Introduction: Hyperthyroidism is a common endocrine disorder in pregnancy, with potentially significant foeto-maternal consequences.
Description of the case: 25 year old lady with auto-immune hyperthyroidism (TRAb>400) was treated with Propranolol and Carbimazole and referred to the Endocrine clinic. She was started on Block and replace therapy. She was soon moved over to Carbimazole as she was contemplating pregnancy. She became hypothyroid in 3 months and anti-thyroid therapy was stopped. In another 2 months she required thyroxine replacement. 3 months later, her TSH started to drop and by 12 months, she was found to be hyperthyroid. 2 months later, she was found to be pregnant and was changed to PTU. During the rest of her pregnancy, her FT3 remained high, FT4 normal with TSH undetectable, despite treatment with PTU 300 mg bd with regular counselling. She delivered a healthy but hyperthyroid baby (FT4: 64, FT3: 31.3, TSH<0.001, TRAb>400) of birthweight 3150 grams at 37 weeks+1 day of gestation. Mums TFTs 1 day postnatal were still in the hyperthyroid state, but when checked after 5 weeks, showed features of hypothyroidism with TSH 9.11. Her PTU was then reduced to 100 mg/day, but she became grossly hypothyroid in 2 months, needing Thyroxine replacement. Within further 2 months, her hyperthyroidism flared up again and is currently being managed by block and replace regimen. The infant is now being treated with Carbimazole and is euthyroid.
Discussion: This case brings forward the following points for discussion: The role of anti-TSH receptor antibodies in fluctuation of thyroid status. The relative contribution of placental glucuronidase system in degradation of PTU for the relative lack of its efficacy seen in this case during pregnancy, which returned after delivery. The close monitoring required in such patients during and after pregnancy.