Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 21 P402

SFEBES2009 Poster Presentations Thyroid (45 abstracts)

Clinical management and outcomes of anti-TSH receptor antibody positive pregnancies

A J Stears 1 , R Stewart 2 , D J Halsall 3 , A L Ogilvy-Stuart 4 , C J Patient 5 , H L Simpson 1 , A Swamy 6 & V K Chatterjee 6


1The Wolfson Diabetes and Endocrine Clinic, Institute of Metabolic Science, Addenbrooke’s Hospital, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK; 2Cambridge University Hospital NHS Foundation Trust, University of Cambridge, Cambridge, UK; 3Department of Clinical Biochemistry, Addenbrooke’s Hospital, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK; 4Department of Paediatrics, Addenbrooke’s Hospital, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK; 5Department of Obstetrics and Gynaecology, The Rosie Hospital, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK; 6Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke’s Hospital, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK.


Introduction: Anti-TSH-receptor binding antibodies can cross the placenta and can stimulate or inhibit the fetal thyroid, causing fetal and neonatal thyroid dysfunction. We test for these antibodies in all pregnant women with a history of thyroid disease using a TSH binding inhibitor immunoglobulin (TBII) assay. Our aims were to audit our management of TBII positive pregnancies and to review pregnancy outcomes.

Methods: Serum TBII concentration was measured using the second-generation BRAHMS TRAK luminescent immunoassay (Hennigsdorf, Germany). The biochemistry database was searched to identify pregnant patients with elevated TBII (>1.0 IU/l) over a 1-year period.

Results: TBII was measured in 109 pregnant women. Of 26/109 had TBII >1.0 IU/l (range 1.1–29.0 IU/l). Maternal thyroid diagnoses were Graves’ disease in 16/26, primary hypothyroidism in 9/26 and hypothyroidism following thyroidectomy for adenoma in 1/26. Third trimester TBII was highest in Graves’ patients either taking antithyroid medication during pregnancy (mean 3.3 IU/l) or euthyroid non-treated Graves’ patients (mean 3.3 IU/l), and was lower in patients with hypothyroidism, either following radioiodine and/or surgery for Graves’ (mean 1.60 IU/l), or with primary hypothyroidism (mean 1.8 IU/l). All pregnancies went successfully to term. Third trimester TBII correlated significantly with first week neonatal fT4 (r=0.67, P=0.006). One fetus had fetal goitre and tachycardia, but had no evidence of clinical or biochemical neonatal thyrotoxicosis. One neonate had transient biochemical thyrotoxicosis, which settled with conservative management. Both were born to mothers with Graves’ requiring antithyroid medication during pregnancy. Cord TSH was elevated in five cases. All had mothers with Graves’ disease, 3/5 mothers had required antithyroid medication during pregnancy, and 2/5 had treated hypothyroidism following previous radioiodine and/or surgery. All settled with conservative management.

Conclusions: Neonatal thyroid dysfunction was most likely with maternal Graves’ disease requiring antithyroid medication during pregnancy, and where 3rd trimester TBII was highest. However neonatal thyroid dysfunction settled spontaneously and overall outcomes were excellent.

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