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Academic literature on the topic 'Tsh-rh'
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Journal articles on the topic "Tsh-rh"
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Pontikides, Nickolaos, Spyridon Karras, Antonios Papagiannis, Athina Kaprara, Panagiotis Anagnostis, George Noussios, Argyrios Doumas, et al. "Recombinant Human Thyrotropin-Aided Radioiodine Therapy in Tracheal Obstruction by an Invading Well-Differentiated Thyroid Carcinoma." Case Reports in Otolaryngology 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/579527.
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Papillary thyroid carcinomas (PTCs) usually extend to lymph nodes in the neck and mediastinum. Rarely, they invade the neighboring upper airway anatomical structures. We report a 56-year-old woman who presented with symptoms of upper airway obstruction. Imaging studies revealed a lesion derived from the thyroid which invaded and obstructed the trachea, which appeared to be a highly differentiated PTC. Total thyroidectomy was performed, with removal of the endotracheal part of the mass along with the corresponding anterior tracheal rings. Two months later, a whole body I131scan after recombinant human thyroid-stimulating hormone (rh-TSH) administration was performed and revealed a residual mass in upper left thyroid lobe. Subsequently, 150 mCi I131were given following rh-TSH administration. Nine months later, there was no sign of residual tumor. This case is the first one reported in the literature regarding rh-TSH administration prior to RAI ablation in a PTC obstructing the trachea.
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Ma, Loretta, AnneMarie Gagnon, Anne Landry, Timothea Le, Fengxia Xiao, Cathy Sun, Heather Lochnan, Dylan Burger, and Alexander Sorisky. "Thyroid-Stimulating Hormone-Stimulated Human Adipocytes Express Thymic Stromal Lymphopoietin." Hormone and Metabolic Research 50, no. 04 (February 19, 2018): 325–30. http://dx.doi.org/10.1055/s-0044-101834.
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AbstractWhen recombinant human (rh) thyroid-stimulating hormone (TSH) is administered to thyroid cancer survivors, an acute extra-thyroidal effect raises pro-inflammatory cytokines and activates platelets. Thymic stromal lymphopoietin (TSLP) is a cytokine recently implicated in platelet activation. Our aim was to measure platelet microparticle levels after rhTSH stimulation in vivo, and to investigate TSLP expression in TSH-stimulated human adipocytes in culture. Blood samples for total and platelet microparticle analysis were obtained from thyroid cancer survivors before (day 1) and after rhTSH administration (day 5). Adipocytes, differentiated from stromal preadipocytes isolated from adipose tissue from surgical patients, were stimulated with TSH. TSLP mRNA expression, protein expression, and protein release into the adipocyte medium were measured. The level of platelet microparticles in thyroid cancer patients rose 5-fold after rhTSH stimulation. TSH upregulated TSLP mRNA expression in adipocytes in culture through a pathway that was inhibited by 66% by H89, a protein kinase A inhibitor. TSLP protein expression rose in response to TSH, and TSH-stimulated TSLP release into the medium was completely blocked by dexamethasone. In conclusion, TSLP is a novel TSH-responsive adipokine. Future studies will be needed to address the potential role of adipocyte-derived TSLP and whether it is linked to TSH-dependent platelet activation.
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Antunes, T. T., A. Gagnon, B. Chen, F. Pacini, T. J. Smith, and A. Sorisky. "Interleukin-6 release from human abdominal adipose cells is regulated by thyroid-stimulating hormone: effect of adipocyte differentiation and anatomic depot." American Journal of Physiology-Endocrinology and Metabolism 290, no. 6 (June 2006): E1140—E1144. http://dx.doi.org/10.1152/ajpendo.00516.2005.
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Adipose cells are extrathyroidal targets of thyroid-stimulating hormone (TSH). TSH stimulates interleukin-6 (IL-6) release from adipocytes. We examined TSH responsiveness as a function of stage of differentiation or adipose tissue depot in cultured adipose cells and determined the effect of TSH on extrathyroidal IL-6 production in vivo. Stromal preadipocytes, isolated from human abdominal subcutaneous or omental adipose tissue, and their differentiated counterparts were studied. IL-6 protein concentration in the medium was measured after TSH stimulation. Basal IL-6 release was greater for preadipocytes than differentiated adipocytes, whether derived from subcutaneous or omental fat depots. A depot-dependent effect (omental > subcutaneous) on basal IL-6 release was observed for preadipocytes (1.6-fold, P < 0.05); a similar trend for differentiated adipocytes was not significant (6.2-fold, P > 0.05). IL-6 responsiveness to TSH was observed upon differentiation, but only for subcutaneous adipocytes (1.9-fold over basal, P < 0.001). To determine if TSH could stimulate IL-6 release from extrathyroidal tissues in vivo, we measured serum IL-6 levels from five thyroidectomized patients who received recombinant human (rh) TSH and found that levels increased by threefold on days 3 and 4 ( P < 0.05) after its administration. Our data demonstrate that stage of differentiation and fat depot origin affect basal and TSH-stimulated IL-6 release from adipose cells in culture. Furthermore, rhTSH elevates serum IL-6 response in thyroidectomized patients, indicating an extrathyroidal site of TSH action.
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Dedov, Ivan I., Pavel O. Rumyantsev, Ksenia S. Nizhegorodova, Konstantin Y. Slashchuk, Valentina S. Yasyuchenya, Marina S. Sheremeta, Michail V. Degtyarev, Larisa V. Nikankina, and Galina A. Melnichenko. "Recombinant human thyrotropin in radioiodine diagnostics and radioiodine ablation of patients with well-differentiated thyroid cancer: the first experience in Russia." Endocrine Surgery 12, no. 3 (December 27, 2018): 128–39. http://dx.doi.org/10.14341/serg9806.
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Background. Traditional endogenous stimulation of thyroid-stimulating hormone (TSH) by means of long-term withdrawal of thyroid hormones for radioiodine diagnostics and radioiodine therapy causes severe hypothyroidism, which worsens patients’ general well-being and may lead to side effects and cause tumor growth and dissemination. Exogenous stimulation with recombinant human TSH (rh-TSH, thyrotropin-alfa) causes short-term increases in TSH levels and does not have the above-mentioned side effects.
Purpose. To estimate the efficacy and safety of rh-TSH in preparation of patients with well-differentiated thyroid cancer for radioiodine diagnostics and radioiodine therapy.
Methods. We conducted an interventional single-center prospective unblinded uncontrolled study of the efficacy and safety of thyrotropin-alfa to prepare patients with well-differentiated thyroid cancer to radioiodine diagnostics and post-surgery radioiodine ablation. The study included 88 patients with well-differentiated thyroid cancer: 54 patients were prepared for post-surgery radioiodine ablation; 34 patients – for radioiodine diagnostics to evaluate combined treatment efficacy and exclusion of tumor recurrence. The level of TSH, thyroglobulin, antibodies to thyroglobulin, whole body scintigraphy, and side effects were measured during exogenous stimulation with thyrotropin-alfa.
Results. The level of TSH reached or exceed the target level (30 mIU/ml) 24 hours after the first injection of recombinant thyrotropin-alfa in 86% of patients; after 48 hours in 100%, the level exceeding 100 IU/ml was observed in 66 (75.1%) patients. The maximum levels of thyroglobulin and antibodies to thyroglobulin were reached 72 and 48 hours after the first injection, respectively. The injections of thyrotropin-alfa were well-tolerated by the patients. In the group for radioiodine diagnostics 2 (5.8%) patients complained of fatigue, 1 (2.9%) patient had signs of dyspeptic disorder, while in the group for radioiodine ablation 4 (7.4%) patients complained of fatigue, 1 (1.8%) patient had marked memory problems that disappeared later (they must have been caused by the patient’s advanced age (82 years)).
Conclusions. Exogenous recombinant human thyroid-stimulating hormone (thyrotropin-alpha) is highly effective in preparation of patients with well-differentiated thyroid cancer for radioiodine diagnostics and radioiodine ablation. It does not have side effects, which are typical of withdrawal of thyroid hormones. The levels of thyroglobulin and antibodies to thyroglobulin measured 72 hours after the first injection of thyrotropin-alfa have the biggest diagnostic informative value.
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Gall, E., M. C. Eberle, E. Deshayes, I. Raingeard, H. Lemoyne-De-Forges, and J. Bringer. "Valeur pronostique du relargage précoce de thyroglobuline au cours de l’irathérapie sous rh-TSH." Annales d'Endocrinologie 76, no. 4 (September 2015): 357. http://dx.doi.org/10.1016/j.ando.2015.07.183.
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Kadambi, Prahlad, MA Ramprakash, Gandi Soujanya, and L Sushanth Prabhath Reddy. "Association between Thyroid Profile and Serum Bilirubin Levels in Term Neonates on Day 3 of Life." Asian Journal of Clinical Pediatrics and Neonatology 8, no. 2 (July 9, 2020): 42–45. http://dx.doi.org/10.47009/ajcpn.2020.8.2.8.
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Background: Neonatal indirect hyperbilirubinemia is a common clinical scenario that manifests as jaundice in the first week of life. Studies have shown that the physiological peak of serum bilirubin (SBR) levels is highest at 72 hours of life as a result of which SBR is measured at 72 hours of life routinely. The American Academy of Pediatricians (AAP) recommends routine screening for congenital hypothyroidism within the first week of life for all neonates. In common practice, both parameters are assessed simultaneously at 72 hours of life. This study aims to correlate thyroid Profile and serum bilirubin levels assessed in term neonates at 72 hours of life. Subjects and Methods: Our retrospective study included 105 term neonates born through cesarean-section at MMCHRI, Kanchipuram; between August 2018 and August 2019. Pre-term, neonates born to eclamptic, pre-eclamptic, diabetic, hypothyroid, Rh-incompatible mothers were excluded from the study. The data collected included Birth Weight, Gestational Age, Thyroid Profile (T3, T4, TSH), SBR (Total and Direct). Data were analyzed using SPSS v16. Results: The mean gestational age of the study population was 268.05 6.25 days, and mean birth weight was 2.997 0.36 kgs. The mean serum levels of total bilirubin were 11.36 3.52 mg/dl. The mean serum fT3, fT4, TSH levels were 8.17 23.2 pg/ml, 2.16 1.68 ng/dl and 4.07 3.4 mIU/ml respectively. A positive association was noted between serum TSH and total serum bilirubin (r= 0.176, p = 0.067) but not statistically significant. Conclusion: Our study has not shown a significant association between serum TSH and SBRT in term neonates. However, the simultaneous assessment remains practical in practice.
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Eberle-Pouzeratte, M. C., and I. Raingeard. "Évaluation d’un protocole de stimulation mixte couplant sevrage court en lévothyroxine et rh-TSH avant irathérapie en Languedoc-Roussillon." Annales d'Endocrinologie 78, no. 4 (September 2017): 261. http://dx.doi.org/10.1016/j.ando.2017.07.131.
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Tiosano, Dov, Lea Even, Zila Shen Orr, and Ze’ev Hochberg. "Recombinant Thyrotropin in the Diagnosis of Congenital Hypothyroidism." Journal of Clinical Endocrinology & Metabolism 92, no. 4 (April 1, 2007): 1434–37. http://dx.doi.org/10.1210/jc.2006-2134.
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Abstract Context: A modern approach to congenital hypothyroidism requires a definitive diagnosis of the underlying mechanisms; this can be achieved within the first weeks of life. When uncertainty persists, treatment is commenced, and the definitive diagnosis of congenital hypothyroidism is deferred to the age of 3 yr. Objectives: The interruption of thyroid replacement treatment is perceived as risky by parents and physicians. The aim of this pilot study was to test the possibility of a definitive diagnosis during thyroid replacement treatment, using stimulation of thyroid tissue by recombinant human (rh)TSH. Subjects: Eight patients, three boys and five girls, age 5–15 yr (mean, 9.5 ± 3.7 yr), with congenital hypothyroidism that had been diagnosed by the neonatal screening program, and having their diagnosis verified between the ages of 3–4 yr, were reevaluated while on thyroid replacement therapy. Interventions: Patients received im 0.6 mg/m2 rhTSH on two consecutive days. Results: rhTSH pharmacokinetics, maximal concentration, t1/2, and area under the curve in children were different as compared with adults. In the patients with intact TSH receptors, free T4 levels decreased after the first and the second injection of rhTSH (P = 0.0137 and P = 0.0149, respectively). All eight children showed identical scintigraphy after rhTSH administration as compared with thyroid replacement withdrawal. Conclusions: The use of rhTSH is effective for definitive diagnosis of congenital hypothyroidism during thyroid replacement treatment, and no safety issues were encountered.
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Nielsen, Viveque Egsgaard, Steen J. Bonnema, and Laszlo Hegedüs. "Transient Goiter Enlargement after Administration of 0.3 mg of Recombinant Human Thyrotropin in Patients with Benign Nontoxic Nodular Goiter: A Randomized, Double-Blind, Crossover Trial." Journal of Clinical Endocrinology & Metabolism 91, no. 4 (April 1, 2006): 1317–22. http://dx.doi.org/10.1210/jc.2005-2137.
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Background: Recombinant human (rh) TSH, in doses from 0.01 to 0.9 mg, has been used to augment the effect of radioiodine (131I) therapy in patients with a benign nontoxic nodular goiter. Transient thyroid enlargement and thyrotoxicosis may be seen following 131I therapy. Aim: The aim of the study was to investigate whether rhTSH per se causes goiter enlargement, until now an issue evaluated only in healthy nongoitrous subjects. Methods: In random order, 10 patients with nontoxic nodular goiter [mean 39.8 ± 20.5 (sd) ml] received either 0.3 mg rhTSH or isotonic saline in a double-blinded crossover design. Thyroid volume (by ultrasound) and function were closely monitored during the following 28 d. Results: Saline injection did not affect thyroid function or size. After rhTSH, median serum TSH increased from baseline 0.97 mU/liter (range 0.39–1.56) to 37.0 mU/liter (range 18.5–55.0) at 24 h (P < 0.01), with a subsequent decline to subnormal levels at d 7. Mean free T4 and free T3 increased significantly from baseline to a maximum at 48 h. Twenty-four hours after rhTSH, the mean goiter volume was significantly increased by 9.8 ± 2.3% (sem) (P = 0.01) and after 48 h by 24.0 ± 5.1% (P = 0.002). The goiter enlargement had reverted at d 7. Nine patients had symptoms of hyperthyroidism and/or cervical compression after rhTSH, as opposed to one during placebo treatment (P < 0.02). Conclusions: A transient average goiter enlargement of up to 24% is seen after 0.3 mg rhTSH. This may lead to a significant cervical compression when used for augmentation of 131I therapy in patients with goiter. The use of lower doses of rhTSH needs to be explored.
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Bãrbuş, Elena, Claudiu Peştean, Maria Iulia Larg, and Doina Piciu. "Quality of life in thyroid cancer patients: a literature review." Medicine and Pharmacy Reports 90, no. 2 (April 26, 2017): 147–53. http://dx.doi.org/10.15386/cjmed-703.
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Introduction. Quality of life (QoL) has received increasing interest in the last years, especially in patients with cancer. This article aims to analyze a selection of medical research papers regarding the quality of life in patients with thyroid carcinoma. We overviewed the main QoL aspects derived from several studies and highlighted those less researched issues, which could represent a solid base for future clinical studies.Method. We used an integrative selection method of medical literature, choosing mostly "free access" studies, as it was considered that they could be easily viewed, searched and researched including by patients.Results. After an integrative literature review, we selected 16 relevant studies. Patients with thyroid cancer have several factors influencing their QoL, with both physical and psychological impact. The decisive factors are the quality of the surgical act, radioiodine therapy, follow-up using rh-TSH vs. hormonal withdrawal, access to behavioral help and the relationship with their physician.Conclusion. We must understand the emotional impact of the cancer diagnosis on the patient and we must collaborate in order to help the patient restore the psychosomatic balance and to recover the quality of life.
Dissertations / Theses on the topic "Tsh-rh"
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Desrues, Laurence. "Contribution à l'étude des mécanismes de couplage stimulus-réponse impliqués dans le contrôle de la sécrétion d'α-MSH par les cellules mélanotropes de l'hypophyse des amphibiens : mode d'action de la TRH, de la dopamine et du GABA." Rouen, 1993. http://www.theses.fr/1993ROUES050.
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Les cellules du lobe intermédiaire sécrètent l'alpha-MSH, une hormone impliquée dans le processus d'homochromie chez les amphibiens. Ces cellules sont soumises à un contrôle hypothalamique complexe. Nous avons recherché les mécanismes intracellulaires impliqués dans la libération d'α-MSH en réponse à la TRH, à la dopamine et au GABA. Chez la grenouille, la TRH est sans effet sur le système adénylate-cyclasique mais induit simultanément une augmentation rapide du taux d'IP3 et une réduction du taux de PIP2 indiquant que les récepteurs de la TRH présents au niveau des cellules mélanotropes sont couplés positivement à la phospholipase C. L'effet de la dopamine sur la sécrétion d'α-MSH est médié par la fermeture de canaux calciques voltage-dépendants et une réduction de l'activité adénylate-cyclasique. De plus, la dopamine provoque une diminution de la production d'IP3 qui participe au maintien de l'effet inhibiteur. L'action du GABA sur la libération d'α-MSH met en jeu principalement des récepteurs [GABA]A dont l'activité est modulée par l'AMPc. Par ailleurs, le GABA stimule des récepteurs [GABA]B négativement couplés à l'adénylate-cyclase ce qui suggère une interaction possible entre les 2 types de récepteurs GABA ergiques. Les agonistes [GABA]A provoquent également une augmentation de la [Ca2+]i médié par l'ouverture de canaux calciques voltage-dépendants de type L; ce phénomène est responsable de l'augmentation transitoire de la sécrétion d'α-MSH produite par le GABA. Le TEA prolonge l'augmentation de la [Ca2+]i induite par les agonistes [GABA]A, suggérant l'intervention de canaux K+ dans l'inhibition de la sécrétion d'α-MSH. Chez le xénope, un traitement de 2 h par la dopamine ou le GABA provoque un blanchiment de la peau et une diminution du taux d'α-MSH circulant sans que les taux des inositols phosphates ne soient modifiés. En revanche, un traitement de 3 jours par l'apomorphine inhibe la production des inositols phosphates suggérant que l'inhibition du turnover des phospholipides inositols induite par la dopamine modulerait la synthèse plus que la libération d'α-MSH. En conclusion, nous montrons que la TRH, la dopamine et le GABA agissent via des récepteurs couplés simultanément à plusieurs mécanismes de transduction. Nos résultats indiquent que l'intégration de l'information au niveau de la cellule mélanotrope ne peut se concevoir comme la simple somme algébrique des effets stimulateurs et inhibiteurs
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Charli, Jean-Louis. "Biosynthese, liberation et inactivation de quelques peptides dans le systeme nerveux central." Paris 6, 1987. http://www.theses.fr/1987PA066304.
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Valentijn, Karine. "Contribution à l'étude du rôle neuroendocrinien des neuropeptides Ps4 et Ps5, deux peptides de connexion issus du précurseur de la thyrolibérine." Rouen, 1998. http://www.theses.fr/1998ROUES018.
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Le précurseur de la thyrotropin-releasing hormone (TRH), un facteur hypophysiotrope impliqué dans la régulation de l'axe hypophyso-thyroïdien, contient plusieurs copies de la TRH reliées entre elles par des peptides intercalaires. L'objectif de notre étude visait à tester l'hypothèse d'une fonction biologique des peptides intercalaires Ps4 (prepro-TRH[160-169]) et Ps5 (prepro-TRH[178-199]), pour lesquels respectivement, des rôles potentialisateurs de la libération de TSH stimulée par la TRH et inhibiteur de la sécrétion de GH ont été rapportés. Nous avons montré que Ps4 et Ps5 sont co-libérés par des tranches d'hypothalamus de rat selon un mécanisme dépendant du potentiel membranaire et du calcium. En revanche, la sécrétion stimulée ne dépend pas de canaux sodiques sensibles a la tétrodotoxine mais fait intervenir des canaux calciques sensibles au voltage dont le profil pharmacologique est différent de celui des canaux de type L et N. Nous avons localisé et caracterisé des sites de liaison d'un analogue radioiodé de Ps4 dans l'hypophyse antérieure et montré que 26% des cellules de la pars distalis possèdent des récepteurs de ce peptide. Une caractérisation immunocytochimique sur coupe semi-fines montre que les récepteurs du Ps4 sont portés par les cellules folliculo-stellaires. Nous avons également montré que le taux de récepteurs antéhypophysaires du Ps4 augmente au cours du développement post-natal et subit des variations au moment du sevrage. L'ensemble de nos données étaie l'hypothèse d'une fonction neuroendocrinienne des peptides Ps4 et Ps5.
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Ebiou, Jean-Claude. "Le rôle biologique de la thyrotropin-releasing hormone (TRH) dans le pancréas endocrine." Paris 7, 1992. http://www.theses.fr/1992PA077056.
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L'objectif de ce travail est la recherche du rôle biologique de la TRH pancréatique. La TRH a été initialement isolée de l'hypothalamus et caractérisée comme pGlu-His-ProNH₂. Elle a ensuite été détectée dans le pancréas endocrine désigne comme deuxième site de synthèse du peptide. La TRH est synthétisée à partir d'un précurseur de haut poids moléculaire. La maturation complète de celui-ci génèrerait 5 molécules de TRH, et 7 peptides de connexion. Nous avons montré que la TRH secrétée par le pancréas a les mêmes caractéristiques chromatographiques que le peptide synthétique. La sécrétion de la TRH pendant le développement est stimulé par le glucose et l'arginine, tandis que ces mêmes secretagogues inhibent la sécrétion chez l'adulte. Fait intéressant, la sécrétion de la TRH augmente avec l’âge, en dépit de la chute des contenus pancréatiques. Nous avons caractérise deux peptides de connexion de la prepro-TRH: prepro-TRH160-169 et prepro-TRH178-199, dans des ilots de Langerhans, et le prepro-TRH178-199 dans le milieu de sécrétion. Concernant le rôle biologique de la TRH pancréatique, nous avons montré que: la TRH exogène stimule la sécrétion basale du glucagon; l'immunoneutralisation de la TRH endogène secrétée par l'anticorps anti-TRH inhibe significativement la sécrétion du glucagon induite par l'arginine, la sécrétion de somatostatine est légèrement inhibée. Sur une fistule pancréatique, la TRH inhibe la sécrétion exocrine des protéines, bicarbonates, et du sodium. Les résultats préliminaires sur les cellules acinaires indiquent une absence d'effet TRH. L'effet TRH, observe in vivo, serait medié par le système nerveux central. Au cours du développement, la TRH n'a pas d'effet sur les secrétions d'insuline et glucagon. Nous pensons qu'elle agirait sur le processus de prolifération des cellules insulaires. La TRH stimule la sécrétion du glucagon des cellules alpha. Il serait intéressant de rechercher l'action biologique des deux peptides de connexion. La détermination du mécanisme d'action de la TRH pancréatique implique la caractérisation des sites de liaison spécifiques. Ce travail a été publié dans: Endocrinology 1992, 130(3):1371-1379; Endocrinology 1992, 131(2) (à paraitre en aout); prostate tumeurs 1991, (7):9-10 et 1992(9):6-7.