scholarly journals Recurrent Thyroid Storm Caused by a Complete Hydatidiform Mole in a Perimenopausal Woman

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Anuradha Jayasuriya ◽  
Dimuthu Muthukuda ◽  
Preethi Dissanayake ◽  
Shyama Subasinghe
Keyword(s):  
Molecular Mimicry ◽  
Hydatidiform Mole ◽  
Gestational Trophoblastic Disease ◽  
Thyroid Storm ◽  
High Dose ◽  
Complete Hydatidiform Mole ◽  
Free Triiodothyronine ◽  
Rare Presentation ◽  
Perimenopausal Woman ◽  
Trophoblastic Disease

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 beta blockers, steroids, and high-dose carbimazole. Her lower abdominal tenderness led to further investigations which revealed tremendously elevated beta-hCG and a snow storm appearance on transabdominal ultrasound suggestive of GTD. She underwent curative surgery and was diagnosed with complete hydatidiform mole postoperatively by histology. Conclusion. Recurrent thyroid crisis in gestational trophoblastic disease is an exceedingly rare presentation and that is highly fatal. This case highlights the importance of early detection and treatment of the etiology of thyrotoxicosis to eliminate mortality.

scholarly journals Perimenopausal giant hydatidiform mole complicated with preeclampsia and hyperthyroidism: A case report and literature review

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 1038-1042
Author(s):  
Yan Wan ◽  
Guoqing Jiang ◽  
Ying Jin ◽  
Zengping Hao
Keyword(s):  
Case Report ◽  
Literature Review ◽  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Hydatidiform Mole ◽  
Gestational Trophoblastic Disease ◽  
Optimal Treatment ◽  
Perimenopausal Woman ◽  
Trophoblastic Disease ◽  
Reproductive Females

Abstract Gestational trophoblastic disease (GTD) commonly occurs in reproductive females, but is extremely rare in perimenopausal females. In this study, we reported a case of hydatidiform mole in a 48-year-old perimenopausal female admitted due to a giant uterine mass of 28 weeks’ gestational size. The serum human chorionic gonadotropin (HCG) level ranged from 944 to 1,286 mIU/mL before treatments. The signs of preeclampsia and hyperthyroidism were relatively prominent. Hysterectomy was performed and chemotherapy was scheduled when the serum HCG level remained at a plateau, about 528 mIU/mL. The symptoms of preeclampsia and hyperthyroidism were relieved after treatment. Accordingly, we concluded that GTD could occur in perimenopausal woman and hysterectomy usually is the optimal treatment.

scholarly journals SUN-513 Severe Hyperthyroidism in a Complete Molar Pregnancy

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Nikoletta Proudan ◽  
Kersthine Andre
Keyword(s):  
Perioperative Complications ◽  
Hydatidiform Mole ◽  
Gestational Trophoblastic Disease ◽  
Thyroid Storm ◽  
Molar Pregnancy ◽  
Free T4 ◽  
Trophoblastic Disease ◽  
Increased Risk ◽  
History Of

Abstract Hydatidiform mole (HM), a type of gestational trophoblastic disease (GTD), is a rare cause of clinical hyperthyroidism. The development of hyperthyroidism requires an elevation of HCG >100,000 mlU/mL for several weeks. Complete mole has a marked HCG elevation compared to partial mole thus presents with a higher incidence of thyrotoxicosis. Surgical uterine evacuation is the treatment of choice for HM. However, untreated hyperthyroidism can pose a risk for the development of thyroid storm and high-output cardiac failure in the perioperative period. To our knowledge, there are no specific guidelines for management at this time. We present a case of hyperthyroidism secondary to complete molar pregnancy successfully treated with propylthiouracil (PTU), potassium iodide (SSKI), and atenolol in the preoperative period. A 42-year-old female with history of migraines presented to her gynecologist with a 3-week history of lower abdominal cramping, vomiting, loss of appetite, and abnormal vaginal bleeding. She also endorsed a 6-pound weight loss, intermittent tachycardia, exertional dyspnea, and increased anxiety. Pregnancy test was positive, and ultrasound was concerning for GTD. Laboratory work up was significant for HCG 797,747 mIU/mL (< 5mlU/mL), TSH <0.005 mIU/mL (0.4-4.0 mlU/mL), Free T4 3.09 ng/dL (0.9-1.9 ng/dL), and Free T3 11.48 pg/dL (1.76-3.78 pg/dL). The patient was admitted to the hospital and started on PTU 100 mg Q6H, SSKI 200 mg TID following the first dose of PTU, and atenolol 25 mg daily. She underwent an uncomplicated D & C the next day. On post-op day 1, HCG decreased to 195,338 mIU/mL and Free T4 to 2.39 ng/dL. The patient was discharged on the aforementioned doses of PTU and atenolol. One-week follow-up labs showed HCG 8,917 mIU/mL and Free T4 1.22 ng/dL. Surgical pathology confirmed a complete hydatidiform mole. PTU was decreased to 50 mg TID. On post-op day 14, HCG had risen to 15,395 mIU/mL with onset of nausea and vomiting. Repeat Free T4 remained within reference range. Patient was taken back to surgery for a laparoscopic total hysterectomy with bilateral salpingectomy. Pathology confirmed an invasive hydatidiform mole. Two-week follow-up lab work showed HCG 155 mIU/mL, TSH 1.5 mIU/mL, and Free T4 1.19 ng/dL. PTU and atenolol were then discontinued. The development of hyperthyroidism in molar pregnancy is largely influenced by the level of HCG and usually resolves with treatment of GTD (1). However, it’s crucial to control thyrotoxicosis to avoid perioperative complications. This case also highlights the importance of monitoring HCG levels following a complete molar pregnancy due to an increased risk for invasive neoplasm. 1. Walkington, L et al. “Hyperthyroidism and human chorionic gonadotrophin production in gestational trophoblastic disease.” British journal of cancer vol. 104,11 (2011): 1665-9. doi:10.1038/bjc.2011.139

scholarly journals Clinicopathological study of Gestational Trophoblastic Disease

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 2344-2349
Author(s):  
Ramesh M. Oswal ◽  
Mahendra A. Patil ◽  
Sujata M. Kumbhar ◽  
Jyoti S. Tele ◽  
Atul B. Hulwan
Keyword(s):  
Risk Factors ◽  
Maternal Age ◽  
Hydatidiform Mole ◽  
Gestational Trophoblastic Disease ◽  
Histopathological Study ◽  
Molar Pregnancy ◽  
Complete Hydatidiform Mole ◽  
Trophoblastic Disease ◽  
Complete Mole ◽  
Clinicopathological Study

Several potential etiologic risk factors have been evaluated for the development of complete hydatidiform mole. The two established risk factors that have emerged are extremes of maternal age and prior molar pregnancy. Advanced or very young maternal age has consistently correlated with higher rates of complete hydatidiform mole. Compared to women aged 21- 35 years, the risk of a complete mole is 1.9 times higher for women both more than 35 years and less than 21 years as well as 7.5 times higher for women more than 40 years. (49, 50) The risk of repeat molar pregnancy after 1 mole is about 1% or about 10-20 times the risk for the general population. The present study on the gestational trophoblastic disease (GTD) was carried out as it is one of the fascinating gynaecological tumours. Hence a clinicopathological study of gestational trophoblastic disease was undertaken with relevance to the histopathological study of GTD and clinical correlation.

scholarly journals A rare presentation of invasive mole with an arterio-venous malformation: a case report

2020 ◽  
Vol 9 (5) ◽  
pp. 2180
Author(s):  
Atmajit Singh Dhillon ◽  
Vartika Pathak
Keyword(s):  
Case Report ◽  
Venous Malformation ◽  
Hydatidiform Mole ◽  
Emergency Admission ◽  
Gestational Trophoblastic Disease ◽  
Severe Bleeding ◽  
Rare Presentation ◽  
Trophoblastic Disease ◽  
Common Etiology ◽  
Invasive Mole

Gestational trophoblastic disease comprises of various pathologies with hydatid form mole bring a common etiology. Emergency admissions of patients of gestational trophoblastic disease is very rare. Here we present a case report of an emergency admission of patient with hydatidiform mole and severe bleeding and then was managed for the same during the course of hospital stay.

Complete Hydatidiform Mole and Coexisting Fetus With Gastroschisis: A Case Report Highlighting the Importance of Diagnostic Genotyping

2021 ◽  
pp. 109352662110248
Author(s):  
Austin McHenry ◽  
Urania Magriples ◽  
Pei Hui ◽  
Raffaella Morotti
Keyword(s):  
Differential Diagnosis ◽  
Hydatidiform Mole ◽  
Gestational Trophoblastic Disease ◽  
Diagnostic Process ◽  
Rare Occurrence ◽  
Complete Hydatidiform Mole ◽  
Trophoblastic Disease ◽  
Increased Risk ◽  
Ancillary Studies

Twin pregnancy with a complete hydatidiform mole and a coexisting fetus (CHMCF) is an extremely rare occurrence, described only by a handful of published series and cases reports. The majority of the literature on CHMCF examines prenatal care and follow-up in relation to the increased risk of gestational trophoblastic neoplasia (GTN). At present, few reports elaborate on the diagnostic process and differential diagnosis, especially in the context of recent molecular advances in risk stratification for GTN. Here, we describe the first known case of a CHMCF with gastroschisis with liveborn delivery at 35 weeks gestation. This report aims to review the pre- and postnatal differential diagnosis and discuss recent updates on the importance of ancillary studies in the diagnosis of gestational trophoblastic disease.

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