scholarly journals Thyroid hormone treatment aiming at reduced, but not suppressed, serum thyroid‐stimulating hormone levels in nontoxic goitre: effects on bone metabolism amongst premenopausal women

1998 ◽  
Vol 243 (2) ◽  
pp. 149-154 ◽  
Author(s):  
Knudsen ◽  
Faber ◽  
SierbÆk‐nielsen ◽  
Badstrup ◽  
SØrensen ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Bone Metabolism ◽  
Premenopausal Women ◽  
Hormone Treatment ◽  
Thyroid Stimulating Hormone ◽  
Hormone Levels ◽  
Stimulating Hormone

scholarly journals Specific Reference Intervals of Serum Triiodothyronine, Thyroxine, and Thyroid-stimulating Hormone in Normal Pregnant Indian Women as per Trimester

2017 ◽  
Vol 21 (1) ◽  
pp. 17-21
Author(s):  
Nandita Hazra ◽  
Binay Mitra ◽  
Reetika Pal
Keyword(s):  
Thyroid Hormone ◽  
Pregnant Women ◽  
Reference Intervals ◽  
Thyroid Stimulating Hormone ◽  
Specific Reference ◽  
Indian Women ◽  
Hormone Levels ◽  
Thyroid Hormone Levels ◽  
Maternal Thyroid ◽  
Stimulating Hormone

ABSTRACT Aim Maternal thyroid hormone levels during pregnancy are vital for the health of the mother as well as the developing child. Fetal growth is affected by maternal thyroid levels. Various physiological changes like alterations of thyroxine-binding globulins, human chorionic gonadotropin level, and changes in iodide metabolism affect maternal thyroid hormone levels. Therefore, reference intervals (RIs) for thyroid hormones in pregnant population require to be established separately from the general population. Materials and methods The RIs of serum triiodothyronine (T3), thyroxine (T4), and thyroid-stimulating hormone (TSH) were determined in healthy pregnant women by enzyme-linked immunosorbent assay (ELISA) technique after segregating them into three trimesters. This study was conducted in a 492-bedded zonal-level hospital. The reference population was chosen from a study population of pregnant women by strict inclusion and exclusion criteria. The assays were done by the most-commonly used, economical ELISA method employing standard kits. Tests were done using accurate and precise methods with proper quality control measures. Results The RIs were calculated from the central 95% of distribution of total T3, total T4, and TSH values located between 2.5 and 97.5 percentile values. The 0.90 confidence intervals for the upper and lower reference limits were calculated. The values thus obtained were different from those provided by the manufacturer kit literature. Conclusion It is recommended to determine one's own laboratory-specific, method-specific, trimester-wise RIs for maternal thyroid hormone status and use them for screening of pregnant women. How to cite this article Chakrabarty BK, Mitra B, Pal R, Hazra N. Specific Reference Intervals of Serum Triiodothyronine, Thyroxine, and Thyroid-stimulating Hormone in Normal Pregnant Indian Women as per Trimester. Indian J Med Biochem 2017;21(1):17-21.

Human Recombinant Interleukin-1β Decreases Plasma Thyroid Hormone and Thyroid Stimulating Hormone Levels in Rats*

Endocrinology ◽  
1988 ◽  
Vol 123 (5) ◽  
pp. 2175-2181 ◽  
Author(s):  
J.-M. DUBUIS ◽  
J-M. DAYER ◽  
C. A. SIEGRIST-KAISER ◽  
A. G. BURGER
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Stimulating Hormone ◽  
Interleukin 1Β ◽  
Hormone Levels ◽  
Stimulating Hormone

scholarly journals Synthetic gene network restoring endogenous pituitary–thyroid feedback control in experimental Graves’ disease

2016 ◽  
Vol 113 (5) ◽  
pp. 1244-1249 ◽  
Author(s):  
Pratik Saxena ◽  
Ghislaine Charpin-El Hamri ◽  
Marc Folcher ◽  
Henryk Zulewski ◽  
Martin Fussenegger
Keyword(s):  
Thyroid Hormone ◽  
Feedback Control ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Hormone Levels ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Thyroid Hormone Levels ◽  
Hormone Homeostasis ◽  
Stimulating Hormone

Graves’ disease is an autoimmune disorder that causes hyperthyroidism because of autoantibodies that bind to the thyroid-stimulating hormone receptor (TSHR) on the thyroid gland, triggering thyroid hormone release. The physiological control of thyroid hormone homeostasis by the feedback loops involving the hypothalamus–pituitary–thyroid axis is disrupted by these stimulating autoantibodies. To reset the endogenous thyrotrophic feedback control, we designed a synthetic mammalian gene circuit that maintains thyroid hormone homeostasis by monitoring thyroid hormone levels and coordinating the expression of a thyroid-stimulating hormone receptor antagonist (TSHAntag), which competitively inhibits the binding of thyroid-stimulating hormone or the human autoantibody to TSHR. This synthetic control device consists of a synthetic thyroid-sensing receptor (TSR), a yeast Gal4 protein/human thyroid receptor-α fusion, which reversibly triggers expression of the TSHAntag gene from TSR-dependent promoters. In hyperthyroid mice, this synthetic circuit sensed pathological thyroid hormone levels and restored the thyrotrophic feedback control of the hypothalamus–pituitary–thyroid axis to euthyroid hormone levels. Therapeutic plug and play gene circuits that restore physiological feedback control in metabolic disorders foster advanced gene- and cell-based therapies.

scholarly journals Graves’ disease coexisted with resistance to thyroid hormone: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Hiroshi Akahori ◽  
Rika Usuda
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Initial Treatment ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Sequencing Analysis ◽  
Resistance To Thyroid Hormone ◽  
Hormone Levels ◽  
Inappropriate Secretion ◽  
Stimulating Hormone

Abstract Background Resistance to thyroid hormone is a rare autosomal dominant disorder characterized by reduced responsiveness to thyroid hormone and can cause syndrome of inappropriate secretion of thyroid stimulating hormone. Although Graves’ disease is a common autoimmune thyroid disorder, the coexistence of these two diseases is extremely rare and makes the diagnosis and treatment complicated, leading to the delayed diagnosis of resistance to thyroid hormone. We describe the case of a Japanese man with resistance to thyroid hormone coexisting with Graves’ disease, in which the correct diagnosis of resistance to thyroid hormone was delayed by masking of the signs of syndrome of inappropriate secretion of thyroid stimulating hormone, with final diagnosis 30 years after the initial treatment for Graves’ disease. Case presentation A 30-year-old Japanese man presented with diffuse goiter and thyrotoxicosis. Anti-thyroid stimulating hormone receptor antibody was positive. He was diagnosed with Graves’ disease. Anti-thyroid medication was chosen as the initial treatment for Graves’ disease. However, this treatment failed to normalize the free triiodothyronine, free thyroxine, and thyroid stimulating hormone levels. His thyroid hormone levels indicated syndrome of inappropriate secretion of thyroid stimulating hormone. After cessation of methimazole treatment by remission of Graves’ disease, his state of syndrome of inappropriate secretion of thyroid stimulating hormone persisted. Magnetic resonance imaging revealed no pituitary tumor lesions. The results of thyroid stimulating hormone-releasing hormone stimulation test showed a normal response of thyroid stimulating hormone. He was suspected to have resistance to thyroid hormone. Direct sequencing analysis of the thyroid hormone receptor β gene identified a heterozygous missense mutation, R282S. Coexistence of resistance to thyroid hormone with Graves’ disease was confirmed. He has no signs of thyrotoxic symptoms, and is capable in activities of daily living at the present time. Conclusion We described a rare case of resistance to thyroid hormone simultaneously existing with Graves’ disease. This case demonstrated that these diseases can coexist, and indicated some of the difficulties in diagnosis of resistance to thyroid hormone with coexisting Graves’ disease. The diagnosis of resistance to thyroid hormone did not become apparent until after anti-hyperthyroidism treatment. Although rare, careful follow-up after the initial treatment of Graves’ disease is necessary. The coexistence of these two diseases should be considered in patients showing occasional syndrome of inappropriate secretion of thyroid stimulating hormone.

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