Endocrine Abstracts

Introduction

During pregnancy, women with Graves’ disease are at risk of maternal and fetal hyperthyroidism caused by stimulating TSH receptor antibody. Here we report the unusual case of a woman with recurrent Graves’ disease who developed central hypothyroidism transiently during pregnancy.

Case report and results

A 26-year-old woman was treated by antithyroid drug for a third episode of hyperthyroidism due to Graves’ disease. At the beginning of her second pregnancy, cervical palpation showed a large vascular goiter. Thiamazole treatment was stopped in the first week of gestation. During the 3^rd month, hormonal monitoring revealed central hypothyroidism: TSH = 1 mU/l (0.27–4.3), fT4 = 0.67 ng/dl (0.81–1.32), fT3 = 2.37 ng/l (2.47–4.1), in presence of anti-TSH receptor antibodies (3.5 UI/l) with stimulating activity (+ 285%) and elevated βHCG levels (153 656 UI/l). During the second half of gestation, substitutive levothyroxine treatment restored an euthyroid state. Furthermore, anti-TSH receptor antibodies titers decreased progressively and were undetectable at the end of the second trimester. The woman gave birth to a healthy euthyroid baby girl (3.2 kg) without goiter. During the postpartum period, she breastfed normally. Her anterior pituitary function was investigated and shown to be normal: spontaneous menstrual periods, anterior pituitary hormones within normal range and normal pituitary IRM at 6-month post-partum. During post-partum follow-up, levothyroxine treatment was progressively decreased and the patient eventually developed ’classical’ recurrence of Graves’ disease with thyrotoxicosis 8 months after delivery.

Conclusion

We report the first case of transient central hypothyroidism during pregnancy in a woman with recurrent episodes of Graves’ disease. Despite the presence of anti-TSH receptor antibodies with stimulating activity detectable during the first two trimesters of pregnancy, we suggest, as a unifying hypothesis to explain this highly unusual clinical and biological pattern, that this woman secreted a variant hCG molecule that binds both to the TSH receptor on follicular thyroid cells and on the folliculo-stellate cells of the anterior pituitary with inhibiting activity resulting in central hypothyroidism.