ODP453 A Lady Changes from Hypothyroid to Hyperthyroid State during Pregnancy

Abstract

Abstract A 34-year-old lady presented to the Endocrine Clinic in 2021 initially for hypothyroidism complicated pregnancy. She volunteered history of Graves’ disease at age 11 and went into remission after taking anti-thyroid medication for 1-2 years. She did not have family history of thyroid disease. She was found to have hypothyroidism during pre-pregnancy check-up in 2017 and started thyroxine (LT4) replacement. The anti-thyroid peroxidase antibody was elevated to 358 (< 35) kIU/l. She had first pregnancy in early 2018 and LT4 was increased to 128 microgram daily which was reduced to 50 microgram daily after delivery. Before the second pregnancy, her TSH was decreasing. The family doctor reduced LT4 to 25 microgram 5 days per week. The TFT just before the patient became pregnant showed TSH 0. 08 (0.35-3.8)mIU/l, fT4 15 (9.5-18.1) pmol/l. At 8th week of pregnancy, her TSH became undetectable, while fT4 was 20.8 (11.8-25.7)pmol/l. At 17th week, her fT4 further increased to 19.9 (10.1-19.4) pmol/l and fT3 was 7.3 (3.25-5.2)pmol/l. TSH remained undetectable. Clinically, she complained of palpitation. She had goiter but no thyroid bruit. Her pulse rate was 118 bpm. LT4 was stopped. She was suspected to have relapse of thyrotoxicosis. Anti-TSH receptor antibody was raised to 3.3 (<1. 0) IU/l. The thyroid stimulating immunoglobulin (TSI) was raised to 155% above baseline activity (nl<140%). At 22th week, her fT4 remained elevated at fT4 19.1 (9.2-17.44), fT3 7.6 (3. 03-4.75) pmol/l. Carbimazole was started at 5mg daily for 2 weeks then 5mg alternate day. At 28th week, her fT4 was still elevated fT4 17.7 (9.2-17.4), fT3 6.9 (3. 03-4.75) pmol/l. She was also noted to have poor maternal weight gain from 61kg pre-pregnancy to 62.4kg at 22th week. She had nausea and vomited once per week. She had iron deficiency anaemia requiring iron supplement. Carbimazole was increased again to 5mg daily for 3 weeks then tailed down to 5mg alternate day. At 33th week, her anti-TSH receptor antibody level reduced to 1.9. At 36th week of gestation, her fT4 level came down to mid normal range 14.1 (9.2-17.4)pmol/l. She delivered at 40th week uneventfully. There are a number of clinical challenges. Usually, the dose of thyroxine is increased by 30% in early pregnancy with TSH aim of 0.5-2. 0mIU/l. But in this patient, the TSH was already low before pregnancy and then became undetectable so LT4 was not increased. Gestational thyrotoxicosis is a differential diagnosis but seldom persisted towards second trimester and TSI is expected to be normal in such case. Graves’ disease usually becomes quiescent during pregnancy due to immunosuppression or haemodilution of autoimmune antibodies. Changing from hypothyroidism to hyperthyroidism is a rare phenomenon. It is related to the concentration and the affinity of anti-thyroid stimulating antibodies and blocking antibodies. The outcome depends on which antibodies predominate. Presentation: No date and time listed