothyroxinemia of prematurity and transient thyroid abnormalities with adverse long term neurodevelopmental outcome in very low birth weight infants.

IntroductionThe association between hypothyroxinemia of prematurity with neurodevelopment was controversial.ObjectivesTo compare 5 year neurodevelopmental outcomes of very low birth weight (VLBW) infants with hypothyroxinemia of prematurity against those without.MethodsRetrospective cohort study in a single tertiary neonatal centre of VLBW infants born between the year 2008 to 2011. Comparisons were made between all abnormal and normal thyroid function controls using cord thyroid function tests, thyroid function tests during admission and pre-discharge thyroid function test done at term equivalent age. At 2 years corrected age, Bayley scales of infant and toddler development–third edition and Vineland II adaptive behaviour scales (VABS) were collected. At 5 years, Wechsler Preschool and Primary Scale of Intelligence (WPPSI-III), Bracken School Readiness Assessment, VABS and Beery Test of Visual-Motor Integration were collected.Results110 subjects were studied at 2 years corrected age and 80 subjects at 5 years old. 29 infants had abnormal thyroid function test (10 infants with hypothyroxinemia of prematurity and 19 infants with transient thyroid abnormalities). There were no significant difference in the 2 years and 5 years developmental outcome between infants with and without hypothyroxinemia of prematurity (p-value>0.05); and between infants with and without transient thyroid abnormalities (p-value>0.05). There were no significant difference in neurological, visual and hearing impairment between infants with or without hypothyroxinemia of prematurity (p-value>0.05).ConclusionsHypothyroxinemia of prematurity or transient thyroid abnormalities in VLBW infants were not associated with poorer neurodevelopment and did not support the need for levothyroxine supplementation.

Hypothyroxinemia in extremely low birth weight infants

Hypothyroxinemia of prematurity (HOP) is a transient alteration in thyroid hormone availabilityfound in more than half of extremely low birth weight infants (ELBW) born at less than 30 weeks [1]. HOP is characterized by very low total T4 (TT4) and free T4 (FT4) levels with a normal or low thyroid stimulating hormone (TSH); TT4 and FT4 show a nadir at 7-10 days of life and they may remained low for the first 3-6 weeks of life depending from the severity of prematurity[2]. The reason for this hypothyroxinemia is multifactorial including the loss of maternal transfer of T4, immaturity of the hypothalamic-pituitary-thyroid axis, limited thyroid capacity to increase synthesis and metabolism, immaturity of peripheral tissue deiodination, reduced iodine availability and excessive losses, drugs affecting thyroid function and other adverse perinatal events [3]. Thyroid hormones are critical for a normal maturation of the developing brain in the fetus and infant, including cerebral neurogenesis, neural migration and differentiation, axonal and dendritic growth and synaptogenesis, gliogenesis, myelogenesis[4,5]. HOP has been associated with adverse neurodevelopmental outcomes such as deficits in developmental of motor, cognitive, language, memory, attention and it seem to be an independent risk factor for cognitive and behavioral deficits [6], however it is not clear the need to treat [7]. In a large trial of prophylacticthyroxine treatment van Wassenaer et al. [8]observed an 18-point improvement in mental development Bayley scores at 2 years postnatal age in infant born at less than 27 weeks gestation but, treated infants of more than 27 weeks had a 10-point deficit in Bayley scores. Overall there is insufficient evidence to determine whether use of thyroid hormones for treatment of preterm infants with transient hypothyroxinemia results in changes in neonatal morbidity and mortality, or reductions in neurodevelopmental impairments, but T4 supplementation may be beneficial in infants born at less than 27 weeks. Recently Scratch et al. [5], contrary to expectations, reported that in children born at less than 30 weeks’ gestation, higher concentrations of free thyroxine over the first 6 weeks of life were associated with poorer cognitive function at 7 years of age. Future studies should be directed in understanding unexpected endocrine patterns after very preterm birth.

Does transient hypothyroxinemia influence metabolic bone disease of prematurity?

Objective: To investigate the relationship between Metabolic Bone Disease (MBD) and Transient Hypothyroxinemia of Prematurity (THOP).Method: One hundred twenty-four infants, born in Marmara University Hospital with a gestational age ≤34 weeks, were enrolled. Clinical features were recorded. Serum TSH, free T4, total T4, calcium, phosphorus and total Alkaline Phosphatase (ALP) levels were determined in the first and third postnatal weeks. MBD was defined as a phosphorus level <4.5 mg/dl and/or ALP >900 IU/l. THOP was defined as a serum free and/or total thyroxine level lower than −1 SD for gestational age at the 7th postnatal day.Result: THOP was diagnosed in nineteen (15.3%) patients. MBD was diagnosed in 52 (41.9%) at the 3rd month. Low birth weight, low gestational age and prolonged parenteral nutrition were associated with MBD. Multivariate analysis documented a significant relationship solely between MBD and gestational age.Conclusion: The risk of MBD does not increase significantly in babies with THOP.

Étude prospective à une semaine de vie de la fonction thyroïdienne chez 97 prématurés consécutifs de terme inférieur à 32 semaines d’aménorrhée

Hypothyroxinemia of prematurity (HTOP) is associated with neurodevelopmental impairment in pre-term newborns born at less than 32 weeks of gestation (WG). HTOP is not clearly defined in the literature and there is no consensus on whether or not treatment of HTOP is beneficial. To describe the epidemiologic characteristics of HTOP and to determine the population at risk of HTOP. Ninety-seven pre-term newborns under 32 WG were prospectively included in this study. FT4 and thyroid-stimulating hormone (TSH) serum levels were assessed between day of life 5 and 7. HTOP was defined as serum level of FT4 0.80 ng/dl or less and TSH less than 20 mUI/l. The HTOP incidence was 29% in pre-term newborns under 32 WG and 64% in pre-term newborns 28 WG or less. FT4 levels were correlated with gestational age (P<0.001). The incidence of hypotension (61% vs 33%; P<0.05), patent ductus arteriosus (50% vs 17%; P<0.05), dopamine treatment (39% vs 16%; P<0.05), and hydrocortisone treatment (25% vs 6%; p<0.05) was higher in the HTOP group. Similarly, severe intracerebral hemorrhage (14% vs 0%; P<0.01) and hypothermic events under 36 °C (1.8 ± 1.7 vs 0.0 ± 0.4; P<0.05) were higher in the HTOP group. Incidence of HTOP is high in pre-term newborns born at less than 28 WG. Morbidity during the first week of life is higher in cases of HTOP. Whether or not treatment of all pre-term with l-thyroxin is beneficial is unknown. However, treatment of the subgroup of pre-term newborns under 28 WG with HTOP should be considered.

Clinical trials with thyroid hormone supplementation in preterm infants with transient hypothyroidism

The morbidity of transient hypothyroxinemia of prematurity （THOP） was high. There is controversial about thyroid hormone supplementation in THOP. Clinical studies suggest that thyroid hormone supplementation can reduce the incidence of patent ductus arteriosus,but no effect on the mortality and the incidence of respiratory disease. Thyroid hormone supplementation can improve the neurodevelopmental outcomes in infants with gestational age less than 28 weeks with THOP, but no effect on infants with gestational age more than 28 weeks. Future research should focus on the normal range of thyroid hormone according to gestational age in preterm infarlts, and randomized clinical trial well- designed stratified according to gestational age to study the long-term neurodevelopmental outcome of thyroid hormone replacement therapy in infants with THOP . Key words: Preterm; Transient hypothyroxinemia of prenmturity

Hypothyroxinemia of prematurity: cause, diagnosis and management

Infants born at extreme prematurity are at a high risk of developmental disability. A major risk factor for disability is having a low level of thyroid hormone, described as hypothyroxinemia, which is recognized to be a frequent phenomenon in these infants. At present, there is uncertainty among clinicians regarding the most appropriate method of managing hypothyroxinemia of prematurity. The literature suggests that some, but not all, forms of thyroid supplementation may reduce the incidence of disability in infants born at extreme prematurity. There is a pressing need to confirm the benefit of treatment and to establish the optimal way to treat transient hypothyroxinemia in these infants.

TRH Testing in Its Infancy

In contrast to primary hypothyroidism (1:3000 to 1:4000 births), central hypothyroidism due to pituitary or hypothalamic dysfunction is rare in newborns, with a prevalence of 1:25,000 to 1:100,000 births (1, 2). Although less common, central hypothyroidism is important to recognize because it is often accompanied by other pituitary hormone deficiencies that can cause life-threatening hypoglycemia. The hypothalamic-pituitary-thyroid axis undergoes dramatic changes in the transition from the fetal to newborn period (3). Thirty minutes after birth, newborns undergo a TSH surge to above 50 IU/liter, followed by a slow decrease to adult levels by 5–7 d of life. The TSH surge is accompanied by a rapid, 50% increase in total T4 levels that fall to normal infant levels by 3–5 d of life. However, the intrinsic variability of a maturing thyroid axis results in normal ranges for TSH and T4 values that vary among neonatal screening programs. Moreover, the trend toward an earlier discharge of infants and mothers from the hospital means that blood samples are being obtained earlier after birth. Considering these changes, interpreting the newborn screen must be done with sensitivity to the time of collection. When the newborn screen identifies a patient with a low T4 and elevated TSH level ( 40 IU/liter), the diagnosis of primary hypothyroidism is certain and therapy is begun. Although less common, other combinations of abnormal thyroid function tests are possible and usually result in additional testing. For example, if a screen is collected after 4–5 d, a case of mild primary hypothyroidism may have only a slightly elevated TSH and low to low-normal T4, mimicking central hypothyroidism. In contrast, patients with central hypothyroidism could experience a modified TSH surge followed by an increase in total T4 over the first 48–72 h of life, enough to push their T4 values into the normal or slightly elevated range. We know very little about the TSH surge in these patients. T4-binding globulin deficiency, euthyroid sick syndrome, and the hypothyroxinemia of prematurity can also cause low T4 associated with a normal TSH level. Importantly in these entities, free T4 values are usually normal. Unfortunately, immunoassays for free T4 are affected by low binding protein concentrations, resulting in falsely low free T4 levels (4), which further complicates their use in infants. To distinguish among these possibilities, additional testing is needed such as repetitive thyroid and pituitary hormone measurements and imaging of the thyroid and pituitary gland. Testing is an expensive and time-consuming approach and does not always result in a certain diagnosis. Therefore, alternative strategies may aid in the evaluation of these infants. In this issue of JCEM, van Tijn et al. (5) present their experience using the TRH stimulation test in a cohort of infants with low total T4 and normal TSH on newborn screen (6) and in whom they later confirmed multiple pituitary hormone deficiencies and pituitary dysmorphology with stimulation testing and imaging. After the synthesis of TRH in 1969, TRH stimulation testing was used to detect subtle states of thyroid gland dysfunction, acting as an amplifier to exaggerate underlying abnormalities in TSH secretion. As third and fourth generation TSH assays became more sensitive, however, the TRH stimulation test fell out of favor. Normal adults experience a maximum increase in serum TSH 30 min after TRH administration, and TSH levels gradually fall to basal levels by 120 min (7). In adults with pituitary or hypothalamic disease, the rise in TSH follows a different pattern. Often there is a delayed rise in TSH after TRH stimulation followed by a sustained increase. Sometimes the TSH rise is blunted or may be absent, which is more likely to be seen with pituitary disease in adults (8). Finally, an exaggerated TSH rise to TRH stimulation is occasionally noted in patients with central hypothyroidism (9, 10). This effect is thought to be due to the release of bioinactive TSH that is equally detected by immunoassays (11). These patterns have been verified in normal children and in children with hypopituitarism (12). Experience with the TRH test in newborns is extremely limited. There are significant differences in T4 metabolism in younger vs. older infants and children, which could produce different TRH stimulation test patterns in health and disease. The few available studies have used different TRH doses, collected TSH values at different times, and studied infants of various ages and clinical conditions (13–15). No other study has

Hypothyroxinemia of prematurity and the risk of cerebral white matter damage

Objective: Infants with hypothyroxinemia of prematurity (HOP) are at increased risk for neurodevelopmental dysfunction. Infants born near the end of the middle trimester are also at increased risk for an echolucency (EL) in the cerebral white matter, which reflects white matter damage and is the cranial ultrasound abnormality that best predicts neurodevelopmental dysfunction. We postulated that some of the increased risk of neurodevelopmental problems associated with HOP reflects an increased risk of EL. Study design: We studied 1414 infants weighing 500 to 1500 g who were born at 4 medical centers between 1991 and 1993. The infants had thyroxine blood levels measured during the first weeks of life, at least 1 of 3 cranial ultrasound scans performed at specified postnatal intervals, and their own and their mother’s hospital charts reviewed. Infants were classified by whether or not their first thyroxine level placed them in the lowest quartile among all infants in this sample (ie, <67.8 nmol/L, our definition of HOP, equivalent to <5.3 μg/dL). Results: After adjusting for such potential confounders as low gestational age and measures of illness severity, infants with HOP had twice the risk of EL as their peers with higher thyroxine levels. Conclusion: Our findings are consistent with the hypothesis that a “normal” blood thyroxine level protects infants born near the end of the middle trimester against the risk of cerebral white matter damage. (J Pediatr 1999;134:706-11)

Thyroid Function in Premature Infants: The Hypothyroxinemia of Prematurity

Advances of perinatal and neonatal medicine have been associated with a progressive reduction in mortality of premature infants and a progressive increase in number of the surviving very low birth weight (VLBW) cohort less than 28 to 32 weeks gestation age. Hypothalamic-pituitary-thyroid (HPT) function is immature in most premature infants, and this is particularly true of the VLBW group. Accumulated information has allowed development of a unique nosology of HPT system disorders in these infants to facilitate thyroid function testing, test interpretation, and patient management.

Hypothyroxinemia of Prematurity--Author's Response

Hypothyroxinemia of Prematurity--Author's Response

The Hypothyroxinemia of Prematurity

The Hypothyroxinemia of Prematurity

Hypothyroxinemia of Prematurity—Author’s Response

Hypothyroxinemia of Prematurity—Author’s Response