scholarly journals Suppression of thyrotropin secretion during roxadustat treatment for renal anemia in a patient undergoing hemodialysis

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Mitsuru Ichii ◽  
Katsuhito Mori ◽  
Daichi Miyaoka ◽  
Mika Sonoda ◽  
Yoshihiro Tsujimoto ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormone Receptor ◽  
Hypoxia Inducible Factor ◽  
Thyroid Stimulating Hormone ◽  
Primary Hypothyroidism ◽  
Renal Anemia ◽  
Case Presentation ◽  
Tsh Secretion ◽  
Levothyroxine Replacement ◽  
Hormone Homeostasis

Abstract Background Inhibition of hypoxia-inducible factor prolyl hydroxylase (HIF-PH) is a novel choice for the treatment of renal anemia, and an oral HIF-PH inhibitor roxadustat was approved for renal anemia. Roxadustat has high affinity to thyroid hormone receptor beta, which may affect thyroid hormone homeostasis. Case presentation We present here a patient undergoing hemodialysis with primary hypothyroidism receiving levothyroxine replacement, who showed decreased free thyroxine (FT4) and thyroid stimulating hormone (TSH) after starting roxadustat. Pituitary stimulation test revealed selective suppression of TSH secretion. Recovery of TSH and FT4 levels after stopping roxadustat suggested the suppression of TSH was reversible. Conclusions Physicians should pay special attention to thyroid hormone abnormalities in treatment with roxadustat.

Thyroid hormone metabolism

2018 ◽  
pp. 25-59
Author(s):  
Helen E. Turner ◽  
Richard Eastell ◽  
Ashley Grossman
Keyword(s):  
Thyroid Hormone ◽  
Anterior Pituitary ◽  
Thyroid Stimulating Hormone ◽  
Hormone Resistance ◽  
Hormone Metabolism ◽  
Endocrine Disease ◽  
Autoimmune Hypothyroidism ◽  
Thyroid Hormone Metabolism ◽  
Tsh Secretion ◽  
Hormone Homeostasis

This chapter describes the thyroid gland, its associated hormones, and metabolism. Thyroid function is regulated most importantly by thyroid-stimulating hormone (TSH), also called thyrotropin. In turn, TSH secretion from the anterior pituitary is stimulated by the hypothalamic factor thyrotropin-releasing hormone (commonly abbreviated as TRH). It investigates genetic thyroid disorders, thyroid hormone resistance, autoimmune hypothyroidism, and Graves’ disease. The chapter lists the modalities of thyroid imaging, including ultrasound and radionuclide imaging (RNI), and describes indications of endocrine disease, like goitre, nodules, and malignancy. It describes thyroid hormone homeostasis and conditions affecting homeostasis. It also describes clinical features, causes, and management for disorders including hypothyroidism, hyperthyroidism, thyroiditis, thyroid nodules, and cancer.

scholarly journals Effect of thiocyanate ingestion through milk on thyroid hormone homeostasis in women

1997 ◽  
Vol 78 (5) ◽  
pp. 679-681 ◽  
Author(s):  
Kishore K. Banerjee ◽  
P. Marimuthu ◽  
Piyali Bhattacharyya ◽  
Malay Chatterjee
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Stimulating Hormone ◽  
Exposed Group ◽  
Control Subjects ◽  
Serum Thiocyanate ◽  
The Mean ◽  
The Difference ◽  
Hormone Homeostasis ◽  
Hormonal Evaluation ◽  
Thiocyanate Concentration

A thyroid-hormonal evaluation of thirty-five women consuming commercially packed milk containing thiocyanate was carried out. The mean serum thiocyanate concentration, which was measured by the FeCl3colour test, was significantly higher (P< 0.01) than that of control subjects. Serum thyroxine (T4), triiodothyronine (T3) and thyroid-stimulating hormone (TSH) concentrations of exposed women were compared with those of thirty-five control subjects. Thiocyanate ingestion was associated with lower levels of T4(P<0.01) and higher levels of TSH (P< 0.01) compared with the control subjects. T3was found to be higher in the women consuming thiocyanate-containing milk but the difference was not significant. The serum T4level was found to be negatively correlated (r−0.359,P<0.05) while the TSH level was positively correlated (r0.354,P< 0.05) with thiocyanate concentration in the exposed group. From this study, it appears that ingestion of milk with added thiocyanate impairs thyroid function.

scholarly journals Thyroid-hormone-dependent negative regulation of thyrotropin beta gene by thyroid hormone receptors: study with a new experimental system using CV1 cells

2004 ◽  
Vol 378 (2) ◽  
pp. 549-557 ◽  
Author(s):  
Keiko NAKANO ◽  
Akio MATSUSHITA ◽  
Shigekazu SASAKI ◽  
Hiroko MISAWA ◽  
Kozo NISHIYAMA ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptor ◽  
Experimental System ◽  
Thyroid Stimulating Hormone ◽  
Negative Regulation ◽  
Dominant Negative ◽  
Negative Effects ◽  
Receptor Isoforms

The molecular mechanism involved in the liganded thyroid hormone receptor suppression of the TSHβ (thyroid-stimulating hormone β, or thyrotropin β) gene transcription is undetermined. One of the main reasons is the limitation of useful cell lines for the experiments. We have developed an assay system using non-pituitary CV1 cells and studied the negative regulation of the TSHβ gene. In CV1 cells, the TSHβ–CAT (chloramphenicol acetyltransferase) reporter was stimulated by Pit1 and GATA2 and suppressed by T3 (3,3´,5-tri-iodothyronine)-bound thyroid hormone receptor. The suppression was dependent on the amounts of T3 and the receptor. Unliganded receptor did not stimulate TSHβ activity, suggesting that the receptor itself is not an activator. Analyses using various receptor mutants revealed that the intact DNA-binding domain is crucial to the TSHβ gene suppression. Co-activators and co-repressors are not necessarily essential, but are required for the full suppression of the TSHβ gene. Among the three receptor isoforms, β2 exhibited the strongest inhibition and its protein level was the most predominant in a thyrotroph cell line, TαT1, in Western blotting. The dominant-negative effects of various receptor mutants measured on the TSHβ–CAT reporter were not simple mirror images of those in the positive regulation under physiological T3 concentration.

Causes and laboratory investigation of hypothyroidism

2011 ◽  
pp. 530-537 ◽  
Author(s):  
Ferruccio Santini ◽  
Aldo Pinchera
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Thyroid Hormone Receptor ◽  
Hormone Secretion ◽  
Thyroid Tissue ◽  
Clinical Manifestations ◽  
Primary Hypothyroidism ◽  
Central Hypothyroidism ◽  
Resistance To Thyroid Hormones

Hypothyroidism is the clinical state that develops as a result of the lack of action of thyroid hormones on target tissues (1). Hypothyroidism is usually due to impaired hormone secretion by the thyroid, resulting in reduced concentrations of serum thyroxine (T4) and triiodothyronine (T3). The term primary hypothyroidism is applied to define the thyroid failure deriving from inherited or acquired causes that act directly on the thyroid gland by reducing the amount of functioning thyroid tissue or by inhibiting thyroid hormone production. The term central hypothyroidism is used when pituitary or hypothalamic abnormalities result in an insufficient stimulation of an otherwise normal thyroid gland. Both primary and central hypothyroidism may be transient, depending on the nature and the extent of the causal agent. Hypothyroidism following a minor loss of thyroid tissue can be recovered by compensatory hyperplasia of the residual gland. Similarly, hypothyroidism subsides when an exogenous inhibitor of thyroid function is removed. Peripheral hypothyroidism may also arise as a consequence of tissue resistance to thyroid hormones due to a mutation in the thyroid hormone receptor. Resistance to thyroid hormones is a heterogeneous clinical entity with most patients appearing to be clinically euthyroid while some of them have symptoms of thyrotoxicosis and others display selected signs of hypothyroidism. The common feature is represented by pituitary resistance to thyroid hormones, leading to increased secretion of thyrotropin that in turn stimulates thyroid growth and function. The variability in clinical manifestations depends on the severity of the hormonal resistance, the relative degree of tissue hyposensitivity, and the coexistence of associated genetic defects (see Chapter 3.4.8).

scholarly journals Combined effects of cadmium and decabrominated diphenyl ether on thyroid hormones in rats

2012 ◽  
Vol 63 (3) ◽  
pp. 255-262 ◽  
Author(s):  
Marijana Ćurčić ◽  
Saša Janković ◽  
Vesna Jaćević ◽  
Sanja Stanković ◽  
Slavica Vučinić ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Thyroid Function ◽  
Wistar Rats ◽  
Diphenyl Ether ◽  
Thyroid Stimulating Hormone ◽  
Combined Effects ◽  
Single Substance ◽  
Hormone Homeostasis ◽  
Stimulating Hormone

The aim of this study was to see how a mixture of cadmium (Cd) and decabrominated diphenyl ether (BDE209) affect thyroid function, namely thyroid-stimulating hormone (TSH), thyroxin (T4), free thyroxin (FT4), triiodothyronin (T3), and free triiodothyronin (FT3) in Wistar rats (eight per group) receiving either a single substance or their combination by gavage for 28 days. Three groups were receiving Cd alone in the doses of 2.5 mg kg-1, 7.5 mg kg-1, or 15 mg kg-1 b. w. a day, three groups were receiving BDE209 in the doses of 1000 mg kg-1, 2000 mg kg-1, or 4000 mg kg-1 b. w. a day, while nine groups were receiving different mixtures of Cd and BDE209 in these doses (3x3 design). The results have indicated that the Cd+BDE209 mixtures more potently disrupt thyroid hormone homeostasis than would be expected from these chemicals alone.

scholarly journals Molecular dynamics approach to the I431V mutational impact on thyroid hormone receptor-beta

BIBECHANA ◽  
2018 ◽  
Vol 16 ◽  
pp. 79-91
Author(s):  
Tika Ram Lamichhane ◽  
Sharma Paudel ◽  
Binod Kumar Yadav ◽  
Hari Prasad Lamichhane
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Point Mutations ◽  
Binding Pocket ◽  
Accessible Surface Area ◽  
Thyroid Stimulating Hormone ◽  
Solvent Accessible Surface Area ◽  
Free Triiodothyronine ◽  
Receptor Beta

The point mutations like I431V on thyroid hormone receptor-beta (THR-β) gene cause resistance to thyroid hormones (RTH) with the clinical diagnosis of elevated free triiodothyronine (T3) and free thyroxin (T4) but not suppressed thyroid stimulating hormone (TSH) on the blood serum. Some ultrasonographic (USG) reports of the patients with RTH show thyroid gland disorder with goiter or nodule(s) or cyst(s) and some USG reports even with RTH are normal. I431V-mutant causes more steric hindrance while binding T3 into THR-β than the native wild type THRT3. The residue on the 431-codon is dynamic in nature showing its flexibility over the course of entry and release of T3-hormone into/from the ligand binding pocket. The more increased solvent accessible surface area of I431V-mutant than that of native I431-residue makes the partial unfolding of the globular THR-β protein. The smaller height of radial distribution function between I431-mutant and T3 shows the decrease in probability of finding the atomic particles nearby T3-hormone in THRT3-MT than in THRT3-WT. The electrostatic interaction energy between native I431 and T3 is negative, but it is positive between I431V and T3. Moreover, the internal energy of I431V-mutant has been found smaller than that of native I431-residue in THRT3 systems.BIBECHANA 16 (2019) 79-91

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