scholarly journals Thyroid‐stimulating hormone receptor antibodies during follow‐up as remission markers in childhood‐onset Graves' disease treated with antithyroid drugs

2020 ◽  
Vol 36 (4) ◽  
pp. 281-286
Author(s):  
Shuo‐Yu Wang ◽  
Chia‐Ti Wang ◽  
Kai‐Jen Tien ◽  
Chao‐Chun Chang ◽  
Ting‐Hsiu Liu
Keyword(s):  
Hormone Receptor ◽  
Thyroid Stimulating Hormone ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Childhood Onset ◽  
Receptor Antibodies ◽  
Stimulating Hormone

scholarly journals Graves’ Disease

2021 ◽  
Author(s):  
Vasudha Bakshi ◽  
Gollapalli Rajeev Kumar
Keyword(s):  
Thyroid Gland ◽  
Hormone Receptor ◽  
Treatment Options ◽  
Positive Family History ◽  
Current Treatment ◽  
Thyroid Stimulating Hormone ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Autoimmune Thyroid ◽  
Stimulating Hormone

Graves’ disease (GD) is an autoimmune thyroid disorder where autoantibodies are produced against TSH (Thyroid Stimulating Hormone) receptor causing thyrotoxicosis. It is characterized by goiter, ophthalmopathy, and occasionally pretibial myxedema. The autoimmune mechanism causing disease is not well understood and it is complex. It involves multifactorial etiology involving environmental and genetic factors. Smoking and positive family history contributing to the development of GD. GD can be diagnosed based on the clinical manifestation and demonstrating low concentration of TSHs, high TRab (Thyroid Stimulating Hormone receptor autoantibodies), and high FT4 (Free thyroxine) concentration. Current treatment options aimed at stable restoration of euthyroidism by following different modalities of suppressing thyroid gland using antithyroid drugs, removing/ablating thyroid gland by surgery, and radioactive iodine treatment with iodine- 131.

Graves Disease in Children: Thyroid-Stimulating Hormone Receptor Antibodies as Remission Markers

2014 ◽  
Vol 164 (5) ◽  
pp. 1189-1194.e1 ◽  
Author(s):  
Roberto Gastaldi ◽  
Elena Poggi ◽  
Alessandro Mussa ◽  
Giovanna Weber ◽  
Maria Cristina Vigone ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Receptor Antibodies ◽  
Stimulating Hormone

scholarly journals Antithyroid drug therapy for Graves’ disease

2021 ◽  
Vol 64 (10) ◽  
pp. 690-698
Author(s):  
Soo Myoung Shin ◽  
Ka Hee Yi
Keyword(s):  
Hormone Receptor ◽  
Adverse Reactions ◽  
Low Dose ◽  
Radioactive Iodine ◽  
Thyroid Stimulating Hormone ◽  
Reproductive Age ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Definitive Therapy ◽  
Stimulating Hormone

Background: Graves’ disease is the most common cause of hyperthyroidism which is caused by stimulating autoantibodies against thyroid-stimulating hormone receptor. There is no etiology-specific treatment for Graves’ disease.Current Concepts: Graves’ disease can be treated with antithyroid drugs (ATDs), radioactive iodine, or thyroidectomy. ATDs are the most preferred first-line therapy, because they do not cause either permanent hypothyroidism or exacerbation of orbitopathy, despite low remission rate. ATDs have serious adverse reactions including agranulocytosis and fulminant hepatic necrosis requiring liver transplantation. Methimazole (MMI) is recommended in every patient starting ATD therapy, except during the first trimester of pregnancy and in cases of thyroid storm, because of relatively lower incidence and severity of serious adverse reactions compared with propylthiouracil. Treatment should be continued for 12 to 18 months, then discontinued if the levels of thyroid-stimulating hormone and thyroid-stimulating hormone receptor antibodies are normalized. In cases of relapse of hyperthyroidism, radioactive iodine or thyroidectomy can be recommended for definitive therapy; however, recent studies support longer-term maintenance of low dose MMI as a favorable alternative therapy. All ATDs may induce congenital anomalies when exposed during early pregnancy. Every female patient of reproductive age should be advised to postpone pregnancy until their thyroid function is maintained within normal range and to stop ATDs when pregnancy is confirmed to avoid the risk of congenital anomalies.Discussion and Conclusion: Longer-term low dose MMI therapy can be a good choice for Graves’ hyperthyroidism with relapse. Before pregnancy, hyperthyroidism should be controlled to stop ATDs during pregnancy.

scholarly journals Prospective Trial of Functional Thyrotropin Receptor Antibodies in Graves Disease

2019 ◽  
Vol 105 (4) ◽  
pp. e1006-e1014 ◽  
Author(s):  
George J Kahaly ◽  
Tanja Diana ◽  
Michael Kanitz ◽  
Lara Frommer ◽  
Paul D Olivo
Keyword(s):  
Predictive Value ◽  
Prospective Trial ◽  
Thyroid Stimulating Hormone ◽  
Luciferase Expression ◽  
Graves Disease ◽  
Thyrotropin Receptor ◽  
Tertiary Referral Center ◽  
Thyrotropin Receptor Antibodies ◽  
Receptor Antibodies

Abstract Context Scarce data exist regarding the relevance of stimulatory (TSAb) and blocking (TBAb) thyrotropin receptor antibodies in the management of Graves disease (GD). Objective To evaluate the clinical utility and predictive value of TSAb/TBAb. Design Prospective 2-year trial. Setting Academic tertiary referral center. Patients One hundred consecutive, untreated, hyperthyroid GD patients. Methods TSAb was reported as percentage of specimen-to-reference ratio (SRR) (cutoff SRR < 140%). Blocking activity was defined as percent inhibition of luciferase expression relative to induction with bovine thyrotropin (TSH, thyroid stimulating hormone) alone (cutoff > 40% inhibition). Main Outcome Measures Response versus nonresponse to a 24-week methimazole (MMI) treatment defined as biochemical euthyroidism versus persistent hyperthyroidism at week 24 and/or relapse at weeks 36, 48, and 96. Results Forty-four patients responded to MMI, of whom 43% had Graves orbitopathy (GO), while 56 were nonresponders (66% with GO; P < 0.01). At baseline, undiluted serum TSAb but not thyroid binding inhibitory immunoglobulins (TBII) differentiated between thyroidal GD-only versus GD + GO (P < 0.001). Furthermore, at baseline, responders demonstrated marked differences in diluted TSAb titers compared with nonresponders (P < 0.001). During treatment, serum TSAb levels decreased markedly in responders (P < 0.001) but increased in nonresponders (P < 0.01). In contrast, TBII strongly decreased in nonresponders (P = 0.002). All nonresponders and/or those who relapsed during 72-week follow-up period were TSAb-positive at week 24. A shift from TSAb to TBAb was noted in 8 patients during treatment and/or follow-up and led to remission. Conclusions Serum TSAb levels mirror severity of GD. Their increase during MMI treatment is a marker for ongoing disease activity. TSAb dilution analysis had additional predictive value.

scholarly journals Central TSH Dysregulation in a Patient with Familial Non-Autoimmune Autosomal Dominant Hyperthyroidism Due to a Novel Thyroid-Stimulating Hormone Receptor Disease-Causing Variant

Medicina ◽  
2021 ◽  
Vol 57 (3) ◽  
pp. 196
Author(s):  
Jasna Suput Omladic ◽  
Maja Pajek ◽  
Urh Groselj ◽  
Katarina Trebusak Podkrajsek ◽  
Magdalena Avbelj Stefanija ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Autosomal Dominant ◽  
Signs And Symptoms ◽  
Thyroid Stimulating Hormone ◽  
Ablation Therapy ◽  
Tsh Secretion ◽  
Tshr Gene ◽  
Adult Male Patient ◽  
Stimulating Hormone

Background and Objectives. Familial non-autoimmune autosomal dominant hyperthyroidism (FNAH) is a rare cause of childhood hyperthyroidism. It is caused by the thyroid-stimulating hormone receptor (TSHR) gene variants. So far, only around 40 families with FNAH have been reported. Patients with activating TSHR variants demonstrated the same classical signs and symptoms of hyperthyroidism as seen in patients with Graves’ disease. Since 2012, ablative therapy is recommended to avoid relapses of hyperthyroidism and its consequences. Case Presentation. We presented a young adult male patient with a novel heterozygous TSHR disease-causing variant p.Arg418Lys (c.1253G>A) in the exon 10, who presented with a mild but progressive FNAH, with a follow-up since infancy. Discussion. Constantly suppressed TSH, including during the euthyreosis in childhood and hypothyreosis after iodine ablation therapy, suggested central dysregulation of the TSH secretion.

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