PITUITARY-THYROID FUNCTION IN THYROTOXIC PATIENTS IN RELATION TO LONG-ACTING THYROID STIMULATOR (LATS) LEVELS

1970 ◽  
Vol 65 (4) ◽  
pp. 577-582 ◽  
Author(s):  
Minoru Fukuchi ◽  
Tohru Matsuoka ◽  
Tadashi Inoue ◽  
Kiyoshi Miyai ◽  
Yuichi Kumahara
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Elevated Serum ◽  
Antithyroid Drug ◽  
Initial Values ◽  
Long Acting ◽  
Serum Tsh

ABSTRACT Serial changes in TSH, LATS, and thyroxine levels in the sera were studied following administration of an antithyroid drug or a thyroid hormone to thyrotoxic patients who became euthyroid after treatment. These changes were simultaneously determined by means of human TSH radioimmunoassay, McKenzie's bioassay. and the method of Murphy, respectively. Administration of 1-methyl-2-mercaptoimidazole (MMI) led to a decrease in thyroxine concentration and to a 6–10 times increase of the initial values in serum TSH concentration. Following administration of thyroxine at the end of the MMI treatment, the elevated serum TSH was rapidly decreased with an increase in thyroxine concentration. LATS activity, however, showed no significant changes throughout these experiments in which the reciprocal changes between TSH and thyroxine concentrations were observed.

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).

scholarly journals Effects of Maternal Levels of Thyroid Hormone (TH) on the Hypothalamus-Pituitary-Thyroid Set Point: Studies in TH Receptor β Knockout Mice

Endocrinology ◽  
2007 ◽  
Vol 148 (11) ◽  
pp. 5305-5312 ◽  
Author(s):  
Manuela Alonso ◽  
Charles Goodwin ◽  
XiaoHui Liao ◽  
David Page ◽  
Samuel Refetoff ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Elevated Serum ◽  
The Other ◽  
Long Term Effects ◽  
Intrauterine Environment ◽  
Set Point ◽  
Other Hand ◽  
Wild Type Phenotype ◽  
Pituitary Thyroid Axis ◽  
Serum Tsh

A level of thyroid hormone (TH) in agreement with the tissue requirements is essential for vertebrate embryogenesis and fetal maturation. In this study we evaluate the immediate and long-term effects of incongruent intrauterine TH levels between mother and fetus using the TH receptor (TR) β−/− knockout mouse as a model. We took advantage of the fact that the TRβ−/− females have elevated serum TH but are not thyrotoxic due to resistance to TH. We used crosses between heterozygotes with wild-type phenotype (TRβ+/−) males and TRβ−/− females, with a hyperiodothyroninemic (high T4 and T3 levels) intrauterine environment (TH congruent with the TRβ−/− fetus and excessive for the TRβ+/− fetus), and reciprocal crosses between TRβ−/− males and TRβ+/− females, providing a euiodothyroninemic intrauterine environment. We found that TRβ−/− dams had reduced litter sizes and pups with lower birth weight but preserved the mendelian TRβ−/− to TRβ+/− ratio at birth, indicating that the incongruous TH levels did not decrease intrauterine survival of a specific genotype. The results of studies in newborns demonstrate that TRβ+/− pups born to TRβ−/− dams have persistent suppression of serum TSH without a peak. On the other hand, TRβ−/− pups born to TRβ+/− dams have lower serum TSH at birth and a tendency to peak higher, compared with TRβ−/− pups born to TRβ−/− dams. The studies in the adult progeny demonstrate that TRβ+/− mice born to TRβ−/− dams and, thus, exposed to higher intrauterine TH levels, have greater resistance to TH at the level of the pituitary when stimulated with TRH. On the other hand, TRβ−/− mice born to TRβ+/− dams and, thus, deprived of TH in uterine life, were more sensitive to TH when similarly stimulated with TRH. Thus, TH exposure in utero has an effect on the regulatory set point of the hypothalamus-pituitary-thyroid axis, which can be seen early in life and persists into adulthood.

Familial Partial Peripheral and Pituitary Resistance to Thyroid Hormone: A Frequently Missed Diagnosis?

PEDIATRICS ◽  
1986 ◽  
Vol 78 (6) ◽  
pp. 1114-1122
Author(s):  
Nancy J. Hopwood ◽  
Sue Ellyn Sauder ◽  
Brahm Shapiro ◽  
James C. Sisson
Keyword(s):  
Thyroid Hormone ◽  
Family Members ◽  
Elevated Serum ◽  
Thyroid Stimulating Hormone ◽  
Thyrotropin Releasing Hormone ◽  
Resistance To Thyroid Hormone ◽  
Releasing Hormone ◽  
Thyroxine Therapy ◽  
Missed Diagnosis ◽  
Serum Tsh

The diagnosis of partial peripheral and pituitary resistance to thyroid hormone was ultimately made in two boys, 7 and 9 years of age, and a 10-year-old girl who had goiters and hyperthyroxinemia. The boys were treated with propythiouracil and/or thyroidectomy or iodine 131 for suspected thyrotoxicosis but had poorly suppressible serum thyroid-stimulating hormone (TSH) post treatment in spite of the usual L-thyroxine replacement. The girl had increasing goiter size while receiving propylthiouracil, 100 mg every eight hours. These findings led to reevaluation of thyroid hormone dynamics in these children and their families. Twelve additional family members, 3 to 38 years of age, compatible with an autosomal dominant inheritance, were also found to have peripheral and pituitary resistance to thyroid hormone. All affected individuals had elevated serum thyroxine and triiodothyronine levels, normal to slightly elevated triiodothyronine resin uptakes, and a nonsuppressed serum TSH. The five individuals who were given thyrotropin-releasing hormone showed exaggerated TSH responses, which normalized on L-thyroxine therapy. Misdiagnosis in six of 15 family members led to significant morbidity (hypothyroidism, delayed growth, and therapy risk). A nonsuppressed serum TSH in a patient with suspected thyrotoxicosis should lead to suspicion of this disorder. Appropriate management for this condition includes L-thyroxine therapy to decrease goiter size and normalize TSH responses to thyrotropin-releasing hormone.

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.

Effect of goitrogen administration on the circadian rhythm of serum thyroid stimulating hormone in the rat

1981 ◽  
Vol 98 (3) ◽  
pp. 396-401 ◽  
Author(s):  
B. Stringer ◽  
D. Wynford-Thomas ◽  
B. Jasani ◽  
E. D. Williams
Keyword(s):  
Circadian Rhythm ◽  
Thyroid Hormone ◽  
Circadian Rhythms ◽  
Thyroid Function ◽  
Diurnal Rhythm ◽  
Thyroid Stimulating Hormone ◽  
Male Rats ◽  
Hormone Synthesis ◽  
Serum Tsh

Abstract. Adult male rats were fed a goitrogen, aminotriazole, for 74 days at a dose known to suppress thyroid function completely. At the end of this period, these animals along with matched controls were killed in groups of seven at 3 hourly intervals throughout a 24 hour period, and serum TSH, T3, T4 and albumin assayed. No significant circadian rhythms of T3, T4 or albumin were found in either, but a highly significant rhythm of TSH was demonstrated both in controls and goitrogen treated groups, with a diminished relative amplitude in the latter. The results indicate that a significant diurnal rhythm of serum TSH persists in the rat despite long-term blockade of thyroid hormone synthesis and that the existence of this rhythm is therefore independent of the presence of circulating T3 or T4.

Effect of diphenylhydantoin on hypothalamic-pituitary-thyroid function in the rat

1980 ◽  
Vol 239 (6) ◽  
pp. E468-E473
Author(s):  
T. Theodoropoulos ◽  
S. L. Fang ◽  
F. Azizi ◽  
S. H. Ingbar ◽  
A. G. Vagenakis ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Direct Effect ◽  
Large Dose ◽  
Inhibitory Effect ◽  
Thyrotropin Releasing Hormone ◽  
Time Dependent ◽  
Tsh Secretion ◽  
Normal Rat ◽  
Serum Tsh

Chronic diphenylhydantoin (DPH) administration (5 mg x 100 g body wt-1 x day-1) to the normal rat is associated with a decrease in the serum thyroxine (T4) and triiodothyronine (T3) concentrations without an appropriate rise in the serum thyrotropin (TSH) concentration, suggesting a possible direct effect of DPH on TSH secretion. To further study this possibility, DPH was administered chronically to thyroidectomized, hypothyroid rats. In the hypothyroid rats treated chronically with DPH, serum TSH did not increase, pituitary TSH content was significantly decreased, and the serum TSH response to thyrotropin-releasing hormone (TRH) was decreased compared to that of diluent-treated, hypothyroid rats. Hypothalamic TRH content was similar in DPH and diluent-treated rats. These findings suggest that DPH suppresses pituitary TSH secretion, probably as a thyroid hormone agonist. The effect of a single large dose of DPH (20 mg/100 g body wt) administered to thyroidectomized rats also decreased serum tSH but, in contrast to the findings in chronically treated rats, hypothalamic TRH and pituitary TSH content and the serum TSH responses to TRH were increased. These differences may be due to the acute inhibitory effect of a large dose of DPH on hypothalamic TRH release. Furthermore, because the effect of thyroid hormone on regulating pituitary TSH synthesis and release is dose and time dependent, the effect of DPH as a thyroid hormone agonist on pituitary TSH dynamics may also be variable.

Genetic and environmental interrelations between measurements of thyroid function in a healthy Danish twin population

2007 ◽  
Vol 292 (3) ◽  
pp. E765-E770 ◽  
Author(s):  
Pia Skov Hansen ◽  
Thomas Heiberg Brix ◽  
Ivan Iachine ◽  
Thorkild I. A. Sørensen ◽  
Kirsten Ohm Kyvik ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Free Triiodothyronine ◽  
Environmental Correlations ◽  
Serum Free ◽  
Hormone Levels ◽  
Opposite Sex ◽  
Thyroid Hormone Levels ◽  
Serum Tsh ◽  
Danish Twin

Serum thyrotropin (TSH), free thyroxine (T4), and free triiodothyronine (T3) levels illustrate the thyroid function set point, but the interrelations between these have never been characterized in detail. The aim of this study was to examine the associations between TSH and thyroid hormone levels in healthy euthyroid twins and to determine the extent to which the same genes influence more than one of these biochemical traits; 1,380 healthy euthyroid Danish twins (284 monozygotic, 286 dizygotic, 120 opposite-sex twin pairs) were recruited. Genetic and environmental associations between thyroid function measurements were examined using quantitative genetic modeling. In bivariate genetic models, the phenotypic relation between two measurements was divided into genetic and environmental correlations. Free T4 and free T3 levels were positively correlated ( r = 0.32, P < 0.0001). The genetic correlation between serum free T4 and free T3 levels was rg = 0.25 (95% CI 0.14–0.35), suggesting that a set of common genes affect both phenotypes (pleiotropy). The correlation between the environmental effects was re = 0.41 (0.32–0.50). From this we calculated that the proportion of the correlation between free T4 and free T3 levels mediated by common genetic factors was 48%. Only 7% of the genetic component of serum free T3 levels is shared with serum free T4. Serum TSH and thyroid hormone levels did not share any genetic influences. In conclusion, thyroid hormone levels are partly genetically correlated genes that affect free T4 levels and exert pleiotropic effects on free T3 levels, although most of the genetic variance for these measurements is trait specific.

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 &lt; 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.

Hyperthyroidism caused by a pituitary thyrotrophin-secreting tumour with excessive secretion of thyrotrophin-releasing hormone and subsequently followed by Graves' disease in a middle-aged woman

1985 ◽  
Vol 110 (3) ◽  
pp. 373-382 ◽  
Author(s):  
Kyuzi Kamoi ◽  
Terunori Mitsuma ◽  
Hiroshi Sato ◽  
Motoharu Yokoyama ◽  
Kazuo Washiyama ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Clinical Signs ◽  
Antithyroid Drug ◽  
Reciprocal Relationship ◽  
Serum Prolactin ◽  
Graves Disease ◽  
Α Subunit ◽  
Thyrotrophin Releasing Hormone ◽  
Aged Woman ◽  
Serum Tsh

Abstract. A 46-year-old woman had signs of thyrotoxicosis and galactorrhoea. Serum immunoreactive TSH and its α-subunit increased in the presence of high serum triiodothyronine (T3), thyroxine (T4), and free T4 concentrations, whereas β-subunit TSH was undetectable. Exogenous TRH failed to increase serum TSH. Serum TSH was markedly suppressed by glucocorticoid, but was increased by antithyroid drug. l-Dopa or bromocriptine partially suppressed, but nomifensine had no influence on serum TSH. Serum prolactin (Prl) was above normal and markedly increased by TRH, but depressed by bromocriptine and not suppressed by nomifensine. Plasma TRH was normal in the hyperthyroid state, but was increased by glucocorticoid and antithyroid drug. Excess thyroid hormone depressed plasma TRH concentrations. Basal serum GH levels were constantly low. Transsphenoidal removal of the tumour normalized serum hormones (T3, T4 free T4, TSH, α-subunit and Prl), and eradicated the clinical signs of hyperthyroidism and galactorrhoea. Histological study of the tumour tissue demonstrated both thyrotrophes and somatotrophes. A reciprocal relationship between serum TSH and T4 concentrations shifted to a higher level before but was normalized after removal of the tumour. Ten months later, the clinical signs of thyrotoxicosis and the increase in serum thyroid hormone recurred without a concomitant increase in serum TSH and its α-subunit. Thyroidal auto-antibodies were slightly positive, but thyrotrophin-binding inhibitor immunoglobulin (TBII) was negative. Administration of antithyroid drug produced a euthyroid state, but 3 years later, discontinuation of the treatment resulted in recurrent hyperthyroidism without suppressed plasma TRH and with no evidence of regrowth of the pituitary tumour. It is suggested that the patient initially had hyperthyroidism owing to excessive TSH secretion from the tumour caused by abnormal TRH secretion, and subsequently had hyperthyroidism owing to Graves' disease.

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