Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2025) 109 P87 | DOI: 10.1530/endoabs.109.P87

SFEBES2025 Poster Presentations Endocrine Cancer and Late Effects (9 abstracts)

Graves’ disease following bone marrow transplantation: a challenging condition to manage

Kyriaki Pieri , Helen E Turner & Christine JH May


Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom


Graves’ disease (GD) following bone marrow transplantation (BMT) is rare. The pathophysiology is uncertain. We present two challenging cases of GD following BMT. Case 1: 45-year-old female, with previous history aged 39 of T-cell lymphoma requiring treatment with CHOP-14 and autologous stem cell transplantation, presented with thyrotoxicosis secondary to GD (TSH <0.01 mU/l; FT4 57.9 pmol/l; FT3 >46.08 pmol/l, TRAb >30 IU/l). She experienced symptoms typical of thyrotoxicosis. There was a small goitre and no thyroid eye disease (TED). Despite compliance with high dose carbimazole for >8 months, thyrotoxicosis persisted (TSH<0.01 mU/l, FT4 32.9-52.4 pmol/l, FT3 >46.08 pmol/l). There was associated liver derangement. She received potassium iodide pre-operatively and underwent thyroidectomy, achieving euthyroidism on levothyroxine. Histology was compatible with GD with minimal inflammation. Case 2: 43-year-old female patient with childhood onset aplastic anaemia, received cyclophosphamide chemotherapy conditioning, total body irradiation and stem cell allograft, complicated by graft versus host disease (GVHD). She was receiving long-term levothyroxine for subclinical hypothyroidism but, presented with new onset thyrotoxicosis despite stopping levothyroxine (TSH <0.01 mU/l, FT4 25.7 pmol/l, FT3 >30.72 pmol/l, TRAb 11.8 IU/l). She started carbimazole, but has persistent thyrotoxicosis, liver derangement, TED CAS 3, diffuse thyroid enlargement and growth of TR3 nodules on thyroid ultrasound. She is awaiting thyroidectomy. Literature reporting GD following BMT is limited to few cases (n = 14) implicating possibility of two mechanisms: GVHD and autoreactivity from transfer of donor lymphocytes. GD onset was reported 5 months to 14 years following BMT. Treatments for GD, where reported, included antithyroid medication (n = 9); surgery first-line/following relapse (n = 3), radioiodine (n = 1). TSH receptor antibody levels were commonly reported as positive/high (TRAb 3.79-34.4 IU/l). Further research into the pathophysiology, monitoring and management is needed to optimise management of such challenging cases.

Volume 109

Society for Endocrinology BES 2025

Harrogate, UK
10 Mar 2025 - 12 Mar 2025

Society for Endocrinology 

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