Category: Thyroid

Monitor: 35


Friday, Apr 26
12:00 PM – 12:30 PM

Objective :

Twin pregnancies with complete hydatiform mole and coexisting normal fetus (CHMCF) are extremely rare with estimated incidence of 1 case for 20,000-100,000 pregnancies. These are associated with both maternal and fetal complications. We present a case of twin pregnancy with CHMCF complicated with trophoblastic hyperthyroidism.

Methods : We reviewed literature in Pubmed.

Results :

Case: A 24 years old female, G4 P3 at 13 weeks gestation presented with vaginal bleeding. She reported dizziness, diaphoresis, tremors, anxiety, palpitation, nausea and edema. Physical examination was significant for gravid uterus, bilateral lower extremity edema, tachypnea and tachycardia.  Patient was found to have twin gestation (live fetus with a complete mole) with Beta HCG of 480,579 mIU/mL on presentation. Work up showed TSH of 0.01 uIU/mL, free t4 of 4.4 ng/dL and total T3 of 405 ng/dL. TSH receptor antibody, anti-thyroid peroxidase antibody and thyroglobulin antibody were negative. After extensive discussion regarding malignancy risk and complications with molar pregnancy, patient opted to proceed with her pregnancy. She was started on Methimazole with dose titration based on free T4 with a  goal free t4 of 1.5ng/dL. She was also on Metoprolol and Nifedipine for hypertension. Pregnancy was complicated with pre-eclampsia, anemia, thrombocytopenia and pulmonary edema. She underwent lower segment cesarean delivery of a viable fetus and evacuation of molar pregnancy at 24 weeks gestation. Methimazole was discontinued after surgery. 4 days after surgery, Beta HCG was 15,942 mIU/mL, TSH was 0.45 uIU/mL and Free t4 was 0.8 ng/dL. Her preterm infant did not have any gross abnormalities and his screen for congenital hypothyroidism was negative.

Discussion :

CHMCF is associated with complications such as spontaneous abortion, intrauterine deaths, preeclampsia and hyperthyroidism. Continuation of CHMCF is an acceptable option but the chance of live birth is 7-37%.  Trophoblastic hyperthyroidism (TH) is often asymptomatic, but 5% develop clinical hyperthyroidism. TH is due to high levels of human chorionic gonadotropin produced by abnormal trophoblast which share the same alpha subunit and amino acid sequence in the beta subunit with thyroid stimulating hormone (TSH), thus interacting with TSH receptor.

Conclusion :

TH usually resolves after surgical uterine evacuation of gestational trophoblastic disease (GTD). Some patients will require anti thyroid therapy until GTD treatment is completed. Lowest possible medication dose should be used to avoid fetal hypothyroidism. Careful surveillance for the development of gestational trophoblastic neoplasia is also needed post GTD treatment.


Edilfavia Mae Uy

Endocrinology Fellow
University of Kentucky
Lexington, Kentucky

I completed my medical degree at Cebu Doctors University, College of Medicine in Cebu, Philippines in 2006. I completed Internal Medicine residency at University of Connecticut in 2012 . I then practiced as an Internal Medicine provider for 6 years doing both inpatient and outpatient practice at Appalachian Regional Healthcare Tug Valley Regional Medical Center in South Williamson, Kentucky. I am currently a first year Endocrinology fellow at the University of Kentucky in Lexington, Kentucky.

Kamyar Asadipooya

Assistant Professor of Medicine, Division of Endocrinology and Molecular Medicine, Department of Medicine,
University of Kentucky

I studied 7 years medical school (9/1992 - 9/1999) and 4 years internal medicine residency (9/2003 - 9/2007) at the Shiraz University of Medical Sciences, Shiraz, Iran. I had 5 years (9/2007 - 9/2012) experiences as an Assistant Professor of Medicine at the Bushehr University of Medical Sciences, Bushehr, Iran. I had 2.5 years (10/2012 - 3/2015) research experience at the Kansas University Medical Center, Kansas City, KS, USA. I had 2 years clinical fellowship of Endocrinology (4/2015 - 4/2017) and 9 months research scientist experience (4/2017 - 12/2017) at the NYU school of Medicine, NYU, NY, USA. I have been Assistant Professor of Medicine at the University of Kentucky, KY, USA since Jan 2018.

Rishi Raj

Clinical Fellow
University of Kentucky
Lexington, Kentucky

I completed my medical school from Patna Medical College, India (08/2007 to 02/2014) and then pursued my residency in Internal Medicine from RWJ Monmouth Medical Center, NJ (07/2015- 06/2018). I also served as Chief Resident between 07/2017-06/2018. Currently, I am doing my training in Endocrinology, Diabetes, and Metabolism at the University of Kentucky, Lexington, KY.

Matthew Hager

Endocrinology Fellow
University Of Kentucky

I completed my medical school from Ross University School of Medicine, Dominica in 2014. I completed my residency in Internal Medicine from University of Kentucky, Lexington, Kentucky and continued my training at University of Kentucky in Endocrinology, Diabetes, and Metabolism where I am currently a second year fellow.