Congenital hypothyroidism in preterm infants: a 3- to 8-year longitudinal study in southern Thailand

2019 ◽  
Vol 32 (11) ◽  
pp. 1275-1282 ◽  
Author(s):  
Somchit Jaruratanasirikul ◽  
Waricha Janjindamai ◽  
Hutcha Sriplung
Keyword(s):  
Preterm Infants ◽  
Congenital Hypothyroidism ◽  
Medical Records ◽  
Neonatal Period ◽  
Initial Dosage ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Function Tests ◽  
Delayed Treatment ◽  
Southern Thailand ◽  
Hpt Axis

Abstract Background Preterm infants are at high risk of developing congenital hypothyroidism (CH) due to the immaturity of the hypothalamic-pituitary-thyroid (HPT) axis, loss of iodine supply from the mother and preterm health problems. Objectives To study the incidence and etiologies of CH in preterm infants who were born or admitted in our institute during 2010–2015. Methods The medical records of preterm infants diagnosed with CH as defined by the thyroid-stimulating hormone (TSH) level at the time of the first or second screening >10 mU/L and/or free T4 < 1.00 ng/dL were reviewed. Results Of 2777 preterm infants, 73 cases (2.6%) were diagnosed as CH. The average TSH levels at the first and second screenings were 20.85 and 15.42 mU/L, respectively. The patients were treated with thyroxine at an average initial dosage of 15 μg/kg/day. At 2–3 years of age, after thyroxine discontinuation for 6–10 weeks and regular thyroid function tests for 2 years, 58 patients (79.5%) were diagnosed as having transient CH and 15 patients (20.5%) were diagnosed as having permanent CH. We found no clinical or laboratory parameters in the neonatal period that could differentiate permanent from transient CH. Thyroid scintigraphy (99 m pertechnetate) revealed two patients (13.3%) with ectopic thyroid, one with thyroid hypoplasia (6.7%), eight with normal thyroid (53.3%) and four with enlarged thyroid (26.7%). Conclusions CH was common in preterm infants with an estimated incidence of 2.6%. Thyroxine should be given to preterm infants with higher initial values of TSH >10 mU/L in order to prevent delayed treatment of permanent CH that could be confirmed later.

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

2021 ◽  
Vol 12 ◽  
Author(s):  
Stephen H. LaFranchi
Keyword(s):  
Thyroid Hormone ◽  
Preterm Infants ◽  
Thyroid Function ◽  
Congenital Hypothyroidism ◽  
Clinical Manifestations ◽  
Thyroid Function Tests ◽  
Term Infants ◽  
Serum T4 ◽  
Preterm Babies ◽  
Hpt Axis

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 &lt;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.

scholarly journals The etiologies and incidences of congenital hypothyroidism before and after neonatal TSH screening program implementation: a study in southern Thailand

2018 ◽  
Vol 31 (6) ◽  
pp. 609-617 ◽  
Author(s):  
Somchit Jaruratanasirikul ◽  
Jutarat Piriyaphan ◽  
Tansit Saengkaew ◽  
Waricha Janjindamai ◽  
Hutcha Sriplung
Keyword(s):  
Congenital Hypothyroidism ◽  
Program Implementation ◽  
Medical Records ◽  
Screening Program ◽  
Thyroid Stimulating Hormone ◽  
Period 2 ◽  
Southern Thailand ◽  
Common Causes ◽  
Before And After ◽  
The Common

Abstract Background: Congenital hypothyroidism (CH) is one of the common causes of intellectual disability which can be prevented by early detection of an elevated thyroid stimulating hormone (TSH) level in the newborn and by treatment with thyroxine. In Thailand, neonatal TSH screening was implemented nationwide in 2005. The objective of the study was to determine the etiologies and the estimated incidences of CH in southern Thailand before and after the implementation of a neonatal TSH screening program in 2005. Methods: The medical records of pediatric patients who were diagnosed with primary CH at Songklanagarind Hospital during 1995–2013 were retrospectively reviewed. The study was divided into two time periods: study period 1 (SP1) (1995–2004) and study period 2 (SP2) (2005–2013), the time before and after TSH program implementation. Results: The most common form of CH during SP1 was overt permanent CH (66%), mostly caused by athyreosis or ectopic thyroid. In SP2, the most common form of CH was mild permanent CH (39%) (mostly due to dyshormonogenesis), followed by overt CH (32%) and transient CH (29%). The overall annual estimated incidence of CH per 10,000 live births in Songkhla Province was 1.69 (1:5021) in SP1, increasing to 4.77 (1:2238) in SP2; in all 14 provinces in southern Thailand, the estimated incidence was 1.24 (1:8094) in SP1 and 2.33 (1:4274) in SP2. Conclusions: Neonatal TSH screening has a significant impact on the increased detection of the mild form of permanent and transient CH cases, which may be important for the prevention of brain damage from less severe CH although this remains to be documented.

Reference intervals for neonatal thyroid function tests in the first 7 days of life

2018 ◽  
Vol 31 (10) ◽  
pp. 1113-1116 ◽  
Author(s):  
Michelle S. Jayasuriya ◽  
Kay W. Choy ◽  
Lit K. Chin ◽  
James Doery ◽  
Alice Stewart ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Medical Records ◽  
Reference Intervals ◽  
Thyroid Stimulating Hormone ◽  
Primary Hypothyroidism ◽  
Specific Reference ◽  
Rapid Decline ◽  
Thyroid Function Tests ◽  
Accurate Identification ◽  
Neonatal Hypothyroidism

Abstract Background: Prompt intervention can prevent permanent adverse neurological effects caused by neonatal hypothyroidism. Thyroid function changes rapidly in the first few days of life but well-defined age-specific reference intervals (RIs) for thyroid-stimulating hormone (TSH), free thyroxine (FT4) and free tri-iodothyronine (FT3) are not available to aid interpretation. We developed hour-based RIs using data mining. Methods: All TSH, FT4 and FT3 results with date and time of collection from neonates aged <7 days during 2005–2015 were extracted from the Monash Pathology database. Neonates with more than one episode of testing or with known primary hypothyroidism, identified by treating physicians or from medical records, were excluded from the analysis. The date and time of birth were obtained from the medical records. Results: Of the 728 neonates qualifying for the study, 569 had time of birth available. All 569 had TSH, 415 had FT4 and 146 had FT3 results. For age ≤24 h, 25–48 h, 49–72 h, 73–96 h, 97–120 h, 121–144 h and 145–168 h of life, the TSH RIs (2.5th–97.5th) (mIU/L) were 4.1–40.2, 3.2–29.6, 2.6–17.3, 2.2–14.7, 1.8–14.2, 1.4–12.7 and 1.0–8.3, respectively; the FT4 RIs (mean ± 2 standard deviation [SD]) (pmol/L) were 15.3–43.6, 14.7–53.2, 16.5–45.5, 17.8–39.4, 15.3–32.1, 14.5–32.6 and 13.9–30.9, respectively; the FT3 RIs (mean±2 SD) (pmol/L) were 5.0–9.4, 4.1–9.1, 2.8–7.8, 2.9–7.8, 3.5–7.2, 3.4–8.0 and 3.8–7.9, respectively. Conclusions: TSH and FT4 were substantially high in the first 24 h after birth followed by a rapid decline over the subsequent 168 h. Use of hour-based RIs in newborns allows for more accurate identification of neonates who are at risk of hypothyroidism.

scholarly journals Hyperoxia Leads to Transient Endocrine Alterations in the Neonatal Rat During Postnatal Development

2021 ◽  
Vol 9 ◽  
Author(s):  
Kowallick Mirjam ◽  
Meray Serdar ◽  
Boyka Markova ◽  
Eva Salveridou ◽  
Ursula Felderhoff-Müser ◽  
...  
Keyword(s):  
Preterm Infants ◽  
Endocrine System ◽  
Thyroid Stimulating Hormone ◽  
Neonatal Rat ◽  
Enzyme Linked Immunosorbent Assay ◽  
High Prevalence ◽  
Pathogenetic Factor ◽  
Short And Long Term ◽  
Hpt Axis ◽  
Endocrine Alterations

Introduction: High oxygen concentrations have been identified as one factor contributing to the pathogenesis of the retinopathia of prematurity, chronic lung disease of the preterm infant and preterm brain injury. Preterm infants also show short- and long-term alterations of the endocrine system. If hyperoxia is one pathogenetic factor has not been investigated yet. With regard to the high prevalence of neurodevelopmental impairments in preterm infants, the hypothalamus-pituitary-thyroid (HPT) axis, the hypothalamus-pituitary-adrenal (HPA) axis and the hypothalamus-pituitary-somatotropic (HPS) axis are of special interest due to their important role in neurodevelopment.Objective: The aim of this study was to investigate the effect of hyperoxia on the endocrine system in the neonatal rat by analyzing the activities of the HPT, HPA and HPS axes, respectively.Methods: Three-days old Wistar rats were exposed to hyperoxia (oxygen 80%, 48 h). On postnatal day 5 (P5) and P11, transcript levels of thyroid-stimulating hormone (TSH), proopiomelanocortin and growth hormone (GH) were analyzed in pituitary sections by in situ hybridization. Serologic quantification of TSH and thyroxine (T4), adrenocorticotropic hormone and GH were performed by Multiplex analysis and Enzyme-linked Immunosorbent Assay.Results: At P5, significantly lower GH levels were observed in pituitaries (mRNA) and in sera of rats exposed to hyperoxia. Serum TSH was significantly elevated without changes in T4.Conclusion: This is the first study demonstrating transient endocrine alterations following hyperoxia in the neonatal rat making oxygen a possible contributor to the pathogenesis of endocrine alterations seen in preterm infants. Considering the detrimental multi-organ effects of hyperoxia on the immature organism, a rational use of therapeutic oxygen in the treatrnent of preterm infants is of utmost importance.

scholarly journals Thyroid dysfunction in preterm infants born before 32 gestational weeks

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Hye-Rim Kim ◽  
Young Hwa Jung ◽  
Chang Won Choi ◽  
Hye Rim Chung ◽  
Min-Jae Kang ◽  
...  
Keyword(s):  
Preterm Infants ◽  
Thyroid Dysfunction ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Function Tests ◽  
Academic Center ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Delayed Maturation ◽  
Levothyroxine Treatment ◽  
Serum Tsh

Abstract Background Thyroid hormones are critical for growth and brain development during the newborn period and infancy. Because of delayed maturation of the hypothalamic-pituitary-thyroid axis in preterm infants, thyroid dysfunction is common, and thyroid stimulating hormone (TSH) elevation is often delayed in preterm infants. The objective of this study was to determine the incidence of thyroid dysfunction requiring levothyroxine treatment and to identify its risk factors in preterm infants. Methods A retrospective cohort study was performed on preterm infants who were born before 32 gestational weeks and admitted to a single tertiary academic center for more than 8 weeks between January 2008 and December 2014. In these infants, serial thyroid function tests (TFTs) measuring serum TSH and free thyroxine (fT4) were routinely performed at 1, 3, and 6 weeks of postnatal age. Results Of the 220 preterm infants enrolled, 180 infants underwent TFTs at 1, 3, and 6 weeks of postnatal age and were included in the study. Of the 180 infants, 35 infants (19.4%) were started on levothyroxine treatment based on the results of serial TFTs. Among the 35 infants who were treated with levothyroxine, 16 infants (45.7%) had normal results on the initial TFT. Three of these 16 infants continued to have normal results on the second TFT. Thyroid dysfunction requiring levothyroxine treatment was significantly associated with maternal pregnancy-induced hypertension (adjusted odds ratio 2.64, 95% confidence interval 1.02–6.81). Conclusions Thyroid dysfunction requiring levothyroxine treatment occurred in nearly one-fifth of preterm infants born before 32 gestational weeks. Nearly half of the preterm infants who were treated with levothyroxine had normal TSH and fT4 levels at 1 week of postnatal age. The findings of the present study suggest that serial TFTs is important to find preterm infants who require levothyroxine treatment.

scholarly journals Delayed Diagnosis of Congenital Hypothyroidism in a Child with Trisomy 21 and Biotinidase Deficiency and Successful Use of Levothyroxine Sodium Oral Solution

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Matthew M. Feldt
Keyword(s):  
Congenital Hypothyroidism ◽  
Trisomy 21 ◽  
Delayed Diagnosis ◽  
Thyroid Stimulating Hormone ◽  
Biotinidase Deficiency ◽  
Subsequent Treatment ◽  
Oral Solution ◽  
Endocrine Disorders ◽  
Thyroid Function Tests ◽  
Treatment Administration

Endocrine disorders are more common and appear earlier in people with trisomy 21 (T21) than in the general population, with thyroid dysfunction being the most common, including both congenital and acquired hypothyroidism. The treatment for biotinidase deficiency, a condition that occurs in approximately 1 : 110,000 people, is with biotin (vitamin B7) supplementation. However, biotin can interfere with endocrine laboratory assays and cause falsely low thyroid-stimulating hormone (TSH) and elevated free thyroxine (FT4) levels. This can interfere with the timely diagnosis and subsequent treatment of congenital hypothyroidism (CH). This case report describes an infant with partial biotinidase deficiency that was confirmed on day 10 of life. Routine screening erroneously reported “normal” TSH that caused delayed diagnosis of CH due to interference with the TSH assay from concurrent biotin use. Once the biotin treatment was withheld for 4 days and the thyroid function tests repeated, an elevated TSH became apparent. Treatment with tablet levothyroxine (L-T4) was started and subsequently changed to L-T4 oral solution (Tirosint®-SOL) to overcome treatment administration difficulties encountered with the tablet form. This resulted in improved TSH control due to more accurate and consistent dosing compared with the tablet formulation. This is the first report of the use of L-T4 oral solution in an infant with T21 and biotinidase deficiency.

scholarly journals DIAGNOSIS OF ENDOCRINE DISEASE: Congenital hypothyroidism: update and perspectives

2018 ◽  
Vol 179 (6) ◽  
pp. R297-R317 ◽  
Author(s):  
C Peters ◽  
A S P van Trotsenburg ◽  
N Schoenmakers
Keyword(s):  
Thyroid Gland ◽  
Congenital Hypothyroidism ◽  
Epidemiological Data ◽  
Developed Countries ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Hormone ◽  
Hormone Production ◽  
Neonatal Hypothyroidism ◽  
Developmental Abnormalities ◽  
Delayed Treatment

Congenital hypothyroidism (CH) may be primary, due to a defect affecting the thyroid gland itself, or central, due to impaired thyroid-stimulating hormone (TSH)-mediated stimulation of the thyroid gland as a result of hypothalamic or pituitary pathology. Primary CH is the most common neonatal endocrine disorder, traditionally subdivided into thyroid dysgenesis (TD), referring to a spectrum of thyroid developmental abnormalities, and dyshormonogenesis, where a defective molecular pathway for thyroid hormonogenesis results in failure of hormone production by a structurally intact gland. Delayed treatment of neonatal hypothyroidism may result in profound neurodevelopmental delay; therefore, CH is screened for in developed countries to facilitate prompt diagnosis. Central congenital hypothyroidism (CCH) is a rarer entity which may occur in isolation, or (more frequently) in association with additional pituitary hormone deficits. CCH is most commonly defined biochemically by failure of appropriate TSH elevation despite subnormal thyroid hormone levels and will therefore evade diagnosis in primary, TSH-based CH-screening programmes. This review will discuss recent genetic aetiological advances in CH and summarize epidemiological data and clinical diagnostic challenges, focussing on primary CH and isolated CCH.

Severe consumptive hypothyroidism caused by multiple infantile hepatic haemangiomas

2018 ◽  
Vol 31 (7) ◽  
pp. 823-827 ◽  
Author(s):  
Enver Simsek ◽  
Meliha Demiral ◽  
Elif Gundoğdu
Keyword(s):  
Congenital Hypothyroidism ◽  
Abdominal Ultrasound ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Function Tests ◽  
Reverse T3 ◽  
Iodothyronine Deiodinase ◽  
Euthyroid Status ◽  
Thyroxine Replacement ◽  
Magnetic Resonance Imaging Mri ◽  
High Index Of Suspicion

Abstract Background Infantile hepatic haemangiomas (IHHs) produce an excess of the thyroid hormone inactivating enzyme type-3 iodothyronine deiodinase (D3), leading to rapid degradation of thyroid hormones and consumptive hypothyroidism. The L-thyroxine replacement dose in patients with consumptive hypothyroidism is inappropriately higher than that in congenital hypothyroidism. Case presentation A 4-month-old boy presented with abdominal distention. Thyroid function tests (TFTs) revealed an elevated thyroid-stimulating hormone (TSH) level of 177 mU/L, normal free thyroxine (fT4) of 1.23 ng/dL, low free tri-iodothyronine (fT3) of 1.55 pg/mL and increased reverse T3 (rT3) of 1240 ng/dL. Abdominal ultrasound and magnetic resonance imaging (MRI) revealed multiple IHHs. Based on his TFTs, ultrasonography and MRI evidence, he was diagnosed with consumptive hypothyroidism, and L-thyroxine replacement at 15 μg/kg/day was started. The L-thyroxine dose was increased gradually to 35 μ/kg/day until a stabilising euthyroid status was achieved. By the age of 8 months, the TSH concentration was decreased to normal levels; the L-thyroxine dose was gradually reduced and finally discontinued at the age of 12 months. Repeat abdominal ultrasound and MRI revealed a reduction in the number and size of the haemangiomas. The TFTs were at normal reference levels. The patient remains in active follow-up. Conclusions Neonatal screening for congenital hypothyroidism is usually negative in cases of IHH, as seen in our case. A high index of suspicion is necessary to diagnose hypothyroidism in cases of IHH. The present case required very high doses of levothyroxine to achieve a euthyroid status. In cases of hypothyroidism in the first year of life with consumptive hypothyroidism caused by hepatic haemangioma, aggressive L-thyroxine replacement is required with no upper limit. The dose should be increased gradually until a stabilising euthyroid status is achieved.

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