Correspondence
GESTATIONAL TRANSIENT THYROTOXICOSIS
To the Editor:—Fifty percent to 90% of pregnant women ex-
perience nausea and vomiting.1 When such patients present to the
ED, treatment with hydration and antiemetics usually suffices.
However, in gestational transient thyrotoxicosis (GTT), emesis
and dehydration tend to be more severe and routine care in the ED
might not be adequate. Presented is a patient whose hyperemesis
resolved only when she was treated for GTT. GGT should be in the
differential diagnosis for pregnant patients with severe emesis or
with repeated ED visits.
A 20-year-old woman presented to the ED with nausea and
vomiting. She was 12 weeks pregnant as shown by pelvic sono-
gram. Throughout her first trimester, she made multiple visits to
labor and delivery and the ED for emesis. On all visits she received
intravenous hydration and antiemetics and was discharged the
same day. For the last 6 –7 weeks, she had vomited multiple times
every day and was persistently nauseated. She did not have ab-
dominal pain, vaginal bleeding or discharge, or diarrhea. She had
no past medical disorders, no surgeries, and no allergies. She was
not on medications other than prenatal vitamins, which precipi-
tated vomiting. The only positive physical examination finding
was tachycardia. Pertinent negatives included a blood pressure of
111/80 mm Hg, a benign abdomen, no edema, and no ovarian or
cervical tenderness. Serum electrolytes revealed a potassium of 2.9
(3.5–5.5 mmol/L) and a bicarbonate of 17 (24 –32 mmol/L). Uri-
nalysis found 2⫹ ketones.
The patient was admitted to the obstetric service after continued
vomiting despite 25 mg of intravenous promethazine hydrochlo-
ride and 3 L of normal saline. She also vomited after ingestion of
potassium chloride.
Nausea, emesis, and tachycardia persisted over the next 24
hours of intravenous fluid and potassium replacement and multiple
antiemetic agents, including ondansetron hydrochloride. GTT was
considered and the following serum tests were obtained: thyroid
stimulating hormone (TSH) ⬍ 0.02 (normal, 0.49 – 4.67 uU/mL),
free thyroxine of 19.9 (normal 4.5–11.0 ␮g/dL), and negative
thyroid antibody titers. The patient denied a history of hyperthy-
roidism and hyperthyroid symptoms. Physical examination re-
vealed no eye findings of hyperthyroidism and a nonpalpable
thyroid. Her emesis and tachycardia continued, and on hospital day
3 specific treatment for GTT was started with 20 mg oral propano-
lol 3 times per day and 100 mg oral propylthioruacil 3 times per
day. Her heart rate decreased to 70 beats/min, and on hospital day
5 she had no vomiting. The next day she was able to eat and drink
and had no gastrointestinal disorders. She remained asymptomatic
and was discharged on her hospital dosage of propanolol and
propylthioruacil. On her 2-week posthospital check, she continued
to be asymptomatic.
GTT is a non-autoimmune hyperthyroidism of variable sever-
ity.2,3 Its prevalence is 2–3% of all pregnancies, which is 10-fold
more common than hyperthyroidism resulting from Graves’ dis-
ease.4 The etiology of GTT is directly related to the thyrotropic
stimulation of the thyroid gland by human chorionic gonadotropin
(hCG).4-7 During normal pregnancy, hCG might lower serum TSH
in the first trimester.5,8 Thyroid-binding globulin levels are ele-
vated and as a result T3 and T4 levels are also increased. However,
active free T3 and T4 are within normal levels.9 In contrast,
patients with GTT have elevated free T3 and T4.9,10
© 2003 Elsevier Inc. All rights reserved.
0735-6757/03/2106-0015$30.00/0
doi:10.1016/S0735-6757(03)00173-6
506
The diagnosis of GTT rests on 4 criteria. The first is the
development of abnormal thyroid function tests in the context of
hyperemesis. Abnormal thyroid tests that precede hyperemesis or
remain after resolution of emesis should prompt a search for
another diagnosis.9,11
The second criterion is no history or evidence of hyperthyroid-
ism before pregnancy. Most patients with hyperthyroidism will
have hyperthyroid symptoms before pregnancy, whereas patients
with GTT will not.9 Therefore, a careful review for symptoms of
hyperthyroidism should be conducted.
Absence of the classic physical findings of hyperthyroidism is the
third criteria. Findings such as goiter, lid lag, proximal muscle wast-
ing, and exophthalmos are not seen in patients with GTT. However,
patients might have mild tachycardia and slight tremor.9 The last
criterion is absence of thyroid autoantibody titers. Such titers are
found in patients with Graves disease but not in patients with GTT.9
GTT usually resolves by 18 weeks gestation.9,11 Hyperemesis
and dehydration might warrant hospitalization for intravenous
hydration and antiemetics. If symptoms persist, they might be
relieved by administration of beta-adrenergic blockers for a short
period, less than 2 months. In rare cases, persistent and severe
clinical manifestations might require treatment with propylthioura-
cil, usually for a few weeks.11
Although this patient required propylthiouracil, most patients
only require supportive therapy. Physicians should be aware of
GTT because patients with this condition might need more exten-
sive treatment than those with nausea and vomiting during a
normal pregnancy. Patients should be informed that GTT does not
lead to a less favorable pregnancy outcome and that GTT is likely
to recur with future pregnancies.13
LISA CHAN, MD
Emergency Department
University of Arizona
Tucson, AZ
References
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