Abstract

Background: Overt hyperthyroidism during pregnancy, though rare (0.1-0.4% of all pregnancies), is alarming as it can lead to many complications such as: preeclampsia, stillbirth, low birth weight, spontaneous abortion, and premature labor. It becomes important to determine the etiology of hyperthyroidism so it can be treated appropriately. The two main etiologies of hyperthyroidism in pregnancy are Graves’ disease, which can be ruled out with TRAb, and hCG-mediated thyrotoxicosis, of which gestational transient thyrotoxicosis (GTT) is a subtype. GTT can present with subclinical hyperthyroidism or a mild overt hyperthyroidism and is more clinically benign than Graves’ disease. It typically resolves by weeks 14-18 of gestation as hCG levels fall. Clinical Case: A 32 year old G1P0 female with subclinical hyperthyroidism presented with a twin pregnancy and abnormal thyroid function tests (TFTs). Prior to pregnancy, she had mildly decreased TSH with normal fT3/fT4 and elevated TPO Ab, but normal thyroglobulin and TRAb. Her thyroid US showed multiple subcentimeter nodules that were too small for biopsy and thyroid parenchyma not consistent with autoimmune thyroid disease or Graves’ disease. The next step was a radioiodine uptake and scan, but it was deferred due to pregnancy. She did not have any symptoms of hyperthyroidism and her physical exam was benign. Her TSH was lower than expected throughout the first month of pregnancy with elevated fT4/fT3, indicating overt hyperthyroidism, which was alarming. Her TRAb was repeated, but was, again, negative, ruling out Graves’ disease. She remained clinically asymptomatic for hyperthyroidism and her TFTs improved during the second trimester and so she was thought likely to have GTT. GTT is a hCG-mediated thyrotoxicosis seen during the end of the first trimester when hCG levels peak. Usually GTT presents with only a mild elevation of fT4/fT3. In this case, the patient presented with a low TSH (even with correction for pregnancy) and higher fT4/fT3 than generally reported for GTT. Graves’ disease was ruled out with negative repeat TRAb, which is important as the management and treatment is very different from GTT. Her abnormal thyroid levels in the setting of GTT were likely related to her multiparity. In twin pregnancies, the placenta produces more hCG for longer period of times and twin pregnancies typically present with lower TSH. Lastly, it was important that her thyroid tests were closely monitored throughout the pregnancy to make sure they downtrended appropriately after the first trimester. Conclusion: GTT in the setting of twin pregnancy may present with thyroid function tests indicating overt hyperthyroidism, but it is important to differentiate it from other etiologies of overt hyperthyroidism in pregnancy so appropriate management can be initiated.

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