MRI/MRA imaging: diagnosing molar pregnancy
Molar pregancy should be considered in women with high serum hCG levels.
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A 39-year-old woman, G5P2, initially presented for a routine prenatal visit at 12 weeks gestational age. Serum thyroid function tests obtained as part of her evaluation were thyroid stimulating hormone (TSH) <0.01 mIU/L and free thyroxine (T4) 3.42 ng/dL (normal 0.89 - 1.80 ng/dL).
She was sent to the endocrine clinic for further evaluation. At her clinic visit, she described mild nausea and vomiting, but denied weight loss. She had occasional palpitations, especially with exertion, and noted that her thyroid had been enlarged and that she had some discomfort with swallowing. She denied any prior history of thyroid dysfunction.
Physical examination revealed a calm woman with a pulse of 88. There was no tremor, and her eyes were normal. Her thyroid was approximately two and one-half times enlarged, very firm, lobular and slightly nodular on the right. Laboratory studies again revealed a suppressed serum TSH of <0.01. Thyroperoxidase (TPO) and thyroglobulin (Tg) antibodies were negative.
A thyroid stimulating immunoglobulin (TSI) was normal at 120%. Serum T4 was strikingly elevated to 24.4 with a T3 uptake of 33.9. The free T4 index was strikingly elevated at 8.3. Serum total triiodothyronine (T3) was also markedly elevated at 575 ng/dL units.
In view of the negative thyroid antibodies and the normal TSI, Graves’ disease was unlikely. Her hyperthyroidism was felt to be too severe to be due to gestational thyrotoxicosis. It was thought most likely that she had a toxic nodular goiter, although this could not be determined definitively because radioactive iodine uptake and scan were contraindicated in the setting of pregnancy.
She was prescribed anti-thyroid medication but did not take it initially because her husband, a medical assistant, told her that it was not appropriate for pregnant women.
When she returned to the obstetric clinic at 16 weeks gestation, no fetal heartbeat could be detected by Doppler. A pelvic ultrasound demonstrated embryonic demise at 11+ weeks.
The placenta had multiple cystic vascular areas consistent with a partial molar pregnancy. Of particular concern was an area of the posterior miduterus with loss of differentiation with the uterine wall and a large plexus of arterial flow, suspicious for myometrial invasion. A quantitative human chorionic gonadotrophin (hCG) measurement was markedly elevated at 306,099 mIU/mL.
In order to further characterize the myometrial invasion, an MRI/MRA was obtained (Figures 1 and 2). This showed uterine enlargement, at 16.7 × 13.1 × 6.3 cm, with a fluid-filled endometrial cavity and a multicystic, enhancing soft tissue endometrial mass measuring 12.5 × 3.9 × 8.8 cm adherent to the posterior wall of the uterus.
Source: EN Pearce |
The right posterior lateral junctional zone appeared indistinct and exhibited hyperenhancement, suggesting invasion into the myometrium. These findings were consistent with gestational trophoblastic disease with likely invasion of the right posterior lateral junctional zone.
The patient was admitted to the hospital and underwent rapid surgical preparation with methimazole, SSKI and dexamethasone. Hysterectomy was performed without complications. Pathology confirmed a partial hydatidiform molar pregnancy. Her hyperthyroidism resolved and serum hCG values decreased to <2 mIU/mL.
hCG and TSH share an identical alpha subunit, and hCG is known to be a weak stimulator of the TSH receptor. The high level of hCG secreted by molar pregnancies, therefore, may cause increased thyroid hormone production. The hCG secreted by molar pregnancies has a decreased sialic acid content, making it an especially potent thyroid stimulator.
Molar pregnancy should be suspected in women with very elevated serum hCG levels, typically at least 100,000 mIU/L. Diagnosis is typically made by pelvic ultrasound; MRI, as obtained for the patient, is rarely required. Removal of the mole cures the thyrotoxicosis.
Elizabeth N. Pearce, MD, MSc, is Assistant Professor of Medicine, Boston University School of Medicine.