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Thyrotoxicosis and Pulmonary Hypertension in the Setting of Molar Pregnancy: A Case Report FREE TO VIEW

Ryan Schroeder, MD; Benjamin Beran, MD; Samih Mawari, MD; Kenneth Presberg, MD; Suzanne Walczak, MD
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Medical College of Wisconsin, Milwaukee, WI

Chest. 2014;146(4_MeetingAbstracts):303A. doi:10.1378/chest.1962994
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SESSION TITLE: Critical Care Student/Resident Case Report Posters II

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM

INTRODUCTION: Thyrotoxicosis is a known cause of pulmonary hypertension (PH), and is also linked to pregnancy, in particular elevated human chorionic gonadotropin (HCG) states. We present a case of thyrotoxicosis causing PH in the setting of a molar pregnancy.

CASE PRESENTATION: A 28-year-old previously healthy African-American female was diagnosed with a molar pregnancy and coexistent normal fetus in the first trimester. At 21 weeks gestation, she presented with lower extremity edema, shortness of breath, and elevated blood pressures. HCG value was 1,164,078 mIU/mL. Thyrotoxicosis was shown by a thyroid-stimulating hormone (TSH) value of <0.005 mIU/L and free thyroxine was 4.17 ng/L. A trans-thoracic echocardiogram (TTE) showed estimated elevated pulmonary artery systolic pressure >60 mmHg, a severely enlarged left atrium, and enlarged right ventricle with mild systolic dysfunction. The patient also developed systemic hypertension. The patient underwent surgical evacuation of pregnancy via abdominal hysterotomy for pre-eclampsia with severe features. Pathology confirmed complete hydatidiform molar pregnancy. Post-operatively, thyroid tests returned to normal with conservative measures within one week. Serial TTEs showed complete normalization of estimated pulmonary artery pressure within four months of pregnancy resolution. Antihypertensive medications were continued for 5 months. Structural abnormalities on TTE also normalized at this point. The patient demonstrated persistent gestational trophoblastic disease requiring intravenous methotrexate therapy seven weeks after the pregnancy. After receiving five cycles of methotrexate, the patient is without signs of disease four months after chemotherapy.

DISCUSSION: HCG shares its α-subunit with TSH and they have a similar β-subunit, which allows HCG to have weakly thyrotropic effects. Thyroid disease is a known cause of Group 5 PH. Multiple reports have shown that thyrotoxicosis can lead to right heart failure with complete reversibility following treatment of the underlying thyroid disease. It is unclear how hyperthyroidism causes PH, several theories exist at this time. With the improvement in her TTE abnormalities, the estimated PA pressures and thyroid function it is likely that her PH was caused by thyrotoxicosis induced by her elevated HCG

CONCLUSIONS: In our patient, her hyperthyroid state resolved after resolution of her molar pregnancy, followed by complete resolution of her PH. This indicates a clear association between this uncommon cause of thyrotoxicosis and PH.

Reference #1: Simonneau G, Robbins IM, Beghetti M, et al. Updated Clinical Classification of Pulmonary Hypertension. J Am Coll Cardiol. 2009;54(1s1):S43-S54.

Reference #2: Conradie M, Koegelenberg C. Conradie M. et al. Pulmonary hypertension and thyrotoxicosis, JEMDSA. 2012;17(2):101-104.

Reference #3: Li J.H., Safford R.E., Aduen J.F., Heckman M.G., Crook J.E., Burger C.D. Pulmonary hypertension and thyroid disease. Chest. 132 2007:793-797.

DISCLOSURE: The following authors have nothing to disclose: Ryan Schroeder, Benjamin Beran, Samih Mawari, Kenneth Presberg, Suzanne Walczak

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