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Endocrine Abstracts (2023) 91 WC9 | DOI: 10.1530/endoabs.91.WC9

East and North Herts NHS Trust, Stevenage, United Kingdom

A 31 year old female patient initially presented with a two month history of unintentional weight loss. Past medical history included multiple sclerosis, for which she had last received alemtuzumab immunotherapy five months previously. Thyroid function tests (TFTs) demonstrated hyperthyroidism, with Thyroid Stimulating Immunoglobulins (TSI) 5.71 iu/l(NR: <0.56). She was diagnosed with Graves’ disease, possibly induced by alemtuzumab, and commenced on carbimazole. She was strongly advised to avoid pregnancy while hyperthyroid, with a plan to switch to propylthiouracil once stable. Concordance with carbimazole was variable over the next few months requiring frequent changes to her treatment regime, although alemtuzumab-induced thyroid dysfunction is also associated with spontaneous, bidirectional switching between hyperthyroidism and hypothyroidism. Carbimazole was gradually titrated to 15 mg daily after nine months. Six weeks later, repeat TFTs demonstrated profound hypothyroidism. She stopped carbimazole and started levothyroxine, which was titrated to 125 mg daily. Six months later, she presented in the tenth week of pregnancy. Levothyroxine was increased to 150 mg daily at booking then adjusted throughout pregnancy. TSI at 28 weeks gestation was significantly elevated at 31.60 iu/l. Serial growth scans were performed, and a decision was made to deliver her baby at 35 weeks for tailing growth and abnormal Dopplers. The baby required CPAP for 24 hours but was otherwise well. TFTs demonstrated suppressed TSH <0.02 mU/lbut normal fT4 corrected for neonatal age. The baby was discharged at 3 days old and subsequent TFTs normalised. The prevalence of Graves’ disease in pregnancy is estimated at 0.2%. Up to 10% of babies born to mothers with Graves’ disease will develop fetal or neonatal thyrotoxicosis, particularly when TSI is significantly elevated. Alemtuzumab-induced Graves’ disease is particularly associated with a rapid elevation in TSI. Pregnant women with current or previous thyrotoxicosis with raised TSI should be offered growth scans and fetal heart rate monitoring at 28, 32 and 36 weeks. Women with hypothyroidism should increase levothyroxine dose by 25 mg on diagnosis of pregnancy with TFTs at least each trimester, aiming TSH <2.0 mU/l. TSI should be checked at 28 weeks to allow assessment of the risk of neonatal hyperthyroidism and antenatal referral to the neonatal team. The baby should have TSI and TFTs checked on day 3-7, with repeat bloods and anti-thyroid drugs as appropriate. Those caring for women with thyroid disease and their babies should be alert to the increased risks to promote healthy outcomes for both.

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