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[PMID]:29320567
[Au] Autor:Gil-Cayuela C; Ortega A; Tarazón E; Martínez-Dolz L; Cinca J; González-Juanatey JR; Lago F; Roselló-Lletí E; Rivera M; Portolés M
[Ad] Endereço:Cardiocirculatory Unit, Health Research Institute of La Fe University Hospital (IIS La Fe), Valencia, Spain.
[Ti] Título:Myocardium of patients with dilated cardiomyopathy presents altered expression of genes involved in thyroid hormone biosynthesis.
[So] Source:PLoS One;13(1):e0190987, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The association between dilated cardiomyopathy (DCM) and low thyroid hormone (TH) levels has been previously described. In these patients abnormal thyroid function is significantly related to impaired left ventricular (LV) function and increased risk of death. Although TH was originally thought to be produced exclusively by the thyroid gland, we recently reported TH biosynthesis in the human ischemic heart. OBJECTIVES: Based on these findings, we evaluated whether the genes required for TH production are also altered in patients with DCM. METHODS: Twenty-three LV tissue samples were obtained from patients with DCM (n = 13) undergoing heart transplantation and control donors (n = 10), and used for RNA sequencing analysis. The number of LV DCM samples was increased to 23 to determine total T4 and T3 tissue levels by ELISA. RESULTS: We found that all components of TH biosynthesis are expressed in human dilated heart tissue. Expression of genes encoding thyroperoxidase (-2.57-fold, P < 0.05) and dual oxidase 2 (2.64-fold, P < 0.01), the main enzymatic system of TH production, was significantly altered in patients with DCM and significantly associated with LV remodeling parameters. Thyroxine (T4) cardiac tissue levels were significantly increased (P < 0.01), whilst triiodothyronine (T3) levels were significantly diminished (P < 0.05) in the patients. CONCLUSIONS: Expression of TH biosynthesis machinery in the heart and total tissue levels of T4 and T3, are altered in patients with DCM. Given the relevance of TH in cardiac pathology, our results provide a basis for new gene-based therapeutic strategies for treating DCM.
[Mh] Termos MeSH primário: Autoantígenos/genética
Cardiomiopatia Dilatada/genética
Oxidases Duais/genética
Iodeto Peroxidase/genética
Proteínas de Ligação ao Ferro/genética
Miocárdio/metabolismo
Receptores da Tireotropina/genética
Hormônios Tireóideos/biossíntese
[Mh] Termos MeSH secundário: Autoantígenos/metabolismo
Biomarcadores/metabolismo
Cardiomiopatia Dilatada/patologia
Estudos de Casos e Controles
Oxidases Duais/metabolismo
Feminino
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Seres Humanos
Iodeto Peroxidase/metabolismo
Proteínas de Ligação ao Ferro/metabolismo
Masculino
Meia-Idade
Receptores da Tireotropina/metabolismo
Remodelação Ventricular
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantigens); 0 (Biomarkers); 0 (Iron-Binding Proteins); 0 (Receptors, Thyrotropin); 0 (Thyroid Hormones); EC 1.11.1.- (Dual Oxidases); EC 1.11.1.7 (TPO protein, human); EC 1.11.1.8 (Iodide Peroxidase); EC 1.6.3.1 (DUOX2 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190987


  2 / 3186 MEDLINE  
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[PMID]:29381976
[Au] Autor:Yu P; Liu S; Zhou X; Huang T; Li Y; Wang H; Yuan G
[Ad] Endereço:Department of Internal Medicine.
[Ti] Título:Thyroid-associated orbitopathy in patients with thyroid carcinoma: A case report of 5 cases.
[So] Source:Medicine (Baltimore);96(47):e8768, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Thyroid-associated orbitopathy (TAO) is most often seen in patients with autoimmune thyroid disease. Data about TAO occurred in patients with thyroid carcinoma are rare. We give a report of 5 patients to present the clinical characteristics, treatment, and prognosis of this type of case. PATIENT CONCERNS: Five thyroid carcinoma patients presented with orbitopathy. Among them, two patients (patient 1 and 4) were hyperthyroid and TSH receptor antibody (TRAb) positive, two patients (patient 3 and 5) were euthyroid and displayed slightly elevated TRAb titres, one patient (patient 2) was euthyroid and TRAb negative. DIAGNOSES: They were diagnosed as thyroid carcinoma and TAO. INTERVENTIONS: Patient 1 underwent total thyroidectomy, intravenous glucocorticoids (GCs) therapy, orbital decompression surgery and oral GCs therapy. Patient 2 and 3 only received total thyroidectomy. Patient 4 received sub-total thyroidectomy and oral GCs therapy. patient 5 didn't received thyroidectomy and underwent intravenous GCs therapy for 2 courses. OUTCOMES: Patient 1,2,3 showed an improvement of TAO at the final follow-up. Patient 4,5 showed no improvement of TAO at the final follow-up. LESSONS: When TAO present in patients with thyroid nodules, the possibility of thyroid carcinoma should be considered, and the nature of these nodules should be carefully evaluated. In some patients with thyroid carcinoma and TAO, the remission of TAO can be seen post total thyroidectomy. But for other patients, besides thyroidectomy, an adequate dose and course of intravenous GCs treatment and even ocular surgery are also needed.
[Mh] Termos MeSH primário: Oftalmopatia de Graves/etiologia
Doenças Orbitárias/etiologia
Neoplasias da Glândula Tireoide/complicações
[Mh] Termos MeSH secundário: Adulto
Feminino
Glucocorticoides/uso terapêutico
Oftalmopatia de Graves/patologia
Oftalmopatia de Graves/terapia
Seres Humanos
Masculino
Meia-Idade
Órbita/patologia
Doenças Orbitárias/patologia
Doenças Orbitárias/terapia
Receptores da Tireotropina/imunologia
Neoplasias da Glândula Tireoide/patologia
Neoplasias da Glândula Tireoide/terapia
Tireoidectomia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucocorticoids); 0 (Receptors, Thyrotropin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008768


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[PMID]:28455095
[Au] Autor:Wang F; Liu C; Jia X; Liu X; Xu Y; Yan S; Jia X; Huang Z; Liu S; Gu M
[Ad] Endereço:Prenatal Diagnosis Center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China; Department of Endocrinology and Metabolism, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
[Ti] Título:Next-generation sequencing of NKX2.1, FOXE1, PAX8, NKX2.5, and TSHR in 100 Chinese patients with congenital hypothyroidism and athyreosis.
[So] Source:Clin Chim Acta;470:36-41, 2017 Jul.
[Is] ISSN:1873-3492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The abnormal expression of certain transcription factors (NKX2.1, FOXE1, NKX2.5, and PAX8) and thyroid stimulating hormone receptor (TSHR) genes has been associated with athyreosis, which is a form of thyroid dysgenesis (TD). We aimed to identify candidate gene mutations in CH patients with athyreosis and to establish the genotype-phenotype correlations in a Chinese population. METHODS: The exons and flanking sequences of NKX2.1, FOXE1, NKX2.5, PAX8, and TSHR were screened by next-generation sequencing and further confirmed by direct Sanger sequencing. The mutation frequencies were calculated and compared against databases. The relationship between genotype and phenotype was also determined. RESULTS: Seven variants were detected in TSHR-p.P52T, p.G132R, p.M164K, p.R450H, p.C700E, p.A522V, and p.R528S. The p. G132R, p. M164K and p. R528S variants were first identified in public databases. Five variants (p.G44D, p.G360V, p.R401Q, p.L418I, and p.E453Q) were found in NKX2.1 and one variant (p.P243T) was detected in FOXE1. In addition, one variant (p.N291I) was found in NKX2.5 and two variants (p.A355V and c.-26G>A) were detected in PAX8. CONCLUSIONS: Our study indicated that TSHR mutations have phenotypic variability and has further expanded the mutation spectrum of TSHR. We also revealed that the rate of NKX2.1, FOXE1, NKX2.5, and PAX8 mutations were low in patients with CH and athyreosis, in contrast to the higher rate of TSHR mutations.
[Mh] Termos MeSH primário: Grupo com Ancestrais do Continente Asiático/genética
Hipotireoidismo Congênito/genética
Análise Mutacional de DNA
Sequenciamento de Nucleotídeos em Larga Escala
Receptores da Tireotropina/genética
Disgenesia da Tireoide/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Criança
Pré-Escolar
Feminino
Fatores de Transcrição Forkhead/genética
Genótipo
Proteína Homeobox Nkx-2.5/genética
Seres Humanos
Masculino
Fator de Transcrição PAX8/genética
Fenótipo
Glândula Tireoide/metabolismo
Fator Nuclear 1 de Tireoide/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FOXE1 protein, human); 0 (Forkhead Transcription Factors); 0 (Homeobox Protein Nkx-2.5); 0 (NKX2-1 protein, human); 0 (NKX2-5 protein, human); 0 (PAX8 Transcription Factor); 0 (PAX8 protein, human); 0 (Receptors, Thyrotropin); 0 (Thyroid Nuclear Factor 1); 0 (Transcription Factors)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


  4 / 3186 MEDLINE  
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[PMID]:28743746
[Au] Autor:Citterio CE; Veluswamy B; Morgan SJ; Galton VA; Banga JP; Atkins S; Morishita Y; Neumann S; Latif R; Gershengorn MC; Smith TJ; Arvan P
[Ad] Endereço:From the Division of Metabolism, Endocrinology and Diabetes, University of Michigan Medical School, Ann Arbor, Michigan 48105.
[Ti] Título: triiodothyronine formation from thyrocytes activated by thyroid-stimulating hormone.
[So] Source:J Biol Chem;292(37):15434-15444, 2017 09 15.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The thyroid gland secretes primarily tetraiodothyronine (T ), and some triiodothyronine (T ). Under normal physiological circumstances, only one-fifth of circulating T is directly released by the thyroid, but in states of hyperactivation of thyroid-stimulating hormone receptors (TSHRs), patients develop a syndrome of relative T toxicosis. Thyroidal T production results from iodination of thyroglobulin (TG) at residues Tyr and Tyr , whereas thyroidal T production may originate in several different ways. In this study, the data demonstrate that within the carboxyl-terminal portion of mouse TG, T is formed independently of deiodination from T We found that upon iodination , T formation in TG was decreased in mice lacking TSHRs. Conversely, T that can be formed upon iodination of TG secreted from PCCL3 (rat thyrocyte) cells was augmented from cells previously exposed to increased TSH, a TSHR agonist, a cAMP analog, or a TSHR-stimulating antibody. We present data suggesting that TSH-stimulated TG phosphorylation contributes to enhanced T formation. These effects were reversed within a few days after removal of the hyperstimulating conditions. Indeed, direct exposure of PCCL3 cells to human serum from two patients with Graves' disease, but not control sera, led to secretion of TG with an increased intrinsic ability to form T upon iodination. Furthermore, TG secreted from human thyrocyte cultures hyperstimulated with TSH also showed an increased intrinsic ability to form T Our data support the hypothesis that TG processing in the secretory pathway of TSHR-hyperstimulated thyrocytes alters the structure of the iodination substrate in a way that enhances T formation, contributing to the relative T toxicosis of Graves' disease.
[Mh] Termos MeSH primário: Processamento de Proteína Pós-Traducional
Receptores da Tireotropina/agonistas
Transdução de Sinais
Tireoglobulina/metabolismo
Células Epiteliais da Tireóide/metabolismo
Tireotropina/metabolismo
Tri-Iodotironina/biossíntese
[Mh] Termos MeSH secundário: Animais
Proteínas de Ligação ao Cálcio/agonistas
Proteínas de Ligação ao Cálcio/genética
Proteínas de Ligação ao Cálcio/metabolismo
Caseína Quinase I/genética
Caseína Quinase I/metabolismo
Linhagem Celular
Células Cultivadas
Proteínas da Matriz Extracelular/agonistas
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Doença de Graves/sangue
Doença de Graves/metabolismo
Doença de Graves/patologia
Halogenação
Seres Humanos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fosforilação
Proteínas Serina-Treonina Quinases/química
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
Ratos
Receptores da Tireotropina/genética
Receptores da Tireotropina/metabolismo
Tireoglobulina/secreção
Células Epiteliais da Tireóide/citologia
Células Epiteliais da Tireóide/patologia
Células Epiteliais da Tireóide/secreção
Tirosina/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Calcium-Binding Proteins); 0 (Extracellular Matrix Proteins); 0 (FAM20C protein, mouse); 0 (Receptors, Thyrotropin); 06LU7C9H1V (Triiodothyronine); 42HK56048U (Tyrosine); 9002-71-5 (Thyrotropin); 9010-34-8 (Thyroglobulin); EC 2.7.11.1 (Casein Kinase I); EC 2.7.11.1 (FAM20C protein, human); EC 2.7.11.1 (Fam20C protein, rat); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171230
[Lr] Data última revisão:
171230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.784447


  5 / 3186 MEDLINE  
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[PMID]:28938449
[Au] Autor:Krieger CC; Perry JD; Morgan SJ; Kahaly GJ; Gershengorn MC
[Ad] Endereço:Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
[Ti] Título:TSH/IGF-1 Receptor Cross-Talk Rapidly Activates Extracellular Signal-Regulated Kinases in Multiple Cell Types.
[So] Source:Endocrinology;158(10):3676-3683, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously showed that thyrotropin (TSH)/insulinlike growth factor (IGF)-1 receptor cross-talk appears to be involved in Graves' orbitopathy (GO) pathogenesis and upregulation of thyroid-specific genes in human thyrocytes. In orbital fibroblasts from GO patients, coadministration of TSH and IGF-1 induces synergistic increases in hyaluronan secretion. In human thyrocytes, TSH plus IGF-1 synergistically increased expression of the sodium-iodide symporter that appeared to involve ERK1/2 activation. However, the details of ERK1/2 activation were not known, nor was whether ERK1/2 was involved in this synergism in other cell types. Using primary cultures of GO fibroblasts (GOFs) and human thyrocytes, as well as human embryonic kidney (HEK) 293 cells overexpressing TSH receptors (HEK-TSHRs), we show that simultaneous activation of TSHRs and IGF-1 receptors (IGF-1Rs) causes rapid, synergistic phosphorylation/activation of ERK1 and ERK2 in all three cell types. This effect is partially inhibited by pertussis toxin, an inhibitor of TSHR coupling to Gi/Go proteins. In support of a role for Gi/Go proteins in ERK1/2 phosphorylation, we found that knockdown of Gi(1-3) and Go in HEK-TSHRs inhibited ERK1/2 phosphorylation stimulated by TSH and TSH plus IGF-1. These data demonstrate that the synergistic effects of TSH plus IGF-1 occur early in the TSHR signaling cascade and further support the idea that TSHR/IGF-1R cross-talk is an important mechanism for regulation of human GOFs and thyrocytes.
[Mh] Termos MeSH primário: Fibroblastos/efeitos dos fármacos
Fator de Crescimento Insulin-Like I/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Receptor Cross-Talk
Receptor IGF Tipo 1/metabolismo
Receptores da Tireotropina/metabolismo
Tireotropina/farmacologia
[Mh] Termos MeSH secundário: Fibroblastos/metabolismo
Oftalmopatia de Graves
Células HEK293
Seres Humanos
Ácido Hialurônico/secreção
Proteína Quinase 1 Ativada por Mitógeno/efeitos dos fármacos
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/efeitos dos fármacos
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Fosforilação/efeitos dos fármacos
Simportadores/efeitos dos fármacos
Simportadores/metabolismo
Células Epiteliais da Tireóide/efeitos dos fármacos
Células Epiteliais da Tireóide/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Thyrotropin); 0 (Symporters); 0 (sodium-iodide symporter); 67763-96-6 (Insulin-Like Growth Factor I); 9002-71-5 (Thyrotropin); 9004-61-9 (Hyaluronic Acid); EC 2.7.10.1 (Receptor, IGF Type 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00528


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[PMID]:28931076
[Au] Autor:Barington M; Brorson MM; Hofman-Bang J; Rasmussen ÅK; Holst B; Feldt-Rasmussen U
[Ad] Endereço:Department of Medical Endocrinology, Rigshospitalet, University Hospital Copenhagen, Copenhagen, Denmark.
[Ti] Título:Ghrelin-mediated inhibition of the TSH-stimulated function of differentiated human thyrocytes ex vivo.
[So] Source:PLoS One;12(9):e0184992, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ghrelin is a peptide hormone produced mainly in the gastrointestinal tract known to regulate several physiological functions including gut motility, adipose tissue accumulation and hunger sensation leading to increased bodyweight. Studies have found a correlation between the plasma levels of thyroid hormones and ghrelin, but an effect of ghrelin on the human thyroid has never been investigated even though ghrelin receptors are present in the thyroid. The present study shows a ghrelin-induced decrease in the thyroid-stimulating hormone (TSH)-induced production of thyroglobulin and mRNA expression of thyroperoxidase in a primary culture of human thyroid cells obtained from paranodular tissue. Accordingly, a trend was noted for an inhibition of TSH-stimulated expression of the sodium-iodine symporter and the TSH-receptor. Thus, this study suggests an effect of ghrelin on human thyrocytes and thereby emphasizes the relevance of examining whether ghrelin also influences the metabolic homeostasis through altered thyroid hormone production.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Grelina/farmacologia
Glândula Tireoide/citologia
Tireotropina/farmacologia
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
Receptores de Grelina/metabolismo
Receptores da Tireotropina/metabolismo
Tireoglobulina/metabolismo
Glândula Tireoide/efeitos dos fármacos
Glândula Tireoide/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ghrelin); 0 (Receptors, Ghrelin); 0 (Receptors, Thyrotropin); 9002-71-5 (Thyrotropin); 9010-34-8 (Thyroglobulin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184992


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[PMID]:28767604
[Au] Autor:Ahn HY; Chung YJ; Cho BY
[Ad] Endereço:Department of Internal Medicine, Chung-Ang University College of Medicine, Seoul, Korea.
[Ti] Título:Serum 25-hydroxyvitamin D might be an independent prognostic factor for Graves disease recurrence.
[So] Source:Medicine (Baltimore);96(31):e7700, 2017 Aug.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Graves disease is the most common cause of thyrotoxicosis. Although medical intervention with antithyroid drugs (ATDs) is commonly the first choice of treatment in Korea, the remission rate associated with this approach is not satisfactory. During ATD therapy, low or undetectable serum levels of thyroid-stimulating hormone (TSH) receptor antibodies (TRAbs) have been reported to affect the incidence of Graves disease remission. This study evaluated the correlation between serum 25-hydroxyvitamin D levels and TRAb levels, as well as the effect of 25-hydroxyvitamin D on the recurrence of Graves disease.A total of 143 patients, who were diagnosed with Graves disease and treated with ATDs, were retrospectively included in our observational study. These patients were followed for more than 1 year after ATD discontinuation. The levels of serum 25-hydroxyvitamin D and TRAb (ie, thyroid-stimulating antibody [TSAb], as detected by bioassay, and TSH-binding inhibitory immunoglobulins [TBIIs]) were measured, and a thyroid function test was performed upon ATD discontinuation. Recurrence was evaluated every 3 months, and was defined as an occurrence of overt thyrotoxicosis during the follow-up period.A total of 95 patients (66.4%) experienced recurrence with a median latency period of 182 days (ranging 28-1219 days). The serum 25-hydroxyvitamin D levels at the time of ATD discontinuation were not correlated with either TBII or TSAb. In the Cox proportional hazard regression analysis, higher free T4 levels (>1.4 ng/dL; hazard ratio [HR], 3.252; 95% confidence interval [CI], 1.022-10.347) and low levels of 25-hydroxyvitamin D (≤14.23 ng/mL) were associated with a higher probability of Graves disease recurrence (HR, 3.016; 95% CI, 1.163-7.819).Lower serum 25-hydroxyvitamin D levels were associated with a higher incidence of Graves disease recurrence. Therefore, serum 25-hydroxyvitamin D might be an independent risk factor for predicting Graves disease recurrence after ATD discontinuation.
[Mh] Termos MeSH primário: Doença de Graves/sangue
Vitamina D/análogos & derivados
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Autoanticorpos/sangue
Biomarcadores/sangue
Feminino
Seguimentos
Doença de Graves/diagnóstico por imagem
Seres Humanos
Masculino
Meia-Idade
Tamanho do Órgão
Prognóstico
Receptores da Tireotropina/imunologia
Recidiva
Estudos Retrospectivos
Glândula Tireoide/diagnóstico por imagem
Vitamina D/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Biomarkers); 0 (Receptors, Thyrotropin); 1406-16-2 (Vitamin D); 64719-49-9 (25-hydroxyvitamin D)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170803
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007700


  8 / 3186 MEDLINE  
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[PMID]:28609287
[Au] Autor:Karponis D; Ananth S
[Ad] Endereço:.
[Ti] Título:The role of thyrostimulin and its potential clinical significance.
[So] Source:Endocr Regul;51(2):117-128, 2017 Apr 25.
[Is] ISSN:1210-0668
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Thyrostimulin is a glycoprotein heterodimer of GPA2 and GPB5, first described in 2002. It is involved in the physiological function of several tissues. Moreover, evidence points towards the ability of thyrostimulin's individual monomers to induce a biological effect, which could denote the circulatory/systemic effects of the molecule when found in higher concentrations. From the evolutionary point of view, thyrostimulin shares a binding epitope with the thyroid-stimulating hormone for the thyroid stimulating hormone receptor, whilst possessing affinity for another unique binding site on the same receptor. Although thyrostimulin can be involved in the hypothalamicpituitary- thyroid axis, its presence in various tissues in an eclectic array of different species renders it multifunctional. From weight loss via increasing metabolic rate to progression of cancer in human ovaries, it is certainly not a signaling molecule to overlook. Furthermore, thyrostimulin has been implicated in bone metabolism, acute illness, and reproductive function. In summary, to our knowledge, this is the first review dealing with the physiological role of thyrostimulin and its potential applications in the clinical practice.
[Mh] Termos MeSH primário: Glicoproteínas/metabolismo
Neoplasias Epiteliais e Glandulares/metabolismo
Neoplasias Ovarianas/metabolismo
Receptores da Tireotropina/metabolismo
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Feminino
Glicoproteínas/química
Glicoproteínas/fisiologia
Seres Humanos
Sistema Hipotálamo-Hipofisário/metabolismo
Sistema Hipotálamo-Hipofisário/fisiologia
Camundongos
Neoplasias Epiteliais e Glandulares/fisiopatologia
Neoplasias Ovarianas/fisiopatologia
Receptores da Tireotropina/fisiologia
Reprodução/fisiologia
Glândula Tireoide/metabolismo
Glândula Tireoide/fisiologia
Perda de Peso/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glycoproteins); 0 (Receptors, Thyrotropin); 0 (thyrostimulin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE


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[PMID]:28439882
[Au] Autor:Diana T; Krause J; Olivo PD; König J; Kanitz M; Decallonne B; Kahaly GJ
[Ad] Endereço:Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany.
[Ti] Título:Prevalence and clinical relevance of thyroid stimulating hormone receptor-blocking antibodies in autoimmune thyroid disease.
[So] Source:Clin Exp Immunol;189(3):304-309, 2017 Sep.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The prevalence and clinical relevance of thyroid stimulating hormone (TSH) receptor (TSHR) blocking antibodies (TBAb) in patients with autoimmune thyroid disease (AITD) was investigated. Serum TBAb were measured with a reporter gene bioassay using Chinese hamster ovary cells. Blocking activity was defined as percentage inhibition of luciferase expression relative to induction with bovine TSH alone (cut-off 40% inhibition). All samples were measured for TSHR stimulatory antibody (TSAb) and TSHR binding inhibiting immunoglobulins (TBII). A total of 1079 unselected, consecutive patients with AITD and 302 healthy controls were included. All unselected controls were negative for TBAb and TSAb. In contrast, the prevalence of TBAb-positive patients with Hashimoto's thyroiditis and Graves' disease was 67 of 722 (9·3%) and 15 of 357 (4·2%). Of the 82 TBAb-positive patients, thirty-nine (48%), 33 (40%) and 10 (12%) were hypothyroid, euthyroid and hyperthyroid, respectively. Ten patients were both TBAb- and TSAb-positive (four hypothyroid, two euthyroid and four hyperthyroid). Thyroid-associated orbitopathy was present in four of 82 (4·9%) TBAb-positive patients, with dual TSHR antibody positivity being observed in three. TBAb correlated positively with TBII (r = 0·67, P < 0·001) and negatively with TSAb (r = -0·86, P < 0·05). The percentage of TBII-positive patients was higher the higher the level of inhibition in the TBAb assay. Of the TBAb-positive samples with  > 70% inhibition, 87% were TBII-positive. Functional TSHR antibodies impact thyroid status. TBAb determination is helpful in the evaluation and management of patients with AITD. The TBAb assay is a relevant and important tool to identify potentially reversible hypothyroidism.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Receptores da Tireotropina/imunologia
Tireoidite Autoimune/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Autoanticorpos/imunologia
Bioensaio
Células CHO
Cricetinae
Cricetulus
Feminino
Doença de Graves/sangue
Doença de Graves/imunologia
Doença de Hashimoto/sangue
Doença de Hashimoto/imunologia
Seres Humanos
Masculino
Meia-Idade
Prevalência
Receptores da Tireotropina/sangue
Glândula Tireoide/imunologia
Glândula Tireoide/patologia
Tireoidite Autoimune/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Receptors, Thyrotropin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12980


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[PMID]:28368444
[Au] Autor:Holthoff HP; Li Z; Faßbender J; Reimann A; Adler K; Münch G; Ungerer M
[Ad] Endereço:Procorde-advanceCOR, D 82152 Martinsried, Germany.
[Ti] Título:Cyclic Peptides for Effective Treatment in a Long-Term Model of Graves Disease and Orbitopathy in Female Mice.
[So] Source:Endocrinology;158(7):2376-2390, 2017 Jul 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A model for human Graves disease in mice was used to compare several treatment approaches. The mice received regular adenovirus (Ad) thyroid-stimulating hormone receptor (TSHR) A subunit immunizations (injections every 4 weeks). The generation of anti-TSHR antibodies, enlarged thyroid sizes (goiter), elevated serum thyroxine levels, retro-orbital fibrosis, and cardiac involvement (tachycardia and hypertrophy) were consistently observed over 9 months. Treatment of established disease in these mice using cyclic peptides that mimic one of the cylindrical loops of the TSHR leucine-rich repeat domain improved or cured all investigated parameters after six consecutive monthly injections. The first significant beneficial effects were observed 3 to 4 months after starting these therapies. In immunologically naïve mice, administration of any of the cyclic peptides did not induce any immune response. In contrast, monthly injections of the full antigenic TSHR A domain as fusion protein with immunoglobulin G crystallizable fragment induced clinical signs of allergy in Ad-TSHR-immunized mice and anti-TSHR antibodies in naïve control mice. In conclusion, cyclic peptides resolved many clinical findings in a mouse model of established Graves disease and orbitopathy. In contrast to blocking TSHR by allosteric modulation, the approach does not incur a direct receptor antagonism, which might offer a favorable side effect profile.
[Mh] Termos MeSH primário: Doença de Graves/tratamento farmacológico
Oftalmopatia de Graves/tratamento farmacológico
Peptídeos Cíclicos/uso terapêutico
Receptores da Tireotropina/química
[Mh] Termos MeSH secundário: Animais
Células CHO
Cricetinae
Cricetulus
Modelos Animais de Doenças
Feminino
Doença de Graves/sangue
Doença de Graves/complicações
Doença de Graves/patologia
Oftalmopatia de Graves/sangue
Oftalmopatia de Graves/patologia
Células HEK293
Seres Humanos
Imunoglobulinas Glândula Tireoide-Estimulantes/sangue
Camundongos
Camundongos Endogâmicos BALB C
Peptídeos Cíclicos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulins, Thyroid-Stimulating); 0 (Peptides, Cyclic); 0 (Receptors, Thyrotropin); 0 (thyrotropin-binding inhibitory immunoglobulin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1845



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