A Hydatidiform Mole Can Cause Severe Gestational Hyperthyroidism PDF

Clinical
Clin Thyroidol 2013;25:298–300. THYROIDOLOGY

CASE REPORT
A Hydatidiform Mole Can Cause Severe
Gestational Hyperthyroidism
Shalini Bhat and Jelena Maletkovic*
OBJECTIVE: To report a new case of molar pregnancy associated with severe thyrotoxicosis.
Background minute. There was no exophthalmos, and her extraoc-

Gestational trophoblastic disease (GTD) is a rare com- ular movements were normal. The thyroid gland was
plication of pregnancy that may be associated with palpable and of normal size. Cardiovascular exami-
thyrotoxicosis. The incidence of hydatidiform mole nation revealed sinus tachycardia without murmurs,
in the United States and other developed countries is rub, or gallops. Breath sounds were equal bilaterally,
about 1 in 1500 live births (1). Complete moles have without rhonchi or wheezes. There was no peripheral
the highest incidence of thyrotoxicosis, predominantly edema. The size of the uterus was compatible with a
affect younger women, and present with vaginal 12-week gestation.
bleeding most of the time. Hyperthyroidism in hyper-
emesis gravidarum occurs with greater frequency Ultrasonography of her enlarged uterus revealed
than in normal pregnancy. We describe a case of that the uterine cavity was significantly distended
hyperthyroidism secondary to molar pregnancy high- and filled with an echogenic soft-tissue mass that
lighting the rare but important evaluation of hyper- had small cystic components, most compatible with
thyroidism in women of child-bearing age. complete molar pregnancy. Her thyroid-function tests
were found to be markedly elevated (Table 1). Her thy-
Case Report rotropin (TSH) was <0.07 mIU/ml (normal range, 0.3
A 20-year-old woman, gravida 2, para 1, presented to 4.2), free thyroxine (FT4) 5.59 ng/dl (normal range,
to the emergency room with a history of nausea, 0.8 to 2.0), triiodothyronine (T3) 465 ng/dl (normal
weight loss of about 20 lb in 6 weeks, and intermit- range, 40 to 180), and human chorionic gonadotropin
tent vaginal bleeding. On examination, she had tachy- (hCG) close to 2 million mIU/ml. Laboratory data on
cardia (108 BPM), a blood pressure of 146/86 mm admission revealed microcytic hypochromic anemia
Hg, and a regular respiration rate of 18 breaths per continued on next page
Table 1. Thyroid-Function Tests
Day 1 Day 2 Day 2 Day 3

(Immediately (1 Day after
after Dilatation Dilatation and
and Curettage) Curettage)
TSH (0.3–4.2 mIU/ml) <0. 07 <0.10 <0.10 <0.07
FT4 (0.8–2.0 ng/dl) 5.59 4.17 3.57 3.03
T3 (40–180 ng/dl) 465 344 257 226
hCG 1,978,770 836,500 580,378
CLINICAL THYROIDOLOGY l DECEMBER 2013 298 VOLUME 25 l ISSUE 12 l © 2013
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CASE REPORT: A Hydatidiform Mole Can Cause Shalini Bhat and Jelena Maletkovic
Severe Gestational Hyperthyroidism
and elevated transaminase and alkaline phosphatase. genic pulmonary edema developed. She required
The remainder of her electrolytes, complete blood intubation and had a prolonged hospitalization but
count, and platelets were normal. Her electrocardio- then stabilized and was discharged in good condition.
gram showed sinus tachycardia. Histopathology of all aborted specimens verified the
diagnosis of partial mole, including a dystrophic fetus.
The patient underwent dilatation and curettage for The hCG values decreased to below detection after 12
evacuation of the mole. During the postoperative weeks, and she was euthyroid at follow up with free
period respiratory failure secondary to noncardio- T4 of 1.1 ng/dl and TSH of 1.42 mU/l.
DISCUSSION AND CONCLUSIONS
GTD with thyrotoxicosis is a rare clinical scenario, (4). The glycoprotein hormone hCG is a specific tumor
but thyroid hyperstimulation by hCG can have severe marker for trophoblastic diseases. The analogy in the
clinical consequences. Complete hydatidiform mole structure between hCG and TSH can cause cross-
most commonly presents with vaginal bleeding, reactivity with their receptors. It has been shown
occurring at 6 to 16 weeks of gestation in 80% to that the homology in the hCG and TSH molecules, as
90% of cases (1). The clinical signs and symptoms, well as in their receptors, is likely to be responsible
such as hyperemesis, have occurred less frequently for the cross-reactivity of hCG with the TSH receptor
in more recent years because of earlier diagnosis (5). Glinoer has estimated that ‘‘for every 10,000 mU/
resulting from widespread use of ultrasonography mL increase in serum hCG, FT4 increases by 0.1 ng/
and accurate tests for hCG. In the past, approximately dL and TSH decreases by 0.1 mIU/mL’’ (6). Molecular
55% to 60% of women with trophoblastic disease variants of hCG found in molar pregnancies have
had clinically evident hyperthyroidism that could be increased thyrotropic potency (7). When gestational
severe at the time of diagnosis. However, in a review trophoblastic disease causes a significant rise in hCG
of 196 patients from the United Kingdom treated for levels, it may induce hyperthyroidism that requires
gestational trophoblastic disease between 2005 and treatment. As expected, thyrotoxicosis resolves with
2010, biochemical hyperthyroidism was present treatment of GTD and normalization of hCG levels.
in 7% and clinical hyperthyroidism in only 2% (2). The development of hyperthyroidism is largely influ-
Hydatidiform moles are commonly associated with enced by the level of hCG and usually resolves with
hCG levels markedly elevated above those of normal treatment of GTD. The consideration of this cause of
pregnancy, as can be seen in our patient, who had an hyperthyroidism in pregnancy should be diagnosed
hCG level close to 2 million mIU/ml. Approximately early and managed efficaciously before imminent dil-
50% of patients with molar pregnancy have preevac- atation and curettage is required for definitive man-
uation hCG levels >100,000 mIU/ml (3). agement of the hydatidiform mole.
Tisne et al. reported the first case of clinical hyperthy- *Endocrinology Division, UCLA School of Medicine,
roidism in a patient with hydatidiform mole in 1955 Los Angeles, CA
continued on next page
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CASE REPORT: A Hydatidiform Mole Can Cause Shalini Bhat and Jelena Maletkovic
Severe Gestational Hyperthyroidism
REFERENCES
1. Lurain JR. Gestational trophoblastic disease I: 5. Yoshimura M, Hershman JM. Thyrotropic action
epidemiology, pathology, clinical presentation and of human chorionic gonadotropin. Thyroid
diagnosis of gestational trophoblastic disease, 1995;5:425-34.
and management of hydatidiform mole. Am J
6. Glinoer D. The regulation of thyroid function in
Obstet Gynecol 2010;203:531-9. Epub August 21,
pregnancy: pathways of endocrine adaptation
2010.
from physiology to pathology. Endocr Rev
2. Garner E, Goldstein DP, Feltmate CM, Berkowitz 1997;18:404-33.
RS. Gestational trophoblastic disease. Clin Obstet
7. Pekary AE, Jackson IM, Goodwin TM, Pang
Gynecol 2007;50:112-22.
XP, Hein MD, Hershman JM. Increased in
3. Menczer J, Modan M, Serr DM. Prospective follow- vitro thyrotropic activity of partially sialated
up of patients with hydatidiform mole. Obstet human chorionic gonadotropin extracted
Gynecol 1980;55:346-9. from hydatidiform moles of patients with
hyperthyroidism. J Clin Endocrinol Metab
4. Tisne L, Barzelatto J, Stevenson C. Study of thyroid
1993;76:70-4.
function during pregnancy-puerperal state with
radioactive iodine. Bol Soc Chil Obstet Ginecol
1955;20:246-51. [in Spanish]
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Clinical

Clin Thyroidol 2013;25:298–300. THYROIDOLOGY

Background minute. There was no exophthalmos, and her extraoc-

Table 1. Thyroid-Function Tests

Day 1 Day 2 Day 2 Day 3

TSH (0.3–4.2 mIU/ml) <0. 07 <0.10 <0.10 <0.07

FT4 (0.8–2.0 ng/dl) 5.59 4.17 3.57 3.03

T3 (40–180 ng/dl) 465 344 257 226

hCG 1,978,770 836,500 580,378

DISCUSSION AND CONCLUSIONS

continued on next page

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