Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2003) 5 P39

BES2003 Poster Presentations Clinical Case Reports (52 abstracts)

Coexisting struma ovarii and Graves' disease

EA Teale & SR Peacey


Department of Diabetes and Endocrinology, Bradford Hospitals NHS Trust, Bradford, UK.


A female presented in 1994 at age 28 with typical symptoms and signs of hyperthyroidism (FT4 39 picomol per litre, TSH < 0.05 milliunit per litre) and associated ophthalmopathy (bilateral exophthalmos, lid retraction and conjunctival inflammation), consistent with Graves' disease. Initially treated successfully with Carbimazole. She relapsed after stopping Carbimazole and in 1998 underwent sub-total thyroidectomy, with residual thyroid tissue left at the inferior poles bilaterally (histological appearance consistent with treated thyrotoxicosis). Postoperatively, her TSH remained undetectable with normal FT4 and TT3 levels. Subsequently she relapsed clinically and biochemically (FT4 28.9 picomol per litre, TT3 3.76 nanomol per litre, TSH <0.05 milliunit per litre). Isotope scanning showed minimal focal uptake bilaterally at the root of the neck [0.08 percent (NR 0.5 to 4.0)]. Carbimazole was restarted and biochemical euthyroidism was maintained. In March 2002 she developed bilateral leg oedema and heavy proteinuria (urinary protein/creatinine ratio 2600, urea 6.8 millimol per litre, creatinine 97 micromol per litre). Ultrasound demonstrated normal kidneys. A complex left ovarian mass was an incidental finding. Surgery was performed in June 2002 for suspected ovarian malignancy. The 555 gram ovarian mass consisted almost entirely of thyroid tissue consistent with struma ovarii, no evidence of malignancy. Hypothyroidism developed postoperatively (FT4 9.7 picomol per litre, TSH 36 milliunit per litre) and thyroid hormone was commenced. TSH receptor stimulating antibody remains positive. Struma ovarii is a rare cause of hyperthyroidism and particularly rare in patients with co-existing Graves' disease. It is likely that her postoperative hyperthyroid relapse was secondary to functioning struma ovarii in view of the low thyroid remnant uptake on isotope scanning and the development of hypothyroidism following removal of the ovarian mass. Circulating TSH receptor stimulating antibodies may have stimulated the ovarian thyroid tissue. Heavy proteinuria has not been described before and its association is as yet unclear.

Volume 5

22nd Joint Meeting of the British Endocrine Societies

British Endocrine Societies 

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