The Association of Thyroid Hormones With β-HCG in Patients With Hydatidiform Mole (original) (raw)
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Human Chorionic Gonadotropin and Thyroid Function in Patients with Hydatidiform Mole
Obstetrical & Gynecological Survey, 1985
In view of the controversy regarding the role of human chorionic gonadotropin as the stimulator of thyroid function in patients with trophoblastic tumors, especially hydatidiform mole, we conducted studies to explore whether a correlation between serum human chorionic gonadotropin levels and thyroid function was demonstrable in such patients. Among 47 patients studied, only one was clinically hyperthyroid, although 10 had serum total thyroxine values exceeding those found in normal pregnancy (8 to 17 11-g/dl). Among 34 patients in whom free thyroxine indices could be calculated, 18 had elevated values for the free thyroxine index (>10.6), and nine had elevated values for both total thyroxine and free thyroxine index. Serum total 3,5,3'-triiodothyronine concentrations were also measured in 17 patients, and only one of them had a value (400 ng/dl) above the normal limit for pregnancy (>350 ng/dl). Among the 13 patients for whom free 3,5,3'-triiodothyronine indices were calculated, three had values above the normal range (>215). A weakly positive correlation (r = 0.35, p < 0.05, n = 47) between the serum human chorionic gonadotropin levels and serum total thyroxine concentrations was observed in these patients. However, no correlation was found between serum human chorionic gonadotropin levels and free thyroxine index values (r = 0.32, p > 0.05, n = 34). Also there was no correlation between serum human chorionic gonadotropin levels and either serum total 3,5,3' -triiodothyronine concentrations (r = 0.32, p > 0.1, n = 17) or free 3,5,3'-triiodothyronine index values (r = 0.27, p > 0.1, n = 13). x 2 Analysis revealed no significant relationship between elevations of serum human chorionic gonadotropin concentration and abnormally high values of the free thyroxine index. These studies do not support the premise that human chorionic gonadotropin per se is the thyroid stimulator of molar pregnancy and suggest that a substance or substances, distinct from human chorionic gonadotropin and elaborated by the gestational trophoblastic tissue, are responsible for thyrotoxicosis observed in patients with trophoblastic tumors. (AM J OBSTET GYNECOL 1984;150:723-8.)
Hyperthyroidism in Gestational Trophoblastic Disease: Review Article
https://www.ijrrjournal.com/IJRR\_Vol.10\_Issue.4\_April2023/IJRR-Abstract11.html, 2023
Gestational trophoblastic disease (GTD) is a collection of illnesses connected to pregnancy that result from aberrant placental trophoblast growth. Some GTD patients experience the rare but possibly fatal consequence of hyperthyroidism, which calls for prompt diagnosis and treatment. There is very little research on hyperthyroidism in GTD. This review examines the epidemiology, pathogenesis, and treatment of this phenomenon. The pathogenesis of hyperthyroidism in GTD has received extensive research. The trophoblastic tissue of the placenta secretes an excessive amount of hCG, which is structurally related to thyroid-stimulating hormone and has increased thyrotropic activity. Worldwide, there are different rates of hyperthyroidism in GTD, with lower rates related to high prenatal screening uptake and early GTD discovery. We were unable to pinpoint any specific risk factors for hyperthyroidism in GTD. Although surgical removal of the uterus can definitively treat hyperthyroidism, serious consequences in GTD have been recorded, including thyroid storm-induced multi-organ failure, ARDS, and pulmonary hypertension. To stop the onset of hyperthyroidism and the difficulties that go along with it, early GTD identification is essential. Women receiving surgery for GTD should be aware of hyperthyroidism as a critical postoperative factor that needs to be adequately managed. Future research should examine the elements contributing to hyperthyroidism in GTD as this may help identify high-risk female patients early.
European Journal of Endocrinology, 2005
Objective: Human chorionic gonadotropin (hCG) is widely used in the management of hydatidiform mole and persistent trophoblastic disease (PTD). Predicting PTD after molar pregnancy might be beneficial since prophylactic chemotherapy reduces the incidence of PTD. Design: A retrospective study based on blood specimens collected in the Dutch Registry for Hydatidiform Moles. A group of 165 patients with complete moles (of which 43 had PTD) and 39 patients with partial moles (of which 7 had PTD) were compared with 27 pregnant women with uneventful pregnancy. Methods: Serum samples from patients with hydatidiform mole with or without PTD were assayed using specific (radio) immunoassays for free α-subunit (hCGα), free β-subunit (hCGβ) and ‘total’ hCG (hCG + hCGβ). In addition, we calculated the ratios hCGα/hCG + hCGβ, hCGβ/hCG + hCGβ, and hCGα/hCGβ. Specificity and sensitivity were calculated and paired in receiver-operating characteristic (ROC) curve analysis, resulting in areas under the...
Alterations in thyroid hormone economy in patients with hydatidiform mole
Journal of Clinical Investigation, 1971
A B S T R A C T Studies of several aspects of thyroid hormone economy have been conducted in 11 patients before and after removal of a molar pregnancy. Before evacuation of the mole, all patients demonstrated moderately to greatly elevated values for thyroidal 'I uptake, absolute iodine uptake, and serum protein-bound-I. Values for serum PBI and serum thyroxine (T4) concentration were consistently and often greatly increased, averaging more than twice those found in normal pregnancy and three times those in normal controls. On the other hand, the maximum binding capacity of the T4binding globulin (TBG) was variably affected, and ranged between the values found in normal controls and those found in normal pregnancy. Values for the absolute concentration of free T4 in serum were, on the average, only moderately elevated, since the proportion of free To was moderately low, although not as low as in normal pregnancy. Sera of patients with molar pregnancy contained high levels of thyroid stimulating activity, as assessed in the McKenzie mouse bioassay system. The stimulator displayed a more prolonged duration of action than that of TSH and did not reveal a major immunological cross-reactivity with either human or bovine TSH, differing in the latter respect from the chorionic thyrotropin of normal human placenta. Abnormalities in iodine metabolism were rapidly ameliorated after removal of the molar pregnancy, and this was associated with the disappearance from serum of the thyroid stimulator.
Recurrent Thyroid Storm Caused by a Complete Hydatidiform Mole in a Perimenopausal Woman
Case Reports in Endocrinology, 2020
Background Gestational trophoblastic disease (GTD) which includes hydatidiform mole, invasive mole, placental site trophoblastic tumor, and choriocarcinoma is a rare cause of hyperthyroidism due to excess production of placental human chorionic gonadotrophin hormone (hCG) by tumor cells. Molecular mimicry between hCG and thyroid stimulating hormone (TSH) leads to continuous stimulation of TSH receptor by extremely high levels of hCG seen in these tumors. Consequently, biochemical and clinical hyperthyroidism ensues and it is potentially complicated by thyrotoxic crisis which is fatal unless urgent therapeutic steps are undertaken. Case Description. We present a 49-year-old perimenopausal woman who presented with recurrent thyroid storm and high output cardiac failure. The initial workup revealed suppressed TSH, high-free thyroxine (FT4), and free triiodothyronine (FT3) levels with increased vascularity of the normal-sized thyroid on ultrasonography. She was managed with parenteral b...
Case Reports in Endocrinology
Context. Gestational trophoblastic disease (GTD) is a rare complication of pregnancy, ranging from molar pregnancy to choriocarcinoma. Twin pregnancies with GTD and coexisting normal fetus are extremely rare with an estimated incidence of 1 case per 22,000–100,000 pregnancies. Molecular mimicry between human chorionic gonadotrophin (hCG) and thyroid-stimulating hormone (TSH) leads to gestational trophoblastic hyperthyroidism (GTH) which is further associated with increased maternal and fetal complications. This is the first reported case in literature describing the delivery of a baby with biochemical euthyroid status following a twin pregnancy with hydatidiform mole (HM) associated with gestational trophoblastic hyperthyroidism (GTH). Case Description. A 24-year-old G4 P3 Caucasian female with twin gestation was admitted to hospital for gestation trophoblastic hyperthyroidism. She was later diagnosed to have twin pregnancy with complete mole and coexisting normal fetus complicated ...
Gestational Trophoblastic Neoplasia (GTN) with Hypertiroidism (Case Report)
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY
Introduction. Gestationaltrophoblastic neoplasia(GTN) is a malignant lesion arising from placental villous and extra-villous trophoblast, occuring in 1:40,000 pregnancies. Invasive mole and choriocarcinoma are the vast majority of GTN, produce substantial amounts of human chorionic gonadotropin (hCG). Hyperthyroidism in GTN is due to stimulation of thyroid gland by hCG which has a similar structure with thyroid stimulating hormone (TSH).Case. A 28-year-old female, suspected with choriocarcinoma and anemia, had history of recurrent vaginal bleeding in 8 months, accompanied with loss of appetite, weight loss, palpitation and tremor. Physical examination: pulse rate 114x/minutes, respiration rate 26x/minutes, temperature 38 0C, conjunctival anemia and dyspneu. Laboratory: anemia, leukocytosis, hypoalbuminemia, hypokalemia, increase ofLDH, increase of bhCG >1,500,000 mIU/mL, T4 14.1 ug/dL (4.40-10.90 ug/dL), FT4 1.95 ng/dL (0.89-1.76 ng/dL), and decrease of TSH. Abdominal CT Scan sug...
Case study: Thyrotoxicosis on women with complete hydatidiform molar pregnancy
Jurnal Kedokteran dan Kesehatan Indonesia
Thyrotoxicosis defined as a clinical manifestation of excess circulating thyroid hormone. Epidemiologic investigation reports 0.2% of thyrotoxicosis is caused by hydatidiform mole. The New England Trophoblastic Disease Centre (NETDC) mentioned that 20% of hydatidiform mole cases have thyrotoxicosis as one of its complications. The basic pathogenesis of thyrotoxicosis is the similarity of the HCG subunit to TSH which results in excessive stimulation of thyroid hormone. We present thethyrotoxicosis case in a 15-weeks pregnant woman with complete hydatidiform mole. The patient admitted to the hospital with blackish-red coloured bleeding and several hyperthyroidism complaints, laboratory test showed elevated levels of HCG and thyroid hormone and decreased TSH. Imaging studies done with ultrasound showed with snowflake pattern. The patient then treated with thyroid hormone suppressant therapy before the hydatidiform mole evacuation. Normalization of thyroid hormone levels should be made immediately before the mole evacuation to avoid lifethreatening thyroid storm complications. Tirotoksikosis merupakan manifestasi klinis akibat kelebihan hormon tiroid yang beredar dalam darah. Hasil epidemiologi mencatat sekitar 0,2% kasus tirotoksikosis dapat disebabkan oleh mola hidatidosa. The New England Thropoblastic Disease Centre (NETDC) menyebutkan 20% kasus mola hidatidosa di benua Asia memiliki komplikasi tirotoksikosis. Patofisiologi dasar tirotoksikosis adalah kemiripan subunit HCG dengan TSH yang mengakibatkan stimulasi produksi hormon tiroid yang berlebihan. Pada kesempatan ini dilaporkan sebuah kasus tirotoksikosis pada seorang wanita hamil usia 15 minggu dengan mola hidatidosa komplit. Pasien mengeluh perdarahan banyak berwarna merah kehitaman, disertai beberapa keluhan hipertiroidisme, hasil laboratorium menunjukkan peningkatan kadar HCG dan hormon tiroid, penurunan TSH disertai gambaran snowflake pattern pada hasil USG. Pasien kemudian diberikan terapi penekan hormon tiroid sebelum dilakukan evakuasi mola. Penekanan kadar hormon tiroid harus dilakukan segera sebelum tindakan evakuasi mola agar komplikasi badai tiroid yang dapat mengancam keadaan pasien dapat dicegah.
The International journal of biological markers
Human chorionic gonadotropin (hCG) is widely used in the management of hydatidiform mole and persistent rophoblastic disease (PTD). Studies on hyperglycosylated human chorionic gonadotropin (invasive trophoblast antigen, ITA) in PTD are limited. In serum samples taken before evacuation of molar pregnancies we measured the concentrations of free hCG -subunit (free hCG ), "total" hCG (hCG+hCG ) and ITA, and determined whether ITA, the two other hCG analytes, or the calculated ratios of hCG /hCG+hCG , hCG /ITA and hCG+hCG /ITA could predict the later development of PTD. A retrospective study based on blood specimens collected in the Dutch Central Registry for Hydatidiform Moles. The study group comprised 97 patients with hydatidiform moles who did not develop PTD after mole evacuation and 33 patients who did develop PTD. Serum samples from 130 patients with hydatidiform mole with or without PTD were assayed using specific (radio) immunoassays for free hCG , total hCG, and ITA...
Malaysian Journal of Medicine and Health Sciences, 2022
A 31-year-old lady presented with abnormal vaginal bleeding during her first trimester of pregnancy. Based on the ultrasound findings and the decreasing hCG trend (from 1040 mIU/mL to 759 mIU/mL), a diagnosis of missed miscarriage was made. A week later, the patient presented with heavy vaginal bleeding. Ultrasound findings showed classic snowstorm appearance suggestive of complete hydatidiform mole. The serum hCG level however, was 357 mIU/mL. In a case of hydatiform mole with inappropriately low hCG, analytical interference was suspected. Postdilution serum hCG of 5,775,000 mIU/mL confirmed the presence of hook effect in a two-site hCG immunoassay. Discordance between serum hCG and clinical findings should be actively investigated by the laboratory to prevent delay in diagnosis and treatment. This case also highlights the need for clinicians to be aware of the hCG assay used in their hospital's laboratory so that they may recognise false negative hCG results.