scholarly journals Thyroid Function Disturbance and Type 3 Iodothyronine Deiodinase Induction after Myocardial Infarction in Rats—A Time Course Study

Endocrinology ◽  
2007 ◽  
Vol 148 (10) ◽  
pp. 4786-4792 ◽  
Author(s):  
Emerson L. Olivares ◽  
Michelle P. Marassi ◽  
Rodrigo S. Fortunato ◽  
Alba C. M. da Silva ◽  
Ricardo H. Costa-e-Sousa ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Thyroid Hormone ◽  
Thyroid Function ◽  
Time Course ◽  
Thyroid Function Tests ◽  
Iodothyronine Deiodinase ◽  
Serum T4 ◽  
Time Course Study ◽  
Type 3 ◽  
Serum Tsh

In humans, there is a significant decrease in serum T3 and increase in rT3 at different time points after myocardial infarction, whereas serum TSH and T4 remain unaltered. We report here a time course study of pituitary-thyroid function and thyroid hormone metabolism in rats subjected to myocardial infarction by left coronary ligation (INF). INF- and sham-operated animals were followed by serial deiodination assays and thyroid function tests, just before, and 1, 4, 8, and 12 wk after surgery. At 4 and 12 wk after INF, liver type 1 deiodinase activity was significantly lower, confirming tissue hypothyroidism. Type 3 deiodinase (D3) activity was robustly induced 1 wk after INF only in the infarcted myocardium. Reminiscent of the consumptive hypothyroidism observed in patients with large D3-expressing tumors, this induction of cardiac D3 activity was associated with a decrease in both serum T4 (∼50% decrease) and T3 (37% decrease), despite compensatory stimulation of the thyroid. Thyroid stimulation was documented by both hyperthyrotropinemia and radioiodine uptake. Serum TSH increased by 4.3-fold in the first and 3.1-fold in the fourth weeks (P < 0.01), returning to the basal levels thereafter. Thyroid sodium/iodide-symporter function increased 1 wk after INF, accompanying the increased serum TSH. We conclude that the acute decrease in serum T4 and T3 after INF is due to increased thyroid hormone catabolism from ectopic D3 expression in the heart.

scholarly journals Thyroid function and effect of aging in combined hetero/homozygous mice deficient in thyroid hormone receptors alpha and beta genes

2002 ◽  
Vol 172 (1) ◽  
pp. 177-185 ◽  
Author(s):  
RE Weiss ◽  
O Chassande ◽  
EK Koo ◽  
PE Macchia ◽  
K Cua ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptors ◽  
Thyroid Function Tests ◽  
Wild Type ◽  
Heterozygous Mouse ◽  
Tsh Secretion ◽  
Homozygous Deletions ◽  
Serum Tsh

The maintenance of thyroid hormone (TH) homeostasis is dependent on the synthesis and secretion of TH regulated by TSH. This is achieved, in turn, by the negative feedback of TH on TSH secretion and synthesis, which requires the interaction with TH receptors (TRs). Derived by alternative splicing of two gene transcription products, three TRs (TRbeta1, TRbeta2 and TRalpha1) interact with TH while another, TRalpha2, binds to DNA but not to TH. In this study we compare the results of thyroid function tests in mice with deletions of the TRalpha and TRbeta genes alone and present novel data on mice that are double homozygous and combined heterozygous. Homozygous deletions of both the TRalpha and TRbeta in the same mouse (TRalphao/o; TRbeta-/-) resulted in serum TSH values only slightly lower than those in athyreotic, Pax8 knockout mice. Whereas the absence of TRalpha alone does not cause resistance to TH, the absence of TRbeta in the presence of TRalpha results in a 205, 169, 544% increase in serum thyroxine (T(4)), triiodothyronine (T(3)) and TSH concentrations respectively. However, in the absence of TRbeta, loss of one TRalpha allele can worsen the resistance to TH with a 243 and 307% increase in T(4) and T(3) respectively. Similarly, while the heterozygous mouse with a single TRbeta allele shows no alteration in thyroid function, the concomitant deletion of TRalpha brings about mild but significant resistance to TH. Furthermore, the severity of the resistance to TH was noted to decrease with age in parallel with the decrease in serum free T(4) values also seen in wild-type mice. These results demonstrate that (1) unliganded TRalpha or TRbeta are not absolutely necessary for the upregulation of TSH; (2) TRbeta but not TRalpha is sufficient for TH-mediated downregulation of TSH; and (3) TRalpha may partially substitute for TRbeta in mediating a partial TH-dependent TSH suppression.

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 <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 Placenta Passage of the Thyroid Hormone Analog DITPA to Male Wild-Type and Mct8-Deficient Mice

Endocrinology ◽  
2014 ◽  
Vol 155 (10) ◽  
pp. 4088-4093 ◽  
Author(s):  
Alfonso Massimiliano Ferrara ◽  
Xiao-Hui Liao ◽  
Pilar Gil-Ibáñez ◽  
Juan Bernal ◽  
Roy E. Weiss ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Monocarboxylate Transporter ◽  
Thyroid Function Tests ◽  
Wild Type ◽  
Peripheral Tissues ◽  
Hormone Analog ◽  
Neurological Phenotype ◽  
Serum T4 ◽  
Mct8 Deficiency ◽  
Serum Tsh

Abstract Monocarboxylate transporter 8 (MCT8) deficiency causes severe X-linked intellectual and neuropsychological impairment associated with abnormal thyroid function tests (TFTs) producing thyroid hormone (TH) deprivation in brain and excess in peripheral tissues. The TH analog diiodothyropropionic acid (DITPA) corrected the TFTs abnormalities and hypermetabolism of MCT8-deficient children but did not improve the neurological phenotype. The latter result was attributed to the late initiation of treatment. Therefore, we gave DITPA to pregnant mice carrying Mct8-deficient embryos to determine whether DITPA, when given prenatally, crosses the placenta and affects the serum TFTs and cerebral cortex of embryos. After depletion of the endogenous TH, Mct8-heterozygous pregnant dams carrying both wild-type (Wt) and Mct8-deficient (Mct8KO) male embryos were given DITPA. Effects were compared with those treated with levothyroxine (L-T4). With DITPA treatment, serum DITPA concentration was not different in the two genotypes, which produced equal effect on serum TSH levels in both groups of pups. In contrast, with L-T4 treatment, TSH did not normalize in Mct8KO pups whereas it did in the Wt littermates and dams despite higher concentration of serum T4. Finally, both treatments similarly modulated the expression of the TH-dependent genes Shh, Klf9, and Aldh1a3 in brain. Thus, the ability of DITPA to cross the placenta, its thyromimetic action on the expression of TH-dependent genes in brain, and its better accessibility to the pituitary than L-T4, as assessed by serum TSH, make DITPA a candidate for the prenatal treatment of MCT8 deficiency.

scholarly journals Challenges in Interpretation of Thyroid Function Tests in Pregnant Women with Autoimmune Thyroid Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Ulla Feldt-Rasmussen ◽  
Anne-Sofie Bliddal Mortensen ◽  
Åse Krogh Rasmussen ◽  
Malene Boas ◽  
Linda Hilsted ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Thyroid Diseases ◽  
Interindividual Variation ◽  
Reference Ranges ◽  
Thyroid Function Tests ◽  
Autoimmune Thyroid ◽  
Function Tests ◽  
Serum Tsh ◽  
In Pregnancy

Physiological changes during gestation are important to be aware of in measurement and interpretation of thyroid function tests in women with autoimmune thyroid diseases. Thyroid autoimmune activity is decreasing in pregnancy. Measurement of serum TSH is the first-line screening variable for thyroid dysfunction also in pregnancy. However, using serum TSH for control of treatment of maternal thyroid autoimmunity infers a risk for compromised foetal development. Peripheral thyroid hormone values are highly different among laboratories, and there is a need for laboratory-specific gestational age-related reference ranges. Equally important, the intraindividual variability of the thyroid hormone measurements is much narrower than the interindividual variation (reflecting the reference interval). The best laboratory assessment of thyroid function is a free thyroid hormone estimate combined with TSH. Measurement of antithyroperoxidase and/or TSH receptor antibodies adds to the differential diagnosis of autoimmune and nonautoimmune thyroid diseases.

scholarly journals The 5′-Deiodinases Are Not Essential for the Fasting-Induced Decrease in Circulating Thyroid Hormone Levels in Male Mice: Possible Roles for the Type 3 Deiodinase and Tissue Sequestration of Hormone

Endocrinology ◽  
2014 ◽  
Vol 155 (8) ◽  
pp. 3172-3181 ◽  
Author(s):  
Valerie Anne Galton ◽  
Arturo Hernandez ◽  
Donald L. St. Germain
Keyword(s):  
Thyroid Hormone ◽  
Male Mice ◽  
Wild Type ◽  
Serum T4 ◽  
The Mean ◽  
Thyroid Hormone Levels ◽  
Tissue Contents ◽  
Type 3 ◽  
Deficient Mice ◽  
Serum Tsh

Fasting in rodents is characterized by decreases in serum T4 and T3 levels but no compensatory increase in serum TSH level. The types 1 and 2 deiodinases (D1 and D2) are postulated to play key roles in mediating these changes. However, serum T4 and T3 levels in fasted 5′-deiodinase-deficient mice decreased by at least the same percentage as that observed in wild-type mice, whereas serum TSH level was unaffected. D3 activity was increased in kidney, muscle, and liver up to 4-fold during fasting, and the mean serum rT3 level was increased 3-fold in fasted D1-deficient mice, compared with fed animals. In wild-type mice, the tissue contents of T4 and T3 in liver, kidney, and muscle were unchanged or increased in fasted animals, and after the administration of [125I]T4 or [125I]T3, the radioactive content in the majority of tissues from fasted mice was increased 2- or 4-fold, respectively. These findings suggest that the observed fasting-induced reductions in the circulating T3 and T4 levels are mediated in part by increased D3 activity and by the sequestration of thyroid hormone and their metabolites in tissues. Studies performed in D3-deficient mice demonstrating a blunting of the fasting-induced decrease in serum T4 and T3 levels were consistent with this thesis. Thus, the systemic changes in thyroid hormone economy as a result of acute food deprivation are not dependent on the D1 or D2 but are mediated in part by sequestration of T4 and T3 in tissues and their enhanced metabolism by the D3.

scholarly journals DIAGNOSTIC DILEMMA IN DISCORDANT THYROID FUNCTION TESTS DUE TO THYROID HORMONE AUTOANTIBODIES

2017 ◽  
Vol 3 (1) ◽  
pp. e22-e25 ◽  
Author(s):  
Panudda Srichomkwun ◽  
Neal H. Scherberg ◽  
Jasminka Jakšić ◽  
Samuel Refetoff
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Thyroid Function Tests ◽  
Diagnostic Dilemma ◽  
Thyroid Hormone Autoantibodies ◽  
Function Tests

scholarly journals AMIODARON SEBAGAI OBAT ANTI ARITMIA DAN PENGARUHNYA TERHADAP FUNGSI TIROID

2013 ◽  
Vol 3 (2) ◽  
Author(s):  
Starry H. Rampengan
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Function ◽  
Hormone Replacement ◽  
Type I ◽  
Peripheral Tissues ◽  
Hormone Synthesis ◽  
Thyroid Hormone Metabolism ◽  
Serum T4 ◽  
Life Threatening

Abstract: Amiodarone is a highly effective anti-arrhythmic agent used in certain arrhythmias from supraventricular tachycardia to life-threatening ventricular tachycardia. Its use is associated with numerous side-effects that could deteriorate a patient’s condition. Consequently, a clinician should consider the risks and benefits of amiodarone before initiating the treatment.The thyroid gland is one of the organs affected by amiodarone. Amiodarone and its metabolite desethyl amiodaron induce alterations in thyroid hormone metabolism in the thyroid gland, peripheral tissues, and probably also in the pituitary gland. These actions result in elevations of serum T4 and rT3 concentrations, transient increases in TSH concentrations, and decreases in T3 concentrations. Both hypothyroidism and hyperthyroidism are prone to occur in patients receiving amiodarone. Amiodarone-induced hypothyroidism (AIH) results from the inability of the thyroid to escape from the Wolff-Chaikoff effect and is readily managed by either discontinuation of amiodarone or thyroid hormone replacement. Amiodarone-induced thyrotoxicosis (AIT) may arise from either iodine-induced excessive thyroid hormone synthesis (type I, usually with underlying thyroid abnormality), or destructive thyroiditis with release of preformed hormones (type II, commonly with apparently normal thyroid glands). Therefore, monitoring of thyroid function should be performed in all amiodarone-treated patients to facilitate early diagnosis and treatment of amiodarone-induced thyroid dysfunction. Key words: Amiodarone, thyroid function, side effect, management, monitoring.     Abstrak: Amiodaron adalah obat antiaritmia yang cukup efektif dalam menangani beberapa keadaaan aritmia mulai dari supraventrikuler takikardia sampai takikardia ventrikuler yang mengancam kehidupan. Namun penggunaan obat ini ternyata menimbulkan efek samping pada organ lain yang dapat menimbulkan perburukan keadaan pasien. Sehingga, dalam penggunaan amiodaron, klinisi juga harus menimbang keuntungan dan kerugian yang ditimbulkan oleh obat ini. Salah satu organ yang dipengaruhi oleh amiodaron adalah kelenjar tiroid. Amiodaron dan metabolitnya desetil amiodaron memengaruhi hormon tiroid pada kelenjar tiroid, jaringan perifer, dan mungkin pada pituitari. Aksi amiodaron ini menyebabkan peningkatan T4, rT3 dan TSH, namun menurunkan kadar T3. Hipotiroidisme dan tirotoksikosis dapat terjadi pada pasien yang diberi amiodaron. Amiodarone-induced hypothyroidism (AIH) terjadi karena ketidakmampuan tiroid melepaskan diri dari efek Wolff Chaikof, dan dapat ditangani dengan pemberian  hormon substitusi T4 atau penghentian amiodaron. Amiodarone-induced thyrotoxicosis (AIT) terjadi karena sintesis hormon tiroid yang berlebihan yang diinduksi oleh iodium (tipe I, biasanya sudah mempunyai kelainan tiroid sebelumnya) atau karena tiroiditis destruktif yang disertai pelepasan hormon tiroid yang telah terbentuk (tipe II, biasanya dengan kelenjar yang normal). Pemantauan fungsi tiroid seharusnya dilakukan pada semua pasien yang diberi amiodaron untuk memfasilitasi diagnosis dan terapi yang dini terjadinya  disfungsi tiroid yang diinduksi amiodaron. Kata Kunci: Amiodaron, fungsi tiroid, efek samping, penanganan, pemantauan.

Iodide Metabolism and Effects

2020 ◽  
pp. 25-33
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Dietary Supplement ◽  
Thyroid Function ◽  
Thyroid Stimulating Hormone ◽  
Hormone Synthesis ◽  
Serum Tsh ◽  
Tsh Stimulation ◽  
Sensitive Marker

Iodine (I2) is essential in the synthesis of thyroid hormones T4 and T3 and functioning of the thyroid gland. Both T3 and T4 are metabolically active, but T3 is four times more potent than T4. Our body contains 20-30 mg of I2, which is mainly stored in the thyroid gland. Iodine is naturally present in some foods, added to others, and available as a dietary supplement. Serum thyroid stimulating hormone (TSH) level is a sensitive marker of thyroid function. Serum TSH is increased in hypothyroidism as in Hashimoto's thyroiditis. In addition to regulation of thyroid function, TSH promotes thyroid growth. If thyroid hormone synthesis is chronically impaired, TSH stimulation eventually may lead to the development of a goiter. This chapter explores the iodide metabolism and effects of Hashimoto's disease.

Subclinical hypothyroidism

2011 ◽  
pp. 543-547
Author(s):  
Jayne A. Franklyn
Keyword(s):  
Thyroid Function ◽  
Subclinical Hypothyroidism ◽  
Expert Panel ◽  
Elevated Serum ◽  
Thyroid Stimulating Hormone ◽  
Free Thyroxine ◽  
Thyroid Function Tests ◽  
Free Triiodothyronine ◽  
Function Tests ◽  
Serum Tsh

Subclinical hypothyroidism is defined biochemically as the association of a raised serum thyroid-stimulating hormone (TSH) concentration with normal circulating concentrations of free thyroxine (T4) and free triiodothyronine (T3). The term subclinical hypothyroidism implies that patients should be asymptomatic, although symptoms are difficult to assess, especially in patients in whom thyroid function tests have been checked because of nonspecific complaints such as tiredness. An expert panel has recently classified individuals with subclinical hypothyroidism into two groups (1): (1) those with mildly elevated serum TSH (typically TSH in the range 4.5–10.0 mU/l) and (2) those with more marked TSH elevation (serum TSH >10.0 mU/l).

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