Trophoblastic hyperthyroidism: Clinical and biochemical features of five cases

Rajatanavin, Rajata; Chailurkit, La‐or; Srisupandit, Suwanee; Tungtrakul, S.; Bunyaratvej, S

doi:10.1016/s0002-9343(88)80351-6

Cited by 33 publications

(9 citation statements)

References 32 publications

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“…64 -66 The precise prevalence of hyperthyroidism in patients with trophoblastic tumors is unknown. It was found in five of 20 patients with trophoblastic disease evaluated at a referral center in 1 year 67 , three of these five thyrotoxic patients had choriocarcinoma, and two had hydatidiform moles. In another study, 30 of 52 patients with gestational trophoblastic tumors were found to be thyrotoxic.…”

Section: Choriocarcinomamentioning

confidence: 98%

Physiological and pathological aspects of the effect of human chorionic gonadotropin on the thyroid

Hershman¹

2004

Best Practice & Research Clinical Endocrinology & Metab

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Human chorionic gonadotropin (hCG) is a glycoprotein hormone that has structural similarity to TSH. At the time of the peak hCG levels in normal pregnancy, serum TSH levels fall and bear a mirror image to the hCG peak. This reduction in TSH suggests that hCG causes an increased secretion of T4 and T3.Women with hyperemisis gravidarum often have high hCG levels that cause transient hyperthyroidsm. In the vast majority of such patients, there will be spontaneous remission of the increased thyroid function when the vomiting stops in several weeks. When there are clinical features of hyperthyroidism, it is be reasonable to treat with antithyroid drugs or a betaadrenergic blocker, but treatment is rarely required beyond 22 weeks of gestation.Hyperthyroidism or increased thyroid function has been reported in many patients with trophoblastic tumors, either hydatiditform mole or choriocarcinoma. The diagnosis of hydatidiform mole is made by ultrasonography that shows a 'snowstorm' appearance without a fetus. Hydatidiform moles secrete large amounts of hCG proportional to the mass of the tumor. The development of hyperthyroidism requires hCG levels of . 200 U/ml that are sustained for several weeks. Removal of the mole cures the hyperthyroidism. There have been many case reports of hyperthyroidism in women with choriocarcinoma and high hCG levels. The principal therapy is chemotherapy, usually given at a specialized center. With effective chemotherapy, longterm survival exceeds 95%.A unique family with recurrent gestational hyperthyroidism associated with hyperemesis gravidarum was found to have a mutation in the extracellular domain of the TSH receptor that made it responsive to normal levels of hCG.Key words: human chorionic gonadotropin; thyrotropin; pregnancy; hyperemesis gravidarum; hydatidiform mole; choriocarcinoma; mutant thyroid-stimulating hormone receptor.

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Section: Choriocarcinomamentioning

confidence: 98%

Physiological and pathological aspects of the effect of human chorionic gonadotropin on the thyroid

Hershman¹

2004

Best Practice & Research Clinical Endocrinology & Metab

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“…The prevalence of hyperthyroidism in patients with hydatidiform mole and choriocarcinoma has been reported as 25-64% (52)(53)(54). Serum T3 levels correlated with serum thyroidstimulating activity, presumably hCG, measured by bioassay (52).…”

Section: Trophoblastic Diseasementioning

confidence: 99%

Thyrotropic Action of Human Chorionic Gonadotropin

Yoshimura¹,

Hershman²

1995

Thyroid

317

146

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Hyperthyroidism or increased thyroid function has been reported in many patients with trophoblastic tumors. In these cases, greatly increased human chorionic gonadotropin (hCG) levels and suppressed TSH levels suggest that hCG has thyrotropic activity. Recent investigations have clarified the structural homology not only in the hCG and TSH molecules but also in their receptors, and this homology suggests the basis for the reactivity of hCG with the TSH receptor. The clinical significance of the thyrotropic action of hCG is now also recognized in normal pregnancy and hyperemesis gravidarum. Highly purified hLH binds to recombinant hTSH receptor and is about 10 times as potent as purified hCG in increasing cAMP. The beta-subunits of hCG and hLH share 85% sequence identity in their first 114 amino acids but differ in the carboxy-terminal peptide because hCG beta contains a 31-amino acid extension (beta-CTP). A recombinant mutant hCG that lacks beta-CTP showed almost identical potency to LH on stimulation of recombinant hTSH receptor. If intact hCG were as potent as hLH in regard to its thyrotropic activity, most pregnant women would become thyrotoxic. One of the roles of the beta-CTP may be to prevent overt hyperthyroidism in the first trimester of pregnancy when a large amount of hCG is produced by the placenta. Nicked hCG preparations, obtained from patients with trophoblastic disease or by enzymatic digestion of intact hCG, showed approximately 1.5- to 2-fold stimulation of recombinant hTSH receptor compared with intact hCG. This suggests that the thyrotropic activity of hCG may be influenced by the metabolism of the hCG molecule itself. Deglycosylation and/or desialylation of hCG enhances its thyrotropic potency. Basic hCG isoforms with lower sialic acid content extracted from hydatidiform moles were more potent in activating adenylate cyclase, and showed high bioactivity/immunoactivity (B/I) ratio in CHO cells expressing human TSH receptors. This is consistent with the finding that the beta-CTP truncated hCG with higher thyrotropic potency is substantially deglycosylated and desialylated in the beta-subunit relative to intact hCG because all four O-linked glycosylation sites occur within the missing C-terminal extension. The desialylated hCG variant also interacts directly with recombinant hTSH receptors transfected into human thyroid cancer cells. There is thyroid-stimulating activity in sera of normal pregnant women, and this correlates with serum hCG levels. The thyroid gland of normal pregnant women may be stimulated by hCG to secrete slightly excessive quantities of T4 and induce a slight suppression of TSH, perhaps being about 1 mU/L less than nongravid levels, but not high enough to induce overt hyperthyroidism. Maternal thyroid glands may secrete more thyroid hormone during early pregnancy in response to the thyrotropic activity of hCG that overrides the normal operation of the hypothalamic-pituitary-thyroid feedback system. Biochemical hyperthyroidism associated with hyperemesis gravidarum has been att...

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“…The production of very high levels of hCG can stimulate the TSH receptor and thus cause hyperthyroidism in patients with choriocarcinoma, molar pregnancy (hydatidiform mole), or testicular cancer (216)(217)(218) (C,C,B). The differential diagnosis with other causes of thyrotoxicosis is based on low thyroid 131 I uptake, high serum gonadotropin levels, and presence of the corresponding producing tumor.…”

Section: How Should Thyrotoxicosis Due To Gonadotropin Hypersecretmentioning

confidence: 99%

Consenso brasileiro para o diagnóstico e tratamento do hipertireoidismo: recomendações do Departamento de Tireoide da Sociedade Brasileira de Endocrinologia e Metabologia

Maia

Scheffel

Meyer

et al. 2013

Arq Bras Endocrinol Metab

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SIntroduction: Hyperthyroidism is characterized by increased synthesis and release of thyroid hormones by the thyroid gland. Thyrotoxicosis refers to the clinical syndrome resulting from excessive circulating thyroid hormones, secondary to hyperthyroidism or due to other causes. This article describes evidence-based guidelines for the clinical management of thyrotoxicosis. Objective: This consensus, developed by Brazilian experts and sponsored by the Department of Thyroid Brazilian Society of Endocrinology and Metabolism, aims to address the management, diagnosis and treatment of patients with thyrotoxicosis, according to the most recent evidence from the literature and appropriate for the clinical reality of Brazil. Materials and methods: After structuring clinical questions, search for evidence was made available in the literature, initially in the database Medline, PubMed and Embase databases and subsequently in SciELO -Lilacs. The strength of evidence was evaluated by Oxford classification system was established from the study design used, considering the best available evidence for each question. Results: We have defined 13 questions about the initial clinical approach for the diagnosis and treatment that resulted in 53 recommendations, including the etiology, treatment with antithyroid drugs, radioactive iodine and surgery. We also addressed hyperthyroidism in children, teenagers or pregnant patients, and management of hyperthyroidism in patients with Graves' ophthalmopathy and various other causes of thyrotoxicosis. Conclusions: The clinical diagnosis of hyperthyroidism usually offers no difficulty and should be made with measurements of serum TSH and thyroid hormones. The treatment can be performed with antithyroid drugs, surgery or administration of radioactive iodine according to the etiology of thyrotoxicosis, local availability of methods and preferences of the attending physician and patient. Arq Bras Endocrinol

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Trophoblastic hyperthyroidism: Clinical and biochemical features of five cases

Cited by 33 publications

References 32 publications

Physiological and pathological aspects of the effect of human chorionic gonadotropin on the thyroid

Physiological and pathological aspects of the effect of human chorionic gonadotropin on the thyroid

Thyrotropic Action of Human Chorionic Gonadotropin

Consenso brasileiro para o diagnóstico e tratamento do hipertireoidismo: recomendações do Departamento de Tireoide da Sociedade Brasileira de Endocrinologia e Metabologia

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