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Endocrine Abstracts (2024) 100 P45 | DOI: 10.1530/endoabs.100.P45

1Bart’s Health NHS Trust, London, United Kingdom; 2Cambridge University Hospital, Cambridge, United Kingdom


A 24-year-old, Bengali female presented to her GP with fatigue. Blood tests demonstrated she was pregnant and had elevated thyroid hormones (Free T4 50.4 pmol/l, NR 10.5-24.5; Free T3 19.9 pmol/l, NR 3.1-6.8) with an inappropriately normal TSH (4.04 mU/l, NR 0.27-4.2), prompting referral to our endocrine unit. Her TFTs were repeated on a different platform which excluded assay interference. She reported a 5-year history of a goitre, associated with symptoms of hyperthyroidism (which had previously been investigated with a normal TSH). She was a primigravida and had no difficulties conceiving. Her past medical history was unremarkable, including no childhood symptoms suggestive of thyroid hormone resistance. She had a significant family history of consanguinity. On examination: BMI 18.39 kg/m2; small, smooth goitre; mildly hyperthyroid (fine tremor, hyper-reflexia); visual fields: concentric reduction to confrontation with red pin. Genetic sequencing identified no abnormality in the thyroid hormone receptor beta. Non-contrast pituitary MRI demonstrated a 21 mm pituitary macroadenoma, in keeping with a TSH-oma. The remainder of her anterior pituitary function was normal. Somatostatin analogues are unlicensed in pregnancy and we sought advice from the UK Teratology Information Service. The patient was counselled carefully on the diagnosis and treatment options. She underwent an octreotide suppression test and commenced 4 weekly long-acting somatostatin analogue therapy at 13+4/40 gestation, resulting in normalisation of her TFTs within 3 days. She was monitored closely, including TFTs, CBG testing and serial fetal growth scans. Non-contrast pituitary MRI at 30/40 gestation demonstrated a significant reduction in the size of the macroadenoma and the patient was planned for a normal vaginal delivery. However, a fetal growth scan at 31+2/40 gestation demonstrated intrauterine growth restriction and oligohydramnios. She underwent an uncomplicated emergency caesarean section at 31+4/40. Her baby boy is well, following 5 weeks on SCBU. To preserve fertility, she will be considered for surgical management after she has completed her family. TSHomas make up less than 1% of all pituitary adenomas; with an incidence of 0.15 per million, although the incidence is increasing, possibly due to more sensitive TSH assays1. To our knowledge, this is the first case in the published literature of TSHoma diagnosed in pregnancy and managed throughout with somatostatin analogues. Somatostatin analogues have been used more routinely in pregnancy in acromegaly, with limited, but favourable safety data. The safety profile in those with TSHomas remains confounded by the initial hyperthyroid state in early pregnancy.

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