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1
Thornes, H. M., D. T. McLeod, and D. Carr. "Economy and efficiency in routine thyroid-function testing: use of a sensitive immunoradiometric assay for thyrotropin in a general hospital laboratory." Clinical Chemistry 33, no. 9 (1987): 1635–38. http://dx.doi.org/10.1093/clinchem/33.9.1635.
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Abstract We measured thyrotropin (TSH) with a sensitive immunoradiometric assay (IRMA) in 2329 consecutive serum samples received for thyroid-function tests from hospital and general practice. Of these, 185 (7.9%) had TSH values less than 0.2 milli-int. unit/L: 33 (1.4%) were hyperthyroid, 20 (0.9%) were being treated for hyperthyroidism, 115 (4.9%) were receiving L-thyroxin, and 17 (0.7%) were clinically euthyroid but had severe non-thyroidal illnesses. In the first 506 serum samples, we also measured free thyroxin, free triiodothyronine (FT3), and total thyroxin. Thyroliberin (thyrotropin-releasing hormone, TRH) tests performed on 84 patients showed that an undetectable initial TSH (usually ascribable to therapy with thyroxin) predicted a flat TRH response. All untreated thyrotoxic patients had undetectable TSH. Experience confirmed that this TSH assay, in conjunction with a supplementary assay of FT3 when the TSH concentration is less than twice the limit of detection, is efficient and economical for routine evaluation of thyroid function in an unselected population.
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Lee, H. Y., A. E. Pekary, V. P. Smith, J. Sladek, and J. M. Hershman. "Immunoenzymatic quantification of low concentrations of thyrotropin." Clinical Chemistry 33, no. 7 (1987): 1223–26. http://dx.doi.org/10.1093/clinchem/33.7.1223.
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Abstract We evaluated an immunoenzymatic assay (Abbott HTSH EIA) for thyrotropin (TSH) as a tool for detecting hyperthyroidism and for monitoring thyroid hormone suppressive therapy in patients with nodular goiter, thyroid carcinoma, and hypopituitarism. We also tested with thyroliberin (TRH), to determine the correlation between peak and basal TSH in suppressed patients. For comparison, we used a nonequilibrium radioimmunoassay optimized for maximum sensitivity (J Clin Endocrinol Metab 1975;41:676). Hyperthyroid patients with values for either or both triiodothyronine and thyroxin above the normal reference interval had Abbott assay values less than or equal to 0.2 milli-int. unit/L, clearly below the Abbott assay normal range, as determined in 116 euthyroid subjects. We detected one-third of the suppressed patients (greater than or equal to 0.3 milli-int. unit/L) with RIA, 69% with the Abbott assay (TSH greater than or equal to 0.04 milli-int. unit/L). Only 20% of patients with undetectable basal TSH values in the Abbott assay responded to TRH with a detectable peak TSH value; the peak TSH value after TRH was proportional to the basal TSH value. A single basal TSH measurement by the Abbott HTSH EIA should be adequate for monitoring the degree of thyroidal suppression in thyroid-hormone-treated patients.
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Ortiga‐Carvalho, Tania M., Maria I. Chiamolera, Carmen C. Pazos‐Moura, and Fredric E. Wondisford. "Hypothalamus‐Pituitary‐Thyroid Axis." Comprehensive Physiology 6, no. 3 (2016): 1387–428. https://doi.org/10.1002/j.2040-4603.2016.tb00708.x.
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ABSTRACTThe hypothalamus‐pituitary‐thyroid (HPT) axis determines the set point of thyroid hormone (TH) production. Hypothalamic thyrotropin‐releasing hormone (TRH) stimulates the synthesis and secretion of pituitary thyrotropin (thyroid‐stimulating hormone, TSH), which acts at the thyroid to stimulate all steps of TH biosynthesis and secretion. The THs thyroxine (T4) and triiodothyronine (T3) control the secretion of TRH and TSH by negative feedback to maintain physiological levels of the main hormones of the HPT axis. Reduction of circulating TH levels due to primary thyroid failure results in increased TRH and TSH production, whereas the opposite occurs when circulating THs are in excess. Other neural, humoral, and local factors modulate the HPT axis and, in specific situations, determine alterations in the physiological function of the axis. The roles of THs are vital to nervous system development, linear growth, energetic metabolism, and thermogenesis. THs also regulate the hepatic metabolism of nutrients, fluid balance and the cardiovascular system. In cells, TH actions are mediated mainly by nuclear TH receptors (210), which modify gene expression. T3 is the preferred ligand of THR, whereas T4, the serum concentration of which is 100‐fold higher than that of T3, undergoes extra‐thyroidal conversion to T3. This conversion is catalyzed by 5′‐deiodinases (D1 and D2), which are TH‐activating enzymes. T4 can also be inactivated by conversion to reverse T3, which has very low affinity for THR, by 5‐deiodinase (D3). The regulation of deiodinases, particularly D2, and TH transporters at the cell membrane control T3 availability, which is fundamental for TH action. © 2016 American Physiological Society. Compr Physiol 6:1387‐1428, 2016.
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Beck-Peccoz, Paolo, and Luca Persani. "Variable biological activity of thyroid-stimulating hormone." European Journal of Endocrinology 131, no. 4 (1994): 331–40. http://dx.doi.org/10.1530/eje.0.1310331.
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Beck-Peccoz P, Persani L. Variable biological activity of thyroid-stimulating hormone. Eur J Endocrinol 1994;131:331–40. ISSN 0804–4643 Thyroid-stimulating hormone (TSH), like the other pituitary glycoprotein hormones, is produced and secreted as a mixture of isoforms, the majority of which represent differences in oligosaccharide structure and possess different bioactivity. When samples are quantified simultaneously by immunometric assay and bioassay, the ratio between bioactivity (B) and immunoreactivity (I) may serve as an index of the overall potency of TSH. Variations of the TSH B/I ratio have been documented in both physiological and pathological conditions associated with alteration of the two most important mechanisms controlling TSH synthesis and secretion, i.e. TRH release and the thyroid hormone feedback system. Major examples of this assumption are the low TSH bioactivity found in samples from patients lacking TRH and thus bearing a hypothalamic hypothyroidism, and the enhanced bioactivity that is invariably found in TSH from patients with thyroid hormone resistance. Moreover, variations of TSH bioactivity have been recorded in normal subjects during the nocturnal TSH surge, in normal fetuses during the last trimester of pregnancy, in patients with primary hypothyroidism and in patients with TSH-secreting pituitary adenoma and non-thyroidal illness. In conclusion, the secretion of TSH molecules with altered bioactivity plays an important pathogenetic role in various thyroid disorders, while in some particular physiological conditions the bioactivity of TSH may vary in order to adjust thyroid hormone secretion to temporary needs. Paolo Beck-Peccoz, Istituto di Scienze Endocrine, Ospedale Maggiore IRCCS, Via F. Sforza 35, 1-20122 Milano, Italy
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Wiersinga, W. M., E. Endert, M. D. Trip, and N. Verhaest-de Jong. "Immunoradiometric assay of thyrotropin in plasma: its value in predicting response to thyroliberin stimulation and assessing thyroid function in amiodarone-treated patients." Clinical Chemistry 32, no. 3 (1986): 433–36. http://dx.doi.org/10.1093/clinchem/32.3.433.
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Abstract We measured thyrotropin in plasma by an ultrasensitive immunoradiometric assay (TSH-IRMA, "Sucrosep," Boots-Celltech), before and after thyroliberin (TRH) stimulation, in 71 patients with suspected thyroid-function disorders. Thirty-three were taking amiodarone; none was receiving (anti)thyroid drugs. The patients were divided into four groups, according to their TSH response to TRH (as measured previously by conventional TSH-RIA) and the concentrations of thyroxin (T4) and triiodothyronine (T3) in their plasma. Observed ranges of plasma TSH-IRMA (milli-int. units/L) before and after TRH were: euthyroid (n = 20), 0.2-3.0 and 1.7-15.5; subclinically hypothyroid (n = 14), 4.3-18.5 and 20-75; hyperthyroid (n = 17), less than 0.09 and less than 0.09-0.4; and subclinically hyperthyroid (n = 20), less than 0.09-1.1 and less than 0.09-2.6. Evidently TSH-IRMA results for a single sample completely distinguish hyperthyroidism from euthyroidism. However, TSH-IRMA values may also be undetectable in subclinical hyperthyroidism. The TSH response to TRH can be predicted from basal TSH-IRMA results less than 0.09 or greater than or equal to 0.8 milli-int. unit/L, intermediate values can be associated with either a normal TSH response (euthyroidism) or a decreased TSH response (subclinical hyperthyroidism only). We advocate TSH-IRMA as the first diagnostic test of thyroid function for amiodarone-treated patients.
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Derkach, Kira V., Alena S. Pechalnova, Viktor N. Sorokoumov, et al. "Effect of a Low-Molecular-Weight Allosteric Agonist of the Thyroid-Stimulating Hormone Receptor on Basal and Thyroliberin-Stimulated Activity of Thyroid System in Diabetic Rats." International Journal of Molecular Sciences 26, no. 2 (2025): 703. https://doi.org/10.3390/ijms26020703.
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The approaches to correct thyroid deficiency include replacement therapy with thyroid hormones (THs), but such therapy causes a number of side effects. A possible alternative is thyroid-stimulating hormone (TSH) receptor activators, including allosteric agonists. The aim of this work was to study the effect of ethyl-2-(4-(4-(5-amino-6-(tert-butylcarbamoyl)-2-(methylthio)thieno[2,3-d]pyrimidin-4-yl)phenyl)-1H-1,2,3-triazol-1-yl) acetate (TPY3m), a TSH receptor allosteric agonist developed by us, on basal and thyroliberin (TRH)-stimulated TH levels and the hypothalamic-pituitary-thyroid (HPT) axis in male rats with high-fat diet/low-dose streptozotocin-induced type 2 diabetes mellitus (T2DM). Single and three-day administration of TPY3m (i.p., 20 mg/kg) was studied, and the effect of TPY3m on the HPT axis was compared with that of levothyroxine. TPY3m increased TH levels when administered to both healthy and diabetic rats, normalizing thyroxine and triiodothyronine levels in T2DM and, unlike levothyroxine, without negatively affecting TSH levels or the expression of hypothalamic and pituitary genes responsible for TSH production. TPY3m pretreatment preserved the stimulatory effects of TRH on TH levels and thyroid gene expression. This indicates the absence of competition between TPY3m and endogenous TSH for TSH receptor activation and is supported by our in vitro results on TPY3m- and TSH-stimulated adenylate cyclase activity in rat thyroid membranes. Morphological analysis of thyroid glands in diabetic rats after three-day TPY3m administration shows an increase in its functional activity without destructive changes. To summarize, TPY3m, with the activity of a partial allosteric agonist of the TSH receptor, was created as a prototype of drugs to correct thyroid insufficiency in T2DM.
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Yu, Anthony A., Robert J. Kemppainen, and John M. MacDonald. "Effect of endotoxin on hormonal responses to thyrotropin and thyrotropin-releasing hormone in dogs." American Journal of Veterinary Research 59, no. 2 (1998): 186–91. http://dx.doi.org/10.2460/ajvr.1998.59.02.186.
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SUMMARY Objective To determine whether administration of endotoxin affects thyroid gland function in dogs. Animals 24 Beagles. Procedure Dogs were given thyrotropin (TSH) or thyrotropin-releasing hormone (TRH) on 2 occasions. Twenty-four hours before the second challenge with TSH or TRH, all dogs were given 5 μg of endotoxin/kg of body weight. Serum concentrations of thyroxine (T4), free T4 (fT4), 3,3′,5-triiodothyronine (T3), reverse T3, autoantibodies to T3, and plasma concentrations of ACTH and cortisol were determined. Results Treatment with endotoxin was associated with reduced baseline concentration of serum T3 and increased baseline concentration of reverse T3 and free T4. Endotoxin treatment resulted in reduced peak serum concentration of T4 after TSH and TRH. However, peak serum concentration of fT4 after TSH and TRH were not affected by endotoxin. Conclusions A single dose of endotoxin affects several aspects of thyroid gland function in dogs, including T4 binding, deiodinase activity, and the thyroidal response to TSH and TRH. Clinical Relevance Acute or chronic nonthyroidal illness may affect thyroid gland function in dogs. Determination of fT4 concentration may provide a means of differentiating the effects of nonthyroidal illness from those of thyroid dysfunction, because endotoxin treatment was associated with increased baseline serum free T4 concentration and unchanged peak serum fT4 concentration after administration of TSH or TRH. (Am J Vet Res 1998;59:186–191)
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Iversen, E., and P. Laurberg. "Thyrotrophin-releasing hormone (TRH) and hormone secretion from the follicular and C-cells of perfused dog thyroid lobes." Acta Endocrinologica 109, no. 4 (1985): 499–504. http://dx.doi.org/10.1530/acta.0.1090499.
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Abstract. Recently we found small amounts of TRH immunoreactivity in the thyroid gland of dogs and pigs. In the present study we investigated if exogenous TRH influences the release of T4, T3 and cAMP from the follicular cells, and calcitonin and somatostatin from the C-cells of perfused dog thyroid lobes. 10−5 mol/l TRH inhibited the TSH induced iodothyronine and cAMP release from the thyroid while 10−8 mol/l TRH had no effect. The relative proportions of T4 and T3 in thyroid secretion were not altered by TRH infusion. TRH did not influence the basal or the Ca++ induced release of somatostatin and calcitonin. Hence TRH has a direct inhibitory effect on the hormone secretion from thyroidal follicular cells. This opens the possibility that TRH in the thyroid participate in the regulation of thyroid hormone secretion. Even though the concentration of TRH found to be effective is high our results may indicate that TRH in the thyroid participates in the regulation of thyroid hormone secretion as an antagonist to TSH.
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Djurica, Snezana, Miroljub Petrovic, Miodrag Rajic, Mladen Davidovic, and Dragoslav Milosevic. "Clinical implications of biochemical alterations induced by hypothalamic thyrotrophin hormone in elderly people." Jugoslovenska medicinska biohemija 22, no. 3 (2003): 243–48. http://dx.doi.org/10.2298/jmh0303243d.
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Thyrotrophin releasing hormone (TRH) test has been done in 62 subjects (females, average age 72), in order to analyze the stimulated TSH action, to assess the immediate thyroid reserve and to make the rational parameters of the thyroid function in the elderly. It was concluded that biochemical alterations provoked by application of hypothalamic thyrothropin hormone are very complex, but important for the clinical practice, giving the possibility of assessment of the actual state of the thyroid's function. It is also concluded that the estimation of TRH stimulated TSH in 20th and 60th minute, and T3 and FT4 in 60th minute of the TRH test provides very solid and rational method of thyroid function estimation, as well as the estimation of the thyroid reserve.
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Chiamolera, Maria Izabel, and Fredric E. Wondisford. "Thyrotropin-Releasing Hormone and the Thyroid Hormone Feedback Mechanism." Endocrinology 150, no. 3 (2009): 1091–96. http://dx.doi.org/10.1210/en.2008-1795.
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Thyroid hormone (TH) plays a critical role in development, growth, and cellular metabolism. TH production is controlled by a complex mechanism of positive and negative regulation. Hypothalamic TSH-releasing hormone (TRH) stimulates TSH secretion from the anterior pituitary. TSH then initiates TH synthesis and release from the thyroid gland. The synthesis of TRH and TSH subunit genes is inhibited at the transcriptional level by TH, which also inhibits posttranslational modification and release of TSH. Although opposing TRH and TH inputs regulate the hypothalamic-pituitary-thyroid axis, TH negative feedback at the pituitary was thought to be the primary regulator of serum TSH levels. However, study of transgenic animals showed an unexpected, dominant role for TRH in regulating the hypothalamic-pituitary-thyroid axis and an unanticipated involvement of the thyroid hormone receptor ligand-dependent activation function (AF-2) domain in TH negative regulation. These results are summarized in the review. The thyrotropin-releasing hormone neuron is well-positioned to integrate information about the environment as well as circulating TH levels and ultimately affect metabolism in response to these physiological changes.
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Derkach, K. V., A. A. Bakhtyukov, V. N. Sorokoumov, I. A. Lebedev, E. A. Didenko, and A. O. Shpakov. "Low molecular inverse agonist of the thyrotropin receptor is active both intraperitoneal and oral administration." Российский физиологический журнал им И М Сеченова 110, no. 1 (2024): 108–21. http://dx.doi.org/10.31857/s0869813924010078.
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Autoimmune hyperthyroidism (Graves’ disease), which is caused by stimulating autoantibodies to the thyroid-stimulating hormone (TSH) receptor, and thyroid gland (TG) tumors, caused by constitutively increased activity of this receptor, are widespread and have a poor prognosis. The drugs used to treat them are not very effective and have many side effects. One of the approaches for the treatment of these thyroid diseases may be the use of allosteric regulators of the TSH receptor with the activity of inverse agonists. The purpose of the work was to study the effects of our previously developed compound TP48 and the new compound TPY5, belonging to the class of thieno[2,3-d]-pyrimidines, on the basal and thyrotropin-releasing hormone (TRH)-stimulated levels of thyroid hormones (THs) in the blood of rats and on the expression of genes responsible for the synthesis of THs in the TG. The effectiveness of TP48 and TPY5 was studied both with intraperitoneal (i.p., 20 mg/kg) and oral (40 mg/kg) administration. Using ELISA, the levels of free (fT4) and total (tT4) thyroxine and free (fT3) and total (tT3) triiodothyronine in the blood were assessed, including during TRH stimulation (intranasally, 300 μg/kg). The gene expression for thyroid peroxidase (Tpo), thyroglobulin (Tg), Na+/I–-symporter (Nis), type 2 deiodinase (Dio2) and TSH receptor (Tshr) in the TG was assessed using PCR. TPY5, with both routes of administration, reduced both basal and TRH-stimulated TH levels, while TP48 suppressed TH production only with i.p. administration. Orally administered TPY5 significantly reduced basal Tpo gene expression and TRH-stimulated Tg and Dio2 gene expression. I.p. administered TP48 reduced only TRH-stimulated expression of the Tg and Dio2 genes. Quite surprisingly, TPY5 (oral) and TP48 (i.p.) reduced basal Tshr gene expression and did not prevent its inhibition by TRH. Thus, the TPY5 compound we developed has the activity of an inverse agonist of the TSH receptor, is effective when administered orally, which is more in demand in medicine, and can be considered as a prototype of drugs to treat autoimmune hyperthyroidism and thyroid tumors.
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Bodó, Enikő, Benedikt Kany, Erzsébet Gáspár, et al. "Thyroid-Stimulating Hormone, a Novel, Locally Produced Modulator of Human Epidermal Functions, Is Regulated by Thyrotropin-Releasing Hormone and Thyroid Hormones." Endocrinology 151, no. 4 (2010): 1633–42. http://dx.doi.org/10.1210/en.2009-0306.
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Several elements of the hypothalamic-pituitary-thyroid axis (HPT) reportedly are transcribed by human skin cell populations, and human hair follicles express functional receptors for TSH. Therefore, we asked whether the epidermis of normal human skin is yet another extrathyroidal target of TSH and whether epidermis even produces TSH. If so, we wanted to clarify whether intraepidermal TSH expression is regulated by TRH and/or thyroid hormones and whether TSH alters selected functions of normal human epidermis in situ. TSH and TSH receptor (TSH-R) expression were analyzed in the epidermis of normal human scalp skin by immunohistochemistry and PCR. In addition, full-thickness scalp skin was organ cultured and treated with TSH, TRH, or thyroid hormones, and the effect of TSH treatment on the expression of selected genes was measured by quantitative PCR and/or quantitative immunohistochemistry. Here we show that normal human epidermis expresses TSH at the mRNA and protein levels in situ and transcribes TSH-R. It also contains thyrostimulin transcripts. Intraepidermal TSH immunoreactivity is up-regulated by TRH and down-regulated by thyroid hormones. Although TSH-R immunoreactivity in situ could not be documented within the epidermis, but in the immediately adjacent dermis, TSH treatment of organ-cultured human skin strongly up-regulated epidermal expression of involucrin, loricrin, and keratins 5 and 14. Thus, normal human epidermis in situ is both an extrapituitary source and (possibly an indirect) target of TSH signaling, which regulates defined epidermal parameters. Intraepidermal TSH expression appears to be regulated by the classical endocrine controls that determine the systemic HPT axis.
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Okamura, Ken, Kaori Sato, Mototaka Yoshinari, et al. "Recovery of the thyroid function in patients with atrophic hypothyroidism and blocking type TSH binding inhibitor immunoglobulin." Acta Endocrinologica 122, no. 1 (1990): 107–14. http://dx.doi.org/10.1530/acta.0.1220107.
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Abstract The prognosis of atrophic hypothyroidism with blocking type TSH-binding inhibitor immunoglobulin was studied. Among 45 patients (16 males and 29 females) with overt hypothyroidism (serum TSH >40 mU/l) without goitre, thyroid autoantibody to microsomal antigen was positive in 38 or 84.4%, and 4 or 8.9% had TSH-binding inhibitor immunoglobulin, which was shown to be a TSH-stimulation blocking antibody by cAMP production assay using cultured porcine thyroid cells. Thyroidal radioactive iodine uptake was low and thyroid hormone replacement therapy was required. Long-term follow up of 2 patients with strongly positive TSH-binding inhibitor immunoglobulin for 2 to 7 years, however, revealed recovery of the thyroid function after steroid therapy or spontaneously with iodide restriction, respectively, correlating with decrease in both TSH-binding inhibitor immunoglobulin and TSH-stimulation blocking antibody activities. Thyroidal radioactive iodine uptake became normal and histological examination of the thyroid in one patient revealed well-preserved thyroid follicles with lymphocytic infiltration. Recovery of thyroid function can be expected with a decrease in TSH-binding inhibitor immunoglobulin activity in atrophic hypothyroidism, which is not necessarily the end stage of chronic thyroiditis.
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Sailer, B., U. Mehl, R. Hörmann, E. Moser, and K. Mann. "Highly Sensitive Determination of TSH in the Follow-Up of TSH-Suppressive Therapy of Patients with Differentiated Thyroid Cancer." Nuklearmedizin 27, no. 01 (1988): 24–28. http://dx.doi.org/10.1055/s-0038-1628906.
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Basal and TRH-stimulated TSH levels were determined in 72 patients with differentiated thyroid cancer on hormonal treatment, using a highly sensitive immunoradiometric assay (IRMAclon, Henning). 43 patients were under treatment with levothyroxine (T4), 29 patients with triiodothyronine (T3). In 33/43 patients (77%) under T4- and in 18/29 patients (62%) under T3-treatment basal TSH levels were below 0.1 mU/l and levels stimulated with 200 µg TRH i.v. were below 0.5 mU/l. 3 patients showed a significant response (to above 0.5 mU/l) in the TRH test despite basal values of less than 0.1 mU/l. In 2 patients with elevated basal TSH levels (0.23 and 0.60 mU/l, resp.) in the IRMAclon, total suppression of TSH secretion was suggested by a failure of TSH to rise after TRH. By retesting these samples in an own TSH IRMA, basal and stimulated TSH values were below 0.1 mU/l. In conclusion, basal and TRH-stimulated TSH levels are well correlated in most patients with thyroid cancer under hormonal treatment. However, in some cases (5/72) determination of basal TSH could not clearly define the degree of thyrotropic suppression. Thus, TRH testing is still necessary to establish definitely complete TSH suppression in patients with thyroid carcinoma under suppressive treatment.
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Castagnoli, Antonio, M. Teresa Rosaria De Cristofaro, Ivano Taddei, Silvana Forni, Cosimo Roberto Russo, and Alberto Pupi. "Usefulness of the Trh Test in the Management of Patients with Differentiated Thyroid Cancer." Tumori Journal 72, no. 6 (1986): 597–600. http://dx.doi.org/10.1177/030089168607200610.
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Thirty patients thyroidectomized for differentiated thyroid cancer were studied. Serum TSH was assayed in basal conditions and after TRH stimulation, while patients were in suppressive therapy with thyroid hormones. The basal TSH was normal in all the patients and less than 2 μ/ml in 20 patients. The TRH test was negative (no TSH response) in 27 patients and in all the cases with the basal TSH lower than 2 μU/ml.
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Wheatley, T., P. M. S. Clark, J. D. A. Clark, P. R. Raggatt, and O. M. Edwards. "Thyroid Stimulating Hormone Measurement by an Ultrasensitive Assay during Thyroxine Replacement: Comparison with other Tests of Thyroid Function." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 24, no. 6 (1987): 614–19. http://dx.doi.org/10.1177/000456328702400611.
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Serum thyroid stimulating hormone (TSH) was measured using a highly sensitive enzyme-amplified immunoassay in 37 clinically euthyroid patients receiving thyroxine replacement therapy and compared with other biochemical tests of thyroid function. A highly significant correlation ( P<0·001) was found between the basal serum TSH and the increase in serum TSH concentration 20 min after the administration of thyrotropin releasing hormone (TRH). The basal serum TSH was negatively correlated with the serum total thyroxine ( P=0·05). When patients results were classified as abnormal or normal many discrepancies were noted between the various thyroid tests. A suppressed serum TSH was found in 65% of patients with a normal serum total thyroxine. However, in patients on thyroxine replacement therapy a basal TSH measured by enzyme-amplified immunoassay provides the same information as a TRH test.
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Abel, E. Dale, Egberto G. Moura, Rexford S. Ahima та ін. "Dominant Inhibition of Thyroid Hormone Action Selectively in the Pituitary of Thyroid Hormone Receptor-β Null Mice Abolishes the Regulation of Thyrotropin by Thyroid Hormone". Molecular Endocrinology 17, № 9 (2003): 1767–76. http://dx.doi.org/10.1210/me.2003-0109.
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Abstract Thyroid hormones, T4 and T3, regulate their own production by feedback inhibition of TSH and TRH synthesis in the pituitary and hypothalamus when T3 binds to thyroid hormone receptors (TRs) that interact with the promoters of the genes for the TSH subunit and TRH. All TR isoforms are believed to be involved in the regulation of this endocrine axis, as evidenced by the massive dysregulation of TSH production in mice lacking all TR isoforms. However, the relative contributions of TR isoforms in the pituitary vs. the hypothalamus remain to be completely elucidated. Thus, to determine the relative contribution of pituitary expression of TR-α in the regulation of the hypothalamic-pituitary-thyroid axis, we selectively impaired TR-α function in TR-β null mice (TR-β−/−) by pituitary restricted expression of a dominant negative TR-β transgene harboring a Δ337T mutation. These animals exhibited 10-fold and 32-fold increase in T4 and TSH concentrations, respectively. Moreover, the negative regulation of TSH by exogenous T3 was completely absent and a paradoxical increase in TSH concentrations and TSH-β mRNA was observed. In contrast, prepro-TRH expression levels in T3-treated TR-β−/− were similar to levels observed in the Δ337/TR-β−/− mice, and ligand-independent activation of TSH in hypothyroid mice was equivalently impaired. Thus, isolated TR-β deficiency in TRH paraventricular hypothalamic nucleus neurons and impaired function of all TRs in the pituitary recapitulate the baseline hormonal disturbances that characterize mice with complete absence of all TRs.
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Magnusson, Ronald P., Bo Yu, and Veronica Brennan. "Effect of serum thyrotropin levels on the concentration of messenger RNA for thyroid peroxidase in the rat." Acta Endocrinologica 126, no. 5 (1992): 460–66. http://dx.doi.org/10.1530/acta.0.1260460.
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The effect of serum TSH on rat thyroid peroxidase mRNA levels was studied in order to investigate the regulation of thyroid peroxidase gene expression in vivo. A nearly full-length rat thyroid peroxidase cDNA clone was isolated from a bacteriophage cDNA library synthesized using poly A+ RNA isolated from the thyroids of propylthiouracil-treated rats. cDNA probes derived from this clone were used to study rat thyroid peroxidase mRNA levels in response to the level of serum TSH. Two major rat thyroid peroxidase mRNA bands were detected on Northern blots of total cellular RNA (at 3.2 kb and at 3.7kb). Injection of thyroxine, which lowered the levels of serum TSH, also lowered the steady-state levels of both rat thyroid peroxidase mRNAs, whereas treatment with methimazole, which increased serum TSH, increased both rat thyroid peroxidase mRNA levels. In hypophysectomized rats 10 days postoperative, very low levels of thyroid peroxidase mRNA were observed. Injection of bovine TSH (1 IU/day) increased rat thyroid peroxidase mRNA expression, preferentially in the 3.2 kb band. These results clearly demonstrate that TSH regulates rat thyroid peroxidase mRNA levels in vivo.
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Le Dafniet, Michèle, Anne-Marie Brandi, Michèle Kujas, Philippe Chanson, and Françoise Peillon. "Thyrotropin-releasing hormone (TRH) binding sites and thyrotropin response to TRH are regulated by thyroid hormones in human thyrotropic adenomas." European Journal of Endocrinology 130, no. 6 (1994): 559–64. http://dx.doi.org/10.1530/eje.0.1300559.
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Le Dafniet M, Brandi A-M, Kujas M, Chanson P, Peillon F. Thyrotropin-releasing hormone (TRH) binding sites and thyrotropin response to TRH are regulated by thyroid hormones in human thyrotropic adenomas. Eur J Endocrinol 1994:130:559–64. ISSN 0804–4643 In order to see whether, in thyrotropic adenomas with thyrotoxicosis, plasma thyroid hormones regulate the thyrotropin-releasing hormone (TRH) binding sites and the thyrotropin (TSH) response to TRH, we investigated: the presence of TRH binding sites in two cases of thyrotropic adenomas associated with hyperthyroidism and in one case of thyrotropic adenoma secondary to thyroid failure; and the in vitro effect, in a perifusion system, of triiodothyronine (T3) on the response of TSH to TRH in three cases of TSH-secreting adenomas associated with hyperthyroidism. The TRH binding sites were absent in the adenomas associated with high levels of circulating thyroid hormones, whereas they were present in the adenoma secondary to primary thyroid failure (K4 =47 nmol/l, Bmax = 40 nmol/ kg membrane proteins). In vitro, the three adenomas spontaneously released TSH in the perifusion medium (1.49 ±0.06 (mean ± sem), 7.25±0.12 and 16.73±0.36 mIU·−1·106 cells−1·2 min−1) and exhibited an ample TSH response to 10−7 mol/l TRH pulses. In two cases, tumoral secretion of fragments was compared with those of fragments maintained since the time of surgical removal in the presence of 10−8 mol/l T3. The TSH responses to TRH were abolished in the presence of T3 in these two cases. We conclude that thyrotropic adenomas associated with hyperthyroidism are still controlled in vivo by T3. In particular, T3 regulates the TSH response to TRH, probably via a down-regulation of the TRH binding sites. Michèle Le Dafniet, Unité INSERM 223, Faculté de Médecine, Pitié-Salpêtrière, 105 Boulevard de l'Hôpital, 75013 Paris, France
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Kariyawasam, Dulanjalee, Latif Rachdi, Aurore Carré, et al. "DYRK1A BAC Transgenic Mouse: A New Model of Thyroid Dysgenesis in Down Syndrome." Endocrinology 156, no. 3 (2015): 1171–80. http://dx.doi.org/10.1210/en.2014-1329.
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Abstract The most common thyroid abnormality among Down syndrome (DS) children corresponds to a mildly elevated TSH, with T4 decreased or in the normal range and thyroid hypoplasia, from the neonatal period onward, which aggravate their mental impairment. Transgenic Dyrk1A mice, obtained by bacterial artificial chromosome engineering (mBACTgDyrk1A), have 3 copies of the Dyrk1A gene. The objective is to determine whether this transgenic Dyrk1A (Dyrk1A+/++) mouse is an adequate murine model for the study of thyroid dysgenesis in DS. Embryonic thyroid development from embryonic day 13.5 (E13.5) to E17.5 was analyzed in wild-type (WT) and Dyrk1A+/++ mice by immunofluorescence with anti-Nkx2–1, anti-thyroglobulin, and anti-T4 antibodies, markers of early thyroid development, hormonogenesis, and final differentiation, respectively. The expression of transcription factors Nkx2–1, Pax8, and Foxe1 involved in thyroidogenesis were studied by quantitative RT-PCR at the same embryonic stages. We then compared the adult phenotype at 8 to 12 weeks in Dyrk1A+/++ and WT mice for T4 and TSH levels, thyroidal weight, and histological analysis. Regarding thyroidal development, at E15.5, Dyrk1A+/++ thyroid lobes are double the size of WT thyroids (P = .01), but the thyroglobulin stained surface in Dyrk1A+/++ thyroids is less than a third as large at E17.5 (P = .04) and their differentiated follicular surface half the size (P = .004). We also observed a significant increase in Nkx2–1, Foxe1, and Pax8 RNA levels in E13.5 and E17.5 Dyrk1A+/++ embryonic thyroids. Dyrk1A+/++ young adult mice have significantly lower plasma T4 (2.4 ng/mL versus WT, 3.7 ng/mL; P = 0.019) and nonsignificantly higher plasma TSH (114 mUI/L versus WT, 73mUI/L; P = .09). In addition, their thyroids are significantly heavier (P = .04) and exhibit large disorganized regions. Dyrk1A overexpression directly leads to thyroidal embryogenetic, functional and morphological impairment. The young adult thyroid phenotype is probably a result of embryogenetic impairment. The Dyrk1A+/++ mouse can be considered a suitable study model for thyroid dysgenesis in DS.
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Yamashita, Kamejiro, Yuji Aiyoshi, Nobuaki Kuzuya, and Yoshinobu Koide. "Alterations of adrenergic systems in thyroid slices from patients with Graves' disease." Acta Endocrinologica 110, no. 3 (1985): 360–65. http://dx.doi.org/10.1530/acta.0.1100360.
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Abstract. The responses to TSH of tissue cAMP levels in thyroid slices from patients with Graves' disease were significantly lower than those in normal thyroid slices. Conversely, tissue cAMP levels in thyroid slices from these patients were greatly increased by β-adrenergic agonists, either isoproterenol or norepinephrine compared with those in normal thyroid slices. The elevation of cAMP levels induced by TSH in normal thyroid slices was significantly reduced by norepinephrine via α-adrenergic action as reported previously in canine thyroid slices, while such an elevation by TSH of cAMP levels in slices of Graves' disease thyroids was not inhibited, or rather increased by norepinephrine. These results indicate that, in addition to low responses to TSH, α- and β-adrenergic systems were functionally altered in thyroid tissues of patients with Graves' disease.
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Lu, Changxue, Li Zhao, Hao Ying, Mark C. Willingham, and Sheue-yann Cheng. "Growth Activation Alone Is Not Sufficient to Cause Metastatic Thyroid Cancer in a Mouse Model of Follicular Thyroid Carcinoma." Endocrinology 151, no. 4 (2010): 1929–39. http://dx.doi.org/10.1210/en.2009-1017.
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TSH is the major stimulator of thyrocyte proliferation, but its role in thyroid carcinogenesis remains unclear. To address this question, we used a mouse model of follicular thyroid carcinoma (FTC) (TRβPV/PV mice). These mice, harboring a dominantly negative mutation (PV) of the thyroid hormone-β receptor (TRβ), exhibit increased serum thyroid hormone and elevated TSH. To eliminate TSH growth-stimulating effect, TRβPV/PV mice were crossed with TSH receptor gene knockout (TSHR−/−) mice. Wild-type siblings of TRβPV/PV mice were treated with an antithyroid agent, propylthiouracil, to elevate serum TSH for evaluating long-term TSH effect (WT-PTU mice). Thyroids from TRβPV/PVTSHR−/− showed impaired growth with no occurrence of FTC. Both WT-PTU and TRβPV/PV mice displayed enlarged thyroids, but only TRβPV/PV mice developed metastatic FTC. Molecular analyses indicate that PV acted, via multiple mechanisms, to activate the integrins-Src-focal adhesion kinase-p38 MAPK pathway and affect cytoskeletal restructuring to increase tumor cell migration and invasion. Thus, growth stimulated by TSH is a prerequisite but not sufficient for metastatic cancer to occur. Additional genetic alterations (such as PV), destined to alter focal adhesion and migration capacities, are required to empower hyperplastic follicular cells to invade and metastasize. These in vivo findings provide new insights in understanding carcinogenesis of the human thyroid.
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D'Arcy, Robert, Steven Hunter, Kirsty Spence, and Margaret McDonnell. "A Case of macro-TSH masquerading as subclinical hypothyroidism." BMJ Case Reports 14, no. 7 (2021): e243436. http://dx.doi.org/10.1136/bcr-2021-243436.
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A 47-year-old man was commenced on levothyroxine following a diagnosis of subclinical hypothyroidism with nonspecific symptoms. Despite increasing doses of levothyroxine, his thyroid-stimulating hormone (TSH) remained elevated and he was referred for further assessment as he was unable to tolerate further titration. On assessment, his thyroid function demonstrated an elevated TSH and elevated free-T4. The initial impression was of iatrogenic thyrotoxicosis, with possible underlying thyroid hormone resistance, TSHoma or assay interference. After discontinuation of levothyroxine, free-T4 normalised but TSH remained elevated. There was a normal response to thyrotropin-releasing hormone (TRH) testing. T3 suppression testing demonstrated free-T4 reduction but persistently high TSH. THRβ sequencing was normal. TSH measurement by alternative assays revealed discrepant results. Gel filtration chromatography revealed the presence of high-molecular weight TSH variant alongside normal TSH. Macro-TSH is a rare phenomenon with spuriously elevated TSH and which may mimic subclinical hypothyroidism. Recognition of macro-TSH avoids misdiagnosis and prevents inappropriate treatment.
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Decroli, Eva, and Alexander Kam. "Dampak Klinis Thyroid-Stimulating Hormone." Jurnal Kesehatan Andalas 6, no. 1 (2017): 222. http://dx.doi.org/10.25077/jka.v6i1.674.
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Thyroid-Stimulating Hormone (TSH), yang disebut juga dengan tirotropin, adalah glikoprotein yang disekresikan oleh bagian anterior dari kelenjar hipofisis. Sintesis dan sekresi dari TSH diatur oleh faktor dari hipotalamus yang didominasi oleh thyrotropin-releasing hormone (TRH) dan faktor perifer yang didominasi oleh kadar hormon tiroid. Setelah disintesis, TSH disekresikan, lalu akan berikatan dengan reseptor yang disebut Thyroid-Stimulating Hormone Receptor (TSHR). Ikatan TSH-TSHR akan memberikan dampak klinis terhadap jaringan dan organ tempat terjadinya ikatan tersebut. Ikatan tersebut bisa terjadi pada kelenjar tiroid dan jaringan ekstratiroid. Jaringan yang sudah dikenal mengekspresikan TSHR adalah jaringan adiposa, hipotalamus, hipofisis anterior, tulang, hati dan sistem imun.
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Kamoi, Kyuzi, Terunori Mitsuma, Hiroshi Sato, et al. "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." Acta Endocrinologica 110, no. 3 (1985): 373–82. http://dx.doi.org/10.1530/acta.0.1100373.
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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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Gauchez, Anne-Sophie, Magali Pizzo, Dany Alcaraz-Galvain, et al. "TSH Isoforms: About a Case of Hypothyroidism in a Down's Syndrome Young Adult." Journal of Thyroid Research 2010 (2010): 1–5. http://dx.doi.org/10.4061/2010/703978.
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Background. For unknown reasons, the prevalence of thyroid autoimmune disorders is higher in patients with Down's syndrome than in the general population. The present case strongly supports a recent evaluation of propagating screening for thyroid disease in this group of patients to assure early diagnosis of hypothyroidism.Methods. In a 25-year-old man diagnosed with Down's syndrome, clinical manifestations of hypothyroidism were lacking, but profound biochemical abnormalities were found with particularly high levels of thyroid stimulating hormone (TSH). Antigenic properties of TSH were characterized using a panel of anti-TSH antibodies.Results. Technical problems not infrequently associated with TSH measurements are convincingly ruled out. Antigenic characterization of the patient's circulating TSH revealed circulating forms of TSH different from pituitary TSH which closely resembled TSH recombinant human hormone.Conclusions. It appears counterintuitive that the bioactivity of TSH decreases in the hypothyroid state as higher bioactivity of TSH is anticipated in hypothyroidism promoted by an increased hypothalamic TRH drive. In contrast, diminished negative thyroid hormone feedback will enhance posttranslational glycosylation of TSH subunits and increase sialylation of the carbohydrate side chains. Both exert a negative effect on TSH bioactivity, only compensated by the very high levels of the hormone as in the present case.
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Kishori, Mokle*1 Gajanan Sanap2. "Review On Thyroid Disease." International Journal in Pharmaceutical Sciences 1, no. 12 (2023): 640–49. https://doi.org/10.5281/zenodo.10427942.
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Thyroid diseases are the most common diseases that occur when conditions affect the thyroid gland. The thyroid gland is an endocrine gland that is a butterfly-shaped and in front of the neck, wrapped around the windpipe (trachea), just below the larynx. The production of hormones thyroxine (T4) and triiodothyronine (T3) is its main purpose. Its function affects nearly every organ of the human body. The thyroid is controlled by the pituitary gland secretes a hormone known as thyroid-stimulating hormone (TSH). TSH then instructed the thyroid gland on how much hormone to make and release. But it also responds to signals from the hypothalamus, secretes thyrotropin-releasing hormone (TRH). TRH then causes the pituitary to release TSH, which signals the thyroid gland. The thyroid creates and releases hormones. When your thyroid makes either too little or too much of these important hormones, it’s called a thyroid disease. When the thyroid gland doesn’t make enough thyroid hormone to meet your body’s needs, this is called hypothyroidism, and when the thyroid gland makes too much thyroid hormone, this is called hyperthyroidism. Hypothyroidism and hyperthyroidism are the two particularly common types of thyroid disease
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Farmaki, Kalistheni, Nicholas Angelopoulos, George Anagnostopoulos, Anastasia Goula, and Christina Pappa. "Thyroid Function in Thalassemic Patients Treated with Combined Chelation Therapy." Blood 108, no. 11 (2006): 1592. http://dx.doi.org/10.1182/blood.v108.11.1592.1592.
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Abstract Recently introduced chelation regimens that combine deferoxamine (DFO) and deferiprone (DFP) have been shown to have greater efficacy in promoting iron excretion than either chelator alone and have been associated with rapid reduction of the iron load in the heart and liver, and with reversal of cardiac dysfunction. It is unclear whether this combined therapy could be associated with a decline in the severity of iron-induced endocrinopathies. The primary endpoint of the present study was to investigate the effects of this therapy on the thyroid function in thalassemic patients with subclinical hypothyroidism (SH) or normal thyroid function. Starting in January 2001, 42 patients with b-tlalassaemia major, previously maintained on subcutaneous DFO only, were switched to combined treatment with DFO and DFP. Before the initiation of combined therapy 14 patients had overt hypothyroidism and were treated with thyroxin substitution. The thyroid function of the remaining patients with normal fasting levels of both FT4 and FT3 was further assessed with TRH test. TSH was measured at 0, 30, 60 and 90 minutes after IV injection of 200 mcg of TRH. 15 patients with normal TSH responses (7 males, 8 females, age 28.86 ± 2.20 years, mean ± SEM), and 13 patients (6 males, 7 females, age 31.15 ± 1.85 years), who were considered suffering from SH were finally enrolled. Criteria for the diagnosis of SH was an elevated basal TSH concentration (>5 TSH μIU/ml) or an increment of the TSH levels during the test more than 20 μIU/ml from the basal value. Combination therapy markedly decreased ferritin levels (585 ± 457 vs. 2124 ± 456 μg/l, P < 0.001 in SH group and 868 ± 339 vs. 2877 ± 552 μg/l, P < 0.001 in eythyroidal group). At the time of reassessment (June 2006), the levels of TSH were decreased at all times during the second TRH test in patients with SH: Basal TSH: 4.12 ± 0.63 vs. 6.27 ± 1.08, P=0.01. TSH At 30′ mins: 22.13 ± 2.18 vs. 34.06 ± 4.75, P=0.005. TSH At 60′ mins: 15.89 ± 1.13 vs. 25.69 ± 3.72, P=0.002. TSH At 90′ mins: 11.83±1.26 vs. 19.44±3.27, P=0.001. TSH quantitative secretion, calculated as the area under the curve, was also significantly decreased with combined therapy (1380±118) compared with the initial assessment (2178±312, P=0.004), while no change occurred in basal FT4 (1.06 ± 0.04 vs. 1.15 ± 0.08 in 2001, normal range 0.71–1.85 ng/ml) and FT3 levels (1.55± 0.07 vs. 1.59± 0.08 in 2001, normal range 1.45–3.48 pg/ml). Nevertheless, 7 patients with previous SH exhibited normal results in the reassessment. In patients with previous normal thyroid function TSH response to TRH stimulus was significantly improved only at 60′ mins (9.78±0.73 vs. 11.49±1.28, P=0.03). This study showed that the combination of DFO and DFP followed by an intensive iron chelation might be associated with an improvement in thyroid function in the early stages of hypothyroidism.
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Müller, Kathrin, Dagmar Führer, Jens Mittag, et al. "TSH Compensates Thyroid-Specific IGF-I Receptor Knockout and Causes Papillary Thyroid Hyperplasia." Molecular Endocrinology 25, no. 11 (2011): 1867–79. http://dx.doi.org/10.1210/me.2011-0065.
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Abstract Although TSH stimulates all aspects of thyroid physiology IGF-I signaling through a tyrosine kinase-containing transmembrane receptor exhibits a permissive impact on TSH action. To better understand the importance of the IGF-I receptor in the thyroid in vivo, we inactivated the Igf1r with a Tg promoter-driven Cre-lox system in mice. We studied male and female mice with thyroidal wild-type, Igf1r+/−, and Igf1r−/− genotypes. Targeted Igf1r inactivation did transiently reduce thyroid hormone levels and significantly increased TSH levels in both heterozygous and homozygous mice without affecting thyroid weight. Histological analysis of thyroid tissue with Igf1r inactivation revealed hyperplasia and heterogeneous follicle structure. From 4 months of age, we detected papillary thyroid architecture in heterozygous and homozygous mice. We also noted increased body weight of male mice with a homozygous thyroidal null mutation in the Igf1r locus, compared with wild-type mice, respectively. A decrease of mRNA and protein for thyroid peroxidase and increased mRNA and protein for IGF-II receptor but no significant mRNA changes for the insulin receptor, the TSH receptor, and the sodium-iodide-symporter in both Igf1r+/− and Igf1r−/− mice were detected. Our results suggest that the strong increase of TSH benefits papillary thyroid hyperplasia and completely compensates the loss of IGF-I receptor signaling at the level of thyroid hormones without significant increase in thyroid weight. This could indicate that the IGF-I receptor signaling is less essential for thyroid hormone synthesis but maintains homeostasis and normal thyroid morphogenesis.
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Inui, T., Y. Ochi, T. Hachiya, et al. "Different binding of stimulatory-type and blocking-type TSH receptor antibody with guinea-pig testis membrane." Acta Endocrinologica 125, no. 5 (1991): 563–69. http://dx.doi.org/10.1530/acta.0.1250563.
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Abstract. A receptor assay using [125I]bTSH-binding to guinea-pig testis membrane was developed. Unlabelled hCG and FSH inhibited [125I]bTSH binding. In patients with Graves' disease and in untreated hyperthyroid patients, almost all long-acting thyroid stimulators and thyroid-stimulating antibodies, respectively did not inhibit [125I]bTSH binding, which on the other hand was inhibited by thyroid stimulation blocking antibodies in patients with primary hypothyroidism. When the inhibitory effect on the binding of [125I]hCG and 125I-synthetic α-subunit peptide (α26-46) of hCG to testis membrane was examined, bTSH resulted in a significant inhibition. However, all three kinds of TSH receptor antibodies had no inhibitory effect. This study demonstrated 1. interaction of α-subunit of TSH and hCG with the testicular receptor; 2. binding of thyroid stimulation-blocking antibody and lack of binding of thyroid-stimulating antibody to the testicular TSH receptor in spite of binding of these TSH receptor antibodies to the thyroidal TSH receptor, and 3. lack of binding of thyroid-stimulating antibody and thyroid stimulation-blocking antibody to the testicular gonadotropin receptor.
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Raj, KC Shiva. "Thyroid function tests and its interpretation." Journal of Pathology of Nepal 4, no. 7 (2014): 584–90. http://dx.doi.org/10.3126/jpn.v4i7.10318.
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Abstract: Thyroid diseases are among the most prevalent of medical conditions. In the patients with obvious features of hypothyroidism or hyperthyroidism thyroid function tests only confirm the diagnosis. Though TSH is widely used as a screening test in suspicion with thyroid disorder, many times TSH alone may be misleading. In this situation TSH along with T4 and T3 should be performed which will resolve the problem. However, thyroid function tests may not concord with each other. Discordant results between TSH, T4 and T3 may be because of various conditions like subclinical hypo- or hyperthyroidism, non-thyroidal illness, drugs etc. Beside that antibody interference and special condition like pregnancy may alter the thyroid hormone concentration. DOI: http://dx.doi.org/10.3126/jpn.v4i7.10318 Journal of Pathology of Nepal (2014) Vol. 4, 584-590
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Meizlik, Paige, Andrew Cucchiara, Lakshmi Kannan, Theresa Scattergood, and Anne Rentoumis Cappola. "TRH Stimulation Testing in Older Individuals with Persistent Subclinical Hypothyroidism: A Randomized, Double-Blind, Cross-Over Study of Levothyroxine and Liothyronine Administration." Journal of the Endocrine Society 5, Supplement_1 (2021): A853—A854. http://dx.doi.org/10.1210/jendso/bvab048.1742.
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Abstract Background: Subclinical hypothyroidism is common in older individuals. To better understand the underlying physiology, we examined the pituitary-thyroid axis using thyrotropin releasing hormone (TRH) stimulation testing both at baseline and after levothyroxine (LT4) and liothyronine (LT3) supplementation. Methods: We conducted a randomized, double-blind, cross-over study in men and women aged 70 years and over without anti-thyroid peroxidase antibodies with persistent subclinical hypothyroidism, defined as having a TSH level between 4.5 and 19.9 µIU/mL with a normal free thyroxine (FT4) level at two consecutive time points. The primary outcome measures were TSH serum concentration area under the curve (AUC), maximum TSH serum concentration (Cmax), and change in free thyroxine (∆FT4) and total triiodothyronine (∆TT3) levels following TRH stimulation, each measured at three time points: once at baseline and once each after achieving euthyroid TSH levels with the two thyroid preparations. The maximal change in TSH (∆TSH); FT4 and TT3 AUCs; and time to maximal TSH, FT4, and TT3 (Tmax) were also analyzed. Results: Thirteen participants [mean (SD) age 77 (5) years], 4 women and 9 men, completed TRH stimulation testing at baseline and after achieving a TSH level of 0.5-1.5 µIU/mL with each therapy. Baseline mean TSH was 4.84 (1.29) µIU/mL. The mean LT4 dose was 105 (36) µg/day and LT4 dose was 34 (9) µg/day. After TRH stimulation, the mean TSH AUC (0-180) at baseline was 3099.5 (1424.4) µIU*min/mL, and significantly decreased after both LT4 [631.4 (315.2), p&lt;0.001] and LT3 [631.5 (317.3), p&lt;0.001]. There was no difference in TSH AUC (0-180) between LT4 and LT3 treatment arms. Baseline mean TSH Cmax was 27.2 (14.5) µIU/mL and significantly decreased after LT4 [5.5 (3.0), p&lt;0.001] and LT3 [5.4 (2.9), p&lt;0.001], with no difference between the LT4 and LT3 treatment arms. The ∆FT4 was 0.11 (0.07) ng/dL at baseline and decreased significantly on LT3. The ∆TT3 was 0.32 (0.09) ng/mL at baseline and significantly decreased on both LT4 and LT3, with no difference between treatment arms. Conclusions: Older individuals with antibody-negative persistent subclinical hypothyroidism have a heterogeneous TSH response to TRH stimulation. Our data show a significantly diminished response to TRH stimulation after thyroid hormone replacement, and they support the pharmacodynamic equivalence of LT4 and LT3 treatment.
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Farmaki, Kallistheni, Ioanna Tzoumari та Christina Pappa. "Reversal of Hypothyroidism in Well Chelated β-Thalassemia Major Patients". Blood 112, № 11 (2008): 3884. http://dx.doi.org/10.1182/blood.v112.11.3884.3884.
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Abstract Thyroid dysfunction is known to occur frequently in β-Thalassemia major patients (TMps), but its prevalence and severity varies in different cohorts according to chelation regimens. Thyroid hormones are critical determinants of brain and somatic development in infants and of metabolic activity in adults affecting the function of virtually every organ system. Thyroid gland mainly secrets T4, whereas 80% of T3 is produced by de-iodination of T4 (liver, kidney, heart and other tissues) and is influenced by a variety of factors. Furthermore, T4 & T3 secretion is tightly regulated within narrow limits by a mechanism that involves the pituitary-secreted TSH which in turn is stimulated by the hypothalamic TRH. Thus, iron overload-related hypothyroidism may be either central (because of deposition in the pituitary or the hypothalamus) and usually associated with other endocrinopathies, or primary (by deposition in the thyroid gland or even other organs). Existing data suggest that the thyroid gland appears to fail before the central components of the axis. In all cases, symptoms occur slowly over time and may vary from subclinical to overt hypothyroidism which is associated with an increased risk of cardiovascular disease. The aim of this study was to investigate the effect of long-term intensive combined chelation therapy on thyroid function in TMps after they were all in negative iron balance. 51 TMps, 25 males 26 females, mean age 29.8±2.03, who were previously maintained on subcutaneous desferrioxamine monotherapy (DFO:40mg/kg, 3–6 days/week) switched to an intensive combined chelation with DFO (40–60mg/kg/d) and Deferiprone (DFP: 75–100mg/kg/d) adapted to individual needs. Thyroid function was assessed initially and after 6 years by TRH stimulation test and TSH, FT4 & FT3 screening. All patients on hormone replacement therapy stopped treatment at least 30 days before the test. This was approved by the Hospital Scientific Committee. Criteria for the diagnosis of subclinical or compensated hypothyroidism was an increase of the TSH levels during the test of more than 20 μIU/ml from the basal value or an elevated basal TSH concentration (>5 μIU/ml) and for overt hypothyroidism a further decrease in FT4 & FT3 levels. With DFO monotherapy 18 TMps were treated with thyroxin therapy. In these patients after combined chelation and an important decrease in iron overload (p<0.0001) as estimated by ferritin levels (2,737±473 vs 450±225mg/dl), MRI liver and heart iron quantification (T2*L & T2*H) and LIC calculated by Ferriscan (13±3 vs. 1.4±0.5mg/gdw), a significant increase was observed in mean FT4 (1.07±0.03 vs. 0.7±0.02ng/ml, p<0.0001) & mean FT3 (2.6±0.1 vs. 1.3± 0.1pg/ml, p<0.0001) and an additional significant decrease in the mean TSH quantitative secretion, calculated as the area under the curve (AUC=1,332±131 vs. 2,231±241, p<0.0001). These 10/18 (56%) TMps with subclinical or compensated hypothyroidism, who normalized TSH, FT4 & FT3 levels and had a normal TRH stimulation test discontinued thyroxin therapy, while another 4/18 (22%) reduced their thyroxin dose. The remaining 4/18 with overt hypothyroidism, while they all improved their TRH stimulation test, only 2 improved to compensated hypothyroidism with TSH levels 5–10mIU/ml and normal FT4 & FT3 levels. Critically, in the other 33/51 euthyroid TMps, no new cases of hypothyroidism were noted after combined chelation and a significant increase (p<0.0001) was observed in the mean FT4 & FT3 levels with a significant decrease (p<0.0001) in the mean TSH quantitative secretion (AUC). This study showed that intensive combined chelation associated with a significant decrease of iron overload may reverse some cases of primary hypothyroidism, either subclinical or compensated, and may prevent progression to overt hypothyroidism, thus influencing the decision to treat with thyroid hormone. It may also improve some cases of overt hypothyroidism suggesting that even iron-induced damage of the thyroid pituitary axis might be ameliorated.
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Mitsuma, Terunori, Tsuyoshi Nogimori, and Masahiro Chaya. "Bombesin inhibits thyrotrophin secretion in rats." Acta Endocrinologica 108, no. 1 (1985): 79–84. http://dx.doi.org/10.1530/acta.0.1080079.
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Abstract. The effects of peripheral administration of bombesin on thyrotrophin-releasing hormone (TRH) and thvrotrophin (TSH) secretion in rats were studied. Bombesin (200 μg/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after bombesin injection, whereas plasma concentrations tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by bombesin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine pre-treated group, the inhibitory effect of bombesin on TSH levels was prevented, but not in the l-Dopa- or 5-hydroxytryptophan pre-treated group. These drugs alone had no effect on plasma TSH levels in terms of the dose used. The inactivation of TRH immunoreactivity in plasma or hypothalamus in vitro after bombesin injection did not differ from that of the controls. These findings suggest that bombesin acts on the hypothalamus to inhibit TRH release, and that its effects are at least partially modified by amines of the central nervous system.
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Mitsuma, Terunori, Tsuyoshi Nogimori, De Heng Sun, and Masahiro Chaya. "Effects of eledoisin on thyrotrophin secretion in rats." Acta Endocrinologica 110, no. 1 (1985): 90–94. http://dx.doi.org/10.1530/acta.0.1100090.
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Abstract. The effect of peripheral administration of eledoisin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. Eledoisin (500 μg/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after eledoisin injection, whereas its plasma concentration tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by eledoisin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine-pretreated group, the inhibitory effect of eledoisin on TSH levels was prevented, but not in the l-dopa- or 5-hydroxytryptophan-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used. The inactivation of TRH immunoreactivity by plasma or hypothalamus in vitro after eledoisin injection did not differ from that of controls. These findings suggest that eledoisin acts on the hypothalamus to inhibit TRH release, and its effects are modified by amines of the central nervous system.
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Bagchi, N., and T. R. Brown. "Repeated thyrotrophin stimulation of thyroid secretion: lack of refractoriness in vivo." Journal of Endocrinology 106, no. 2 (1985): 153–57. http://dx.doi.org/10.1677/joe.0.1060153.
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ABSTRACT It has been reported that prior exposure of thyroid tissue to TSH in vitro induces a state of refractoriness to new challenges of the hormone. We have investigated the effect of repeated TSH treatment on thyroid secretion to determine whether such refractoriness exists in vivo. The rate of thyroid secretion was estimated by measuring the rate of hydrolysis of labelled thyroglobulin from mouse thyroid glands in vitro. The thyroid glands were labelled in vivo with 131I and then cultured for 20 h in the presence of mononitrotyrosine, an inhibitor of iodotyrosine deiodinase. The rate of hydrolysis of labelled thyroglobulin was measured as the percentage of radioactivity released as free iodotyrosines and iodothyronines into the gland and the medium at the end of incubation. Thyrotrophin was administered in vivo at hourly intervals for 2–4 injections. The corresponding control group received saline injections every hour except for the last injection when they received TSH. The peak rates of thyroglobulin hydrolysis, measured 2 h following the last injection, were similar in animals receiving two, three or four TSH injections and were not different from those in the control groups. Serum tri-iodothyronine and thyroxine concentrations 2 h after the last injection were higher in the groups receiving multiple TSH injections. Thyroidal cyclic AMP accumulation in response to TSH was markedly depressed in the group receiving multiple injections compared with the group receiving a single injection of TSH in vivo. These data indicate that (1) the stimulatory effect of TSH on thyroidal secretion is not diminished by prior administration of the hormone in vivo, (2) repeated TSH administrations in vivo cause refractoriness of the adenylate cyclase response to TSH and (3) a dichotomy exists between the secretory response and the adenylate cyclase response to repeated administrations of TSH. J. Endocr. (1985) 106, 153–157
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Kakezono, Fumiko, Shunichi Yamashita, Naokata Yokoyama, et al. "Stimulation of thyroid adenylate cyclase activity by sera from patients with non-thyroidal illness." Acta Endocrinologica 113, no. 3 (1986): 340–45. http://dx.doi.org/10.1530/acta.0.1130340.
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Abstract. We have previously shown that sera from many hypothyroid patients stimulated adenylate cyclase activity as measured by serum bioactive TSH concentrations produced by FRTL-5 cell line. This TSH-stimulating activity did not correlate with serum immunoreactive TSH. IgG fractions of these sera did not stimulate FRTL-5 cells. The present study was, therefore, undertaken to investigate the thyroid stimulating activity of sera from patients with non-thyroidal illness. Studies were performed in 36 patients with various non-thyroidal illness. In these patients, serum concentrations of T4, free thyroxine, T3, and TSH were determined. In addition, sera were incubated with FRTL-5 cells or porcine thyroid cells in primary culture in the presence of 0.4 mm MIBX, and medium cAMP concentrations were determined by radioimmunoassay. Sera obtained from some patients with various non-thyroidal illness increased cAMP concentrations in culture media of FRTL-5 cells as well as that of porcine thyroid cells. The thyroid stimulating effects of sera were not disease specific and significantly correlated inversely with serum T3 and T4 concentrations. Serum TSH concentrations in these patients were within the normal range even by the newly developed ultrasensitive assay. Although the nature of substance(s) present in sera of patients with low T3 syndrome which stimulates thyroid adenylate cyclase is not entirely known, it is conceivable that there exist mechanisms independent of TSH to compensate the decreased serum T3 levels in low T3 syndrome.
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Maulidiyanti, Ellies Tunjung Sari. "Hubungan Kadar TSH Terhadap Kadar FT4 Pada Pasien Tiroid Di Bangkalan." JOURNAL OF MUHAMMADIYAH MEDICAL LABORATORY TECHNOLOGIST 1, no. 2 (2018): 21. http://dx.doi.org/10.30651/jmlt.v1i2.1487.
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AbstractThyroid disorder disease ranks second most in the list of metabolic diseases after diabetes mellitus (DM). Thyroid disease or Thyroid abnormalities is a condition of abnormalities in a person due to the disorder of the thyroid gland. TSH is a primary factor that controls thyroid cell growth and synthesis also thyroid hormone secretion. TSH secretion is stimulated by low levels of T3 and T4 and by the hormone TRH (Thyroid Releasing Hormone) the hypothalamus is inhibited by elevated levels of T3 and T4. T3 and T4 are circulating in the plasma, most of which are bound with proteins, Thyroid Binding Globulin (TBG) and a small part in free form that are Free Triiodotironine (FT3) and Free Thyroxine (FT4). The free hormone (FT3 and FT4) is an actively metabolic fraction which is known to be quantitative. Currently the measurement of free hormone levels should be part of a complete examination of the status of the thyroid gland. The purpose analyzes the levels of TSH, FT4 and proves the relationship between the two in patients with thyroid disorders. This examination by using ELISA method is with EIA competitive principles and sandwiches. The samples are serum of patients with thyroid disorders at RSUD Bangkalan and Farmalab Laboratory from October to November 2017.The 30 samples obtaines an average result of TSH level of 1.9 mIU / L and an average FT4 level of 2.8 ng / dl. Next test Kolmogorov-Smirnov and Spearrman's test results obtained if the variable one value rose (high) then the other variable down (low). It can be concluded that there is an opposite relationship between TSH levels and FT4 levels, if TSH levels increase, the FT4 level decreases, and so it is also in contrast Keywords: TSH, FT4, thyroid disorders
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Williams, Gareth, Marius Kraenzlin, Laurence Sandier, et al. "Hyperthyroidism due to non-tumoural inappropriate TSH secretion." Acta Endocrinologica 113, no. 1 (1986): 42–46. http://dx.doi.org/10.1530/acta.0.1130042.
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Abstract. Inappropriate hypersecretion of TSH was investigated in a 25 year old man whose hyperthyroidism had relapsed 4 years after subtotal thyroidectomy. Serum TSH levels were further increased by both TRH and metoclopramide and were partially suppressed by triiodothyronine (120 μ/day). The serum α-subunit: TSH molar ratio was < 1.0, and computerised axial tomography showed no evidence of a pituitary tumour. These features are characteristic of inappropriate TSH secretion due to thyrotroph resistance to thyroid hormones. A long-acting somatostatin analogue (SMS 201-995), 50 μg injected sc twice-daily for three days, suppressed TSH levels and nearly normalised thyroid hormone levels. Somatostatin analogues may be therapeutically useful in thyrotoxicosis due to non-tumoural inappropriate TSH hypersecretion.
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Pasqualini, Titania, June McCalla, Stacy Berg, et al. "Subtle primary hypothyroidism in patients treated for acute lymphoblastic leukemia." Acta Endocrinologica 124, no. 4 (1991): 375–80. http://dx.doi.org/10.1530/acta.0.1240375.
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Abstract. We evaluated serum thyroid hormone and thyroid antibody levels, the serum TSH response to TRH, and the circadian pattern of serum TSH in 10 children and adolescents after radiation therapy for acute lymphoblastic leukemia. Four patients had received central nervous system preventive cranial irradiation and intrathecal chemotherapy, and the remaining 6 patients were treated with craniospinal irradiation for central nervous system relapse. Serum total T4 and T3 concentrations were within the normal range and thyroid antibodies were negative in all patients. Four patients who had received craniospinal irradiation had low free T4 levels. Prior to TRH administration, the overall mean serum TSH concentration was 5.4±1.3 mU/l, and the mean peak response to TRH was 33±6.5 mU/l. Both were significantly increased when compared to the levels observed in our control population (p<0.05 and <0.025, respectively). The overall mean nadir diurnal TSH was 3.6±0.8 mU/l, and the mean peak nocturnal TSH was 6.9±1.3 mU/l, both significantly elevated when compared to normal children (p<0.025). The mean nocturnal TSH surge, however, was not significantly different from normal. Four of 6 children treated with craniospinal irradiation, and one of four children treated with cranial irradiation had increased basal and peak serum TSH concentrations in response to TRH. One of the patients treated with cranial irradiation had an abnormal nocturnal TSH surge. We conclude that subtle primary hypothyroidism is relatively common in patients with acute lymphoblastic leukemia, particularly in those who have been treated with craniospinal irradiation.
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Gayo, L., B. Bonet, A. S. Herranz, R. Iglesias, M. J. Toro, and E. Montoya. "Postnatal development of brain TRH, serum TSH and thyroid hormones in the male and female rat." Acta Endocrinologica 112, no. 1 (1986): 7–11. http://dx.doi.org/10.1530/acta.0.1120007.
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Abstract. The postnatal development of immunoreactive TRH in the central nervous system (CNS), serum TSH and thyroid hormones was studied in both male and female normal rats. While in most structures of the CNS, TRH increased until day 20–30, serum TSH values peaked at day 15 as did T4. Significant differences were also obtained between both sexes in these parameters. These data further support the fact that pituitary-thyroid axis maturation is independent of brain TRH.
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Chung, Shinjae, Xiao-Hui Liao, Caterina Di Cosmo, et al. "Disruption of the Melanin-Concentrating Hormone Receptor 1 (MCH1R) Affects Thyroid Function." Endocrinology 153, no. 12 (2012): 6145–54. http://dx.doi.org/10.1210/en.2011-1435.
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Abstract Melanin-concentrating hormone (MCH) is a peptide produced in the hypothalamus and the zona incerta that acts on one receptor, MCH receptor 1 (MCH1R), in rodents. The MCH system has been implicated in the regulation of several centrally directed physiological responses, including the hypothalamus-pituitary-thyroid axis. Yet a possible direct effect of the MCH system on thyroid function has not been explored in detail. We now show that MCH1R mRNA is expressed in thyroid follicular cells and that mice lacking MCH1R [MCH1R-knockout (KO)] exhibit reduced circulating iodothyronine (T4, free T4, T3, and rT3) levels and high TRH and TSH when compared with wild-type (WT) mice. Because the TSH of MCH1R-KO mice displays a normal bioactivity, we hypothesize that their hypothyroidism may be caused by defective thyroid function. Yet expression levels of the genes important for thyroid hormones synthesis or secretion are not different between the MCH1R-KO and WT mice. However, the average thyroid follicle size of the MCH1R-KO mice is larger than that of WT mice and contained more free and total T4 and T3 than the WT glands, suggesting that they are sequestered in the glands. Indeed, when challenged with TSH, the thyroids of MCH1R-KO mice secrete lower amounts of T4. Similarly, secretion of iodothyronines in the plasma upon 125I administration is significantly reduced in MCH1R-KO mice. Therefore, the absence of MCH1R affects thyroid function by disrupting thyroid hormone secretion. To our knowledge, this study is the first to link the activity of the MCH system to the thyroid function.
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Hoermann, Rudolf, Mark J. Pekker, John E. M. Midgley, and Johannes W. Dietrich. "The role of supporting and disruptive mechanisms of FT3 homeostasis in regulating the hypothalamic–pituitary–thyroid axis." Therapeutic Advances in Endocrinology and Metabolism 14 (January 2023): 204201882311581. http://dx.doi.org/10.1177/20420188231158163.
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Background: Thyroid hormones are controlled by the hypothalamic–pituitary–thyroid (HPT) axis through a complex network of regulatory loops, involving the hormones TRH, TSH, FT4, and FT3. The relationship between TSH and FT4 is widely used for diagnosing thyroid diseases. However, mechanisms of FT3 homeostasis are not well understood. Objective: We used mathematical modelling to further examine mechanisms that exist in the HPT axis regulation for protecting circulating FT3 levels. Methods: A mathematical model consisting of a system of four coupled first-order parameterized non-linear ordinary differential equations (ODEs) was developed, accounting for the interdependencies between the hormones in the HPT axis regulation. While TRH and TSH feed forward to the pituitary and thyroid, respectively, FT4 and FT3 feed backward to both the pituitary and hypothalamus. Stable equilibrium solutions of the ODE system express homeostasis for a particular variable, such as FT3, if this variable stays in a narrow range while certain other parameter(s) and system variable(s) may vary substantially. Results: The model predicts that (1) TSH-feedforward protects FT3 levels if the FT4 production rate declines and (2) combined negative feedback by FT4 and FT3 on both TSH and TRH production rates keeps FT3 levels insensitive to moderate changes in FT4 production rates and FT4 levels. The optimum FT4 and FT3 feedback and TRH and TSH-feedforward ranges that preserve FT3 homeostasis were found by numerical continuation analysis. Model predictions were in close agreement with clinical studies and individual patient examples of hypothyroidism and hyperthyroidism. Conclusions: These findings further extend the concept of HPT axis regulation beyond TSH and FT4 to integrate the more active sister hormone FT3 and mechanisms of FT3 homeostasis. Disruption of homeostatic mechanisms leads to disease. This provides a perspective for novel testable concepts in clinical studies to therapeutically target the disruptive mechanisms.
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Abdulkareem Salman, Mustafa. "Prevalence Of Thyroid Hormones Test Abnormality In Females At Reproductive Age Attending Al-batool Maternity Teaching Hospital." Diyala Journal of Medicine 24, no. 2 (2023): 93–99. http://dx.doi.org/10.26505/djm.24027111208.
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Background: Although there is little information about the prevalence of thyroid disorders in young women, but they are common in Iraq. Objective: To prevalence of thyroid hormones test abnormality in females at reproductive age attending al-batool maternity teaching hospital Patients and Methods: This study involved 1570 of reproductive female ages patients at the Al-batool Maternity Hospital in Diyala Province, Iraq. Serum levels of T3, T4, and TSH were measured in this study. According to the conventional definitions of T3, T4, and TSH levels of overt hyper- and hypothyroidism patients were grouped according to their thyroid status at the time of testing. Results: A total of 1570 subjects were screened of whom 152 subjects (18.6%) had abnormal TSH. The overall prevalence of hyperthyroidism with elevated TSH was 17.4%, of which 1.2% had hypothyroidism with elevated TSH. A low TSH was seen in 1.3% of the study population (P= 0.001). Generally, thyroxin hormone (T4) abnormalities were totaled at 12.02%, of which 10.22% were hypothyroidism and 1.8% was hyperthyroidism. Furthermore, the triiodothyroxin hormone T4 abnormality percentage was 14.84%, compared to hypothyroidism of 3.12% and hyperthyroidism of 11.72%. Conclusion: Thyroid dysfunction was common in young women. Therefore, females more susceptible to thyroid disorders. Keywords: prevalence, thyroid‑stimulating hormone, hyperthyroidism, hypothyroidism, Iraq, women
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Kalsoom, Ume, and Niaz Ali. "Effect of Carbamazepine on the serum level of Thyrotropin Releasing Hormone." International Journal of Basic & Clinical Pharmacology 8, no. 6 (2019): 1349. http://dx.doi.org/10.18203/2319-2003.ijbcp20192201.
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Background: The thyroid gland is endocrine gland located in front and lower side of neck. Thyroid gland secretes two types of thyroid hormones that are triiodothyronine (T3) and tetraiodothyronine (T4). The hypothalamus is a center for regulation of thyroid hormones. It senses the low hormone levels and in turn releases thyrotropin-releasing hormone (TRH). TRH stimulates anterior pituitary to release TSH which then acts on the thyroid gland to maintain normal level of T3 and T4. The objective of study is to determine the effects of carbamazepine on TRH in euthyroid rabbits.Methods: An experimental study performed on 30 rabbits. These were divided into three groups having 10 rabbits in each group. 10 rabbits were treated with 10mg/kg/day of CBZ (OD), other 10 with 35mg/kg/day CBZ (three divided doses) and 10 rabbits served as control. T3, FT4, TSH and TRH levels were evaluated at baseline and after 21 days of treatment in all three groups by Electro-chemiluminescence immunoassay and ELISA respectively.Results: Comparison of the hormone levels of the group and the group having a dose of 10 mg/kg/day 21 days of treatment. Comparative results showed serum level of T3 (P=0.031), FT4 (P=0.030), and TRH (P=0.044) levels significantly lower than the control group and TSH (P=0.057) levels remain unaltered. It was also found that group having a dose of 35 mg/kg/day; TDS showed decrease in T3 (P value 0.001), FT4 (P=0.001), TSH (P=0.003) and TRH (P=0.001) level as compared to control group.Conclusions: Our data suggest that Carbamazepine monotherapy does alter thyroid hormones and its central regulatory hormone TRH. Decrease in TRH level increase level of depression and suicidal thoughts and also risk of tertiary hypothyroidism. These findings could have very important clinical implications.
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Oliveira, K. J., T. M. Ortiga-Carvalho, A. Cabanelas, et al. "Disruption of neuromedin B receptor gene results in dysregulation of the pituitary–thyroid axis." Journal of Molecular Endocrinology 36, no. 1 (2006): 73–80. http://dx.doi.org/10.1677/jme.1.01892.
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The level of thyrotropin (TSH) secretion is determined by the balance of TSH-releasing hormone (TRH) and thyroid hormones. However, neuromedin B (NB), a bombesin-like peptide, highly concentrated in the pituitary, has been postulated to be a tonic inhibitor of TSH secretion. We studied the pituitary–thyroid axis in adult male mice lacking NB receptor (NBR-KO) and their wild-type (WT) littermates. At basal state, NBR-KO mice presented serum TSH slightly higher than WT (18%, P< 0.05), normal intra-pituitary TSH content, and no significant changes in α and β TSH mRNA levels. Serum thyroxine was normal but serum triiodothyronine (T3) was reduced by 24% (P< 0.01) in NBR-KO mice. Pituitaries of NBR-KO mice exhibited no alteration in prolactin mRNA expression but type I and II deiodinase mRNA levels were reduced by 53 and 42% respectively (P< 0.05), while TRH receptor mRNA levels were importantly increased (78%, P< 0.05). The TSH-releasing effect of TRH was significantly higher in NBR-KO than in WT mice (7.1-and 4.0-fold respectively), but, while WT mice presented a 27% increase in serum T3 (P< 0.05) after TRH, NBR-KO mice showed no change in serum T3 after TRH. NBR-KO mice did not respond to exogenous NB, while WT showed a 30% reduction in serum TSH. No compensatory changes in mRNA expression of NB or other bombesin-related peptides and receptors (gastrin-releasing peptide (GRP), GRP-receptor and bombesin receptor subtype-3) were found in the pituitary of NBR-KO mice. Therefore, the data suggest that NB receptor pathways are importantly involved in thyrotroph gene regulation and function, leading to a state where TSH release is facilitated especially in response to TRH, but probably with a less-bioactive TSH. Therefore, the study highlights the important role of NB as a physiological regulator of pituitary–thyroid axis function and gene expression.
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Ertek, Sibel. "Molecular economy of nature with two thyrotropins from different parts of the pituitary: pars tuberalis thyroid-stimulating hormone and pars distalis thyroid-stimulating hormone." Archives of Medical Science 17, no. 1 (2021): 189–95. http://dx.doi.org/10.5114/aoms/102476.
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Thyrotropin (TSH) is classically known to be regulated by negative feedback from thyroid hormones and stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus. At the end of the 1990s, studies showed that thyrotroph cells from the pars tuberalis (PT) did not have TRH receptors and their TSH regulation was independent from TRH stimulation. Instead, PT-thyrotroph cells were shown to have melatonin-1 (MT-1) receptors and melatonin secretion from the pineal gland stimulates TSH- subunit formation in PT. Electron microscopy examinations also revealed some important differences between PT and pars distalis (PD) thyrotrophs. PT-TSH also have low bioactivity in the peripheral circulation. Studies showed that they have different glycosylations and PT-TSH forms macro-TSH complexes in the periphery and has a longer half-life. Photoperiodism affects LH levels in animals via decreased melatonin causing increased TSH- subunit expression and induction of deiodinase-2 (DIO-2) in the brain. Mammals need a light stimulus carried into the suprachiasmatic nucleus (which is a circadian clock) and then transferred to the pineal gland to synthesize melatonin, but birds have deep brain receptors and they are stimulated directly by light stimuli to have increased PT-TSH, without the need for melatonin. Photoperiodic regulations via TSH and DIO 2/3 also have a role in appetite, seasonal immune regulation, food intake and nest-making behaviour in animals. Since humans have no clear seasonal breeding period, such studies as recent ‘’domestication locus’’ studies in poultry are interesting. PT-TSH that works like a neurotransmitter in the brain may become an important target for future studies about humans.
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Ertek, Sibel. "Molecular economy of nature with two thyrotropins from different parts of the pituitary: pars tuberalis thyroid-stimulating hormone and pars distalis thyroid-stimulating hormone." Archives of Medical Science 17, no. 1 (2021): 189–95. http://dx.doi.org/10.5114/aoms/102476.
Full textAbstract:
Thyrotropin (TSH) is classically known to be regulated by negative feedback from thyroid hormones and stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus. At the end of the 1990s, studies showed that thyrotroph cells from the pars tuberalis (PT) did not have TRH receptors and their TSH regulation was independent from TRH stimulation. Instead, PT-thyrotroph cells were shown to have melatonin-1 (MT-1) receptors and melatonin secretion from the pineal gland stimulates TSH- subunit formation in PT. Electron microscopy examinations also revealed some important differences between PT and pars distalis (PD) thyrotrophs. PT-TSH also have low bioactivity in the peripheral circulation. Studies showed that they have different glycosylations and PT-TSH forms macro-TSH complexes in the periphery and has a longer half-life. Photoperiodism affects LH levels in animals via decreased melatonin causing increased TSH- subunit expression and induction of deiodinase-2 (DIO-2) in the brain. Mammals need a light stimulus carried into the suprachiasmatic nucleus (which is a circadian clock) and then transferred to the pineal gland to synthesize melatonin, but birds have deep brain receptors and they are stimulated directly by light stimuli to have increased PT-TSH, without the need for melatonin. Photoperiodic regulations via TSH and DIO 2/3 also have a role in appetite, seasonal immune regulation, food intake and nest-making behaviour in animals. Since humans have no clear seasonal breeding period, such studies as recent ‘’domestication locus’’ studies in poultry are interesting. PT-TSH that works like a neurotransmitter in the brain may become an important target for future studies about humans.
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Scheepers, Max H. M. C., Zaid J. J. Al-Difaie, Nicole D. Bouvy, Bas Havekes, and Alida A. Postma. "Four-Dimensional Dual-Energy Computed Tomography-Derived Parameters and Their Correlation with Thyroid Gland Functional Status." Tomography 11, no. 3 (2025): 22. https://doi.org/10.3390/tomography11030022.
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Purpose: Dual-energy computed tomography (DECT) allows for the measurement of iodine concentration, a component for the synthesis of thyroid hormones. DECT can create virtual non-contrast (VNC) images, potentially reducing radiation exposure. This study explores the correlations between thyroid function and iodine concentration, as well as the relationship between thyroid densities in true non-contrast (TNC) and virtual non-contrast (VNC) images and thyroid function. Methods: The study involved 87 patients undergoing 4D-CT imaging with single and dual-energy scans for diagnosing primary hyperparathyroidism. Thyroid densities and iodine concentrations were measured across all scanning phases. These measurements were correlated with thyroid function, indicated by TSH and FT4 levels. Differences in thyroid density between post-contrast phases and TNC phases (ΔHU) were analyzed for correlations with thyroid function and iodine concentrations. Results: Positive correlations between iodine concentrations and TSH were found, with Spearman’s coefficients (R) of 0.414, 0.361, and 0.349 for non-contrast, arterial, and venous phases, respectively. Thyroid density on TNC showed significant positive correlations with TSH levels (R = 0.436), consistently across both single- (R = 0.435) and dual-energy (R = 0.422) scans. Thyroid densities on VNC images did not correlate with TSH or FT4. Differences in density between contrast and non-contrast scans (ΔHU) negatively correlated with TSH (p = 0.002). Conclusions: DECT-derived iodine concentrations and thyroid densities in non-contrast CT scans demonstrated positive correlations with thyroid function, in contrast to thyroid densities on VNC scans. This indicates that VNC images are unsuitable for this purpose. Correlations between ΔHU and TSH suggest a potential link between the thyroid’s structural properties to capture iodine and its hormonal function. This study underscores the potential value of (DE-) CT imaging for evaluating thyroid function as an additional benefit in head and neck scans.
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Rawat, Renu, Rimpy Saini, Ruby Rani Agarwal, and Shashi Kant Tiwari. "ASSESSMENT OF RASA, RAKTA, MAMSA AND MEDO DHATU LEVEL IN HY-POTHYROIDISM." International Ayurvedic Medical Journal 13, no. 02 (2025): 417–21. https://doi.org/10.46607/iamj1713022025.
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Ayurveda, an age-old Indian medical system, is well-known for its natural remedies and comprehensive approach to wellness. Thyroid hormones are an essential part of the human endocrine system and play a significant role in the metabolism, growth and development of tissues. Thyrotropin-releasing hormone (TRH) produced by the hypothalamus acts on the pituitary to stimulate the synthesis and release of TSH. TSH stimulates the thyroid to secrete mainly T4 and T3. An increase in the level of thyroid hormones inhibits the release of TRH from the hypothalamus and TSH from the pituitary, while a fall in the level of thyroid hormones leads to an increase in the level of TRH and TSH. As per Ayurvedic doctrine, health and disease assessment are determined by the status of Agni, Dosha, Dhatu, Mala, and Srotas in the body. Metabolic activities are linked to the development and function of Dhatus, and it has been observed that hypothyroidism impairs this metabolism. Agni is fundamental to health and disease and is crucial to metabolism. Therefore, assessment of the Dhatu and agni is a key factor in determining the severity of hypothyroidism. The relationship between Dhatu Kshaya Vridhi and hypothyroidism can help in providing a new line of Ayurvedic treatment.