Changing presentation of complete hydatidiform mole at the New England Trophoblastic Disease Center over the past three decades: Does early diagnosis alter risk for gestational trophoblastic neoplasia?

2015 ◽  
Vol 138 (1) ◽  
pp. 46-49 ◽  
Author(s):  
Sue Yazaki Sun ◽  
Alexander Melamed ◽  
Donald P. Goldstein ◽  
Marilyn R. Bernstein ◽  
Neil S. Horowitz ◽  
...  
2016 ◽  
Vol 26 (5) ◽  
pp. 984-990 ◽  
Author(s):  
Antonio Braga ◽  
Valéria Moraes ◽  
Izildinha Maestá ◽  
Joffre Amim Júnior ◽  
Jorge de Rezende-Filho ◽  
...  

ObjectiveThe aim of the study was to evaluate potential changes in the clinical, diagnostic, and therapeutic parameters of complete hydatidiform mole in the last 25 years in Brazil.MethodsA retrospective cohort study was conducted involving the analysis of 2163 medical records of patients diagnosed with complete hydatidiform mole who received treatment at the Rio de Janeiro Reference Center for Gestational Trophoblastic Disease between January 1988 and December 2012. For the statistical analysis of the natural history of the patients with complete molar pregnancies, time series were evaluated using the Cox-Stuart test and adjusted by linear regression models.ResultsA downward linear temporal trend was observed for gestational age of complete hydatidiform mole at diagnosis, which is also reflected in the reduced occurrence of vaginal bleeding, hyperemesis and pre-eclampsia. We also observed an increase in the use of uterine vacuum aspiration to treat molar pregnancy. Although the duration of postmolar follow-up was found to decline, this was not accompanied by any alteration in the time to remission of the disease or its progression to gestational trophoblastic neoplasia.ConclusionsEarly diagnosis of complete hydatidiform mole has altered the natural history of molar pregnancy, especially with a reduction in classical clinical symptoms. However, early diagnosis has not resulted in a reduction in the development of gestational trophoblastic neoplasia, a dilemma that still challenges professionals working with gestational trophoblastic disease.


1986 ◽  
Vol 67 (5) ◽  
pp. 690-694 ◽  
Author(s):  
DOO SANG KIM ◽  
HYUNG MOON ◽  
KYUNG TAI KIM ◽  
YOUNG JIN MOON ◽  
YOUN YEOUNG HWANG

2018 ◽  
Vol 148 (1) ◽  
pp. 161-167 ◽  
Author(s):  
Izildinha Maestá ◽  
Roni Nitecki ◽  
Neil S. Horowitz ◽  
Donald P. Goldstein ◽  
Marjory de Freitas Segalla Moreira ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Anuradha Jayasuriya ◽  
Dimuthu Muthukuda ◽  
Preethi Dissanayake ◽  
Shyama Subasinghe

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.


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