Starting Dose of Levothyroxine for the Treatment of Congenital Hypothyroidism

Hrytsiuk, Ihor; Gilbert, Ruth; Logan, Stuart; Pindoria, Sima; Brook, C. G. D.

doi:10.1001/archpedi.156.5.485

Cited by 52 publications

(32 citation statements)

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“…Moreover long-term follow-up studies found that high starting dose of L-T4 might cause more behavior problems reflecting increased anxiety, social withdrawal, and poorer concentration (Rovet and Ehrlich, 1995;Oerbeck et al, 2003). The starting dose of L-T4 we used is in conformity with what Campos and Rovet reported, but is much lower than the commonly used dose of 8~15 µg/(kg·d) or the 10.1~15.0 µg/(kg·d) reported from previous studies (Gruters et al, 1997;Hrytsiuk et al, 2002;Salerno et al, 2002). Patients with permanent CH require long-term substitution with a large dose of thyroxin (Rovet and Ehrlich, 1995).…”

Section: Discussionsupporting

confidence: 79%

Treatment and follow-up of children with transient congenital hypothyroidism

Yang

Zhu

Zhou

et al. 2005

J. Zhejiang Univ. - Sci. B

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Abstract:Objective: To study the clinical therapy and prognosis in children with transient congenital hypothyroidism (CH). Methods: Fifty-seven children with CH diagnosed after neonatal screening were treated with low-dosage levothyroxine (L-T4). Follow-up evaluation included the determination of TT3, TT4 and TSH serum levels and the assessment of thyroid gland morphology, bone age, growth development and development quotients (DQ). A full check-up was performed at age 2, when the affected children first discontinued the L-T4 treatment for 1 month, and one year later. Development quotients were compared with a control group of 29 healthy peers. Results: The initial L-T4 dosage administered was 3.21~5.81 µg/(kg·d) with an average of (16.25±3.87) µg/d. Mean duration of therapy was (28.09±9.56) months. No significant difference was found between study group and control group in the DQ test (average score (106.58±14.40) vs (102.4±8.6), P>0.05) and 96.49% of the CH children achieved a test score above 85. Bone age, 99mTc scans and ultrasonographic findings were all normal, and evaluation of physical development was normal too, as were the serum levels of TT3, TT4 and TSH after one year of follow-up. Conclusion: A L-T4 dosage of 3.21~5.81 µg/(kg·d) was found sufficient for the treatment of transient CH. The treated children showed satisfactory overall mental and physical development at age 2. So it is possible for CH children to stop taking medicine if their laboratory findings and physical development are all normal after regular treatment and 2~3 years of follow-up.

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Section: Discussionsupporting

confidence: 79%

Treatment and follow-up of children with transient congenital hypothyroidism

Yang

Zhu

Zhou

et al. 2005

J. Zhejiang Univ. - Sci. B

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“…Clinical and experimental studies have demonstrated that THs are essential for normal brain development. This was documented initially in children with congenital hypothyroidism (Leneman et al, 2001;Hindmarsh, 2002;Hrytsiuk et al, 2002;Salerno et al, 2002;Rovet and Daneman, 2003). These findings were followed by animal studies mainly focused on cerebellar development, which occurs largely postnatally (Koibuchi and Chin, 2000;Thompson and Potter, 2000;Morte et al, 2002;Singh et al, 2003).…”

Section: Nervous Systemmentioning

confidence: 97%

Thyroid hormones and the control of cell proliferation or cell differentiation: Paradox or duality?

Kress

Samarut

Plateroti

2009

Molecular and Cellular Endocrinology

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Thyroid hormones and the control of cell proliferation or cell differentiation: paradox or duality?. Molecular and Cellular Endocrinology, Elsevier, 2009, 313 (1-2) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. SummaryAmphibian metamorphosis perfectly illustrates a key paradox: thyroid hormones control diverse cellular processes depending on the tissue context. This point is also reinforced by a recent accumulation of evidence. For example, thyroid hormones and their nuclear receptor TRs have been described to function in different systems in synergy and/or in antagonism with other signaling pathways. This interaction helps explain their pleiotropic roles. This review summarizes the most important advances in this field, focusing in particular on the key action of thyroid hormones in controlling the balance between the processes of cell proliferation and cell differentiation in a few organs, with special attention paid to the intestine. We highlight similarities between the cellular and molecular events occurring during postnatal intestinal maturation at metamorphosis in amphibians, and comparable events observed at weaning in mice. 1-Introduction1.1 Thyroid hormone production Thyroid hormones (THs), L-thyroxine or T4 and 3,5,3'-L-triiodothyronine or T3, are essential for the development of several organs, including the central nervous system, skeleton, heart, intestine, skeletal muscle and sensory organs. Moreover, they also have important regulatory effects on oxygen consumption and metabolic rate (Oppenheimer et al., 1987). The follicular cells of the thyroid gland synthesize and secrete both hormones, but T4 is the most abundant. This process is under the control of circulating THs levels through the hypothalamuspituitary-thyroid feedback regulatory loop (rev. in Fredric and Wondisford, 2004). The intracellular concentration of T3 is dependent upon the uptake of T3 and T4, and their subsequent metabolism (Bianco and Kim, 2006). In fact, both hormones are actively transported across the cell membrane by specific transporter proteins, of which monocarboxylate transporter-8 is the best characterized (Dumitrescu et al., 2004;Friesema et al., 2004; rev. in Refetoff andDumitrescu, 2007 andVisser et al., 2007). Three iodothyronine deiodinase selenoenzymes (D1, D2 and D3) regulate TH activation and catabolism (Bianco and Kim, 2006). D1 and D2 catalyze the 5'-deiodination of T4 to its active metabolite T3. T3 is generated from the activity of D1, which is the main source of circulating T3. In contrast, D2 is the isoenzyme primarily responsible for local production of T3 in target cells. T3 derived from ...

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“…16 Indeed, it is not decided what constitutes the best initial dose level, which still remains an issue of considerable discussion, if not controversy. [20][21][22] Studies examining intellectual outcome in children with CH identified by newborn screening describe an average lowering of ϳ6 to 7 IQ points, 23 with values varying according to a number of methodologic factors. Such factors include the particular sample characteristics; treatment and management factors including starting dose and the particular age at which children were treated; test age; and the IQ test that was used and when it was given in relation to when test norms were developed.…”

mentioning

confidence: 99%

Children With Congenital Hypothyroidism and Their Siblings: Do They Really Differ?

Rovet

2005

Pediatrics

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ABSTRACT. Objective. Although favorable outcome is typically described in follow-up studies of children with congenital hypothyroidism (CH) identified by newborn screening, IQ reductions and persistent cognitive deficits are still reported. These findings are accounted for by disease and treatment variables as well as methodologic factors including choice of comparison group. Although siblings are ideal because they control for genetic and environmental influences, by definition they have different ages when tested, which can also introduce bias. Because we followed children with CH and their siblings over an extended period of time, there were a number of occasions when both groups were tested at the same age. The purpose of this study was to compare the results of children with CH and their unaffected siblings at the same age and with the same test. Methods. The sample consisted of 42 children with CH detected between 1975 and 1985 and their 42 siblings, all of whom were tested with the McCarthy or WechslerIntelligence Scale for Children-Revised (WISC-R) intelligence tests. Nineteen pairs of children were evaluated at 6 years with the McCarthy, and 30 pairs of children were evaluated at 7 or 9 years with the WISC-R. Recorded for children with CH were disease etiology, bone age and thyroxine levels at diagnosis, age at onset of treatment, and starting dosage of levothyroxine.Results. Paired t tests revealed that the CH group scored lower than siblings by 8.1 IQ points on the McCarthy and 6.2 points on the WISC-R. Factors contributing to the size of the CH-sibling IQ difference were (1) the etiology of hypothyroidism, reflecting the larger differences by those with athyreosis or an ectopic gland than dyshormonogenesis, and (2) the starting dosage of levothyroxine, with those initially treated with >8.2 g/kg per day having smaller CH-sibling differences than those given lower starting doses. There were no effects of bone age, thyroxine levels at diagnosis, or age at treatment onset. Conclusion It is now Ͼ2 decades since newborn screening programs for congenital hypothyroidism (CH) were first implemented. 1-3 A large number of studies on children so identified 4 have revealed that although screening and early treatment are beneficial in preventing the mental retardation associated previously with cretinism, 5 some children still experience subtle selective cognitive deficits 6-9 that persist into adolescence 10 and adulthood. 11 Their specific deficits depend on disease and treatment-related factors including etiology of hypothyroidism 12 and starting dosage of replacement hormone therapy. [13][14][15][16] Etiology is relevant because it reflects if and when the disease began in utero. 17 Although the fetal thyroid is supplemented by the maternal thyroid, it does not totally compensate all late gestational fetal needs. 18 Treatment factors are relevant because they determine the period of postnatal hypothyroidism. Although prompt treatment with a high initial dose level of levothyroxine (L-T4) is associated with ...

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Starting Dose of Levothyroxine for the Treatment of Congenital Hypothyroidism

Cited by 52 publications

References 53 publications

Treatment and follow-up of children with transient congenital hypothyroidism

Treatment and follow-up of children with transient congenital hypothyroidism

Thyroid hormones and the control of cell proliferation or cell differentiation: Paradox or duality?

Children With Congenital Hypothyroidism and Their Siblings: Do They Really Differ?

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