Endocrine Abstracts

A 64-year-old man presented with mild biochemical hyperthyroidism – TSH <0.01 mU/l (NR 0.35–4.90), FT4 19.4 pmol/l (NR 9–19) in 2005. He was treated by his general practitioner with a 9 months course of carbimazole. Six months later, TSH became suppressed (0.05 mU/l) but with a normal fT4 (17 pmol/l). He was referred to a ‘One-Stop’ Thyroid Clinic and was seen there 3 months later. Thyroid isotope scan showed a toxic multinodular goitre. He was treated with radioiodine (RAI) at this initial visit but without repeating his thyroid function tests (TFTs).

He was seen in the Thyroid Clinic 6 weeks post-RAI and was thought to be hypothyroid with a 4 weeks history of tiredness, constipation, dyspnoea and husky voice. TFTs, however, revealed a TSH of <0.02 mU/l and fT4 of 32.4 pmol/l. He was advised to recheck TFTs 6 weeks later.

He was referred to our unit 3 months post-RAI for a second opinion. He was clinically and biochemically thyrotoxic (TSH <0.02 mU/l (NR 0.34–5.6), fT4 >72 pmol/l (NR 7.5–21.1)) and was commenced on carbimazole 60 mg daily. Within 6 weeks, however, he became profoundly hypothyroid (TSH 1.57 mU/l, fT4 2.49 pmol/l). As it was difficult to determine whether the hypothyroidism was secondary to carbimazole treatment or the previous RAI, his carbimazole was stopped. Four weeks later his thyrotoxicosis relapsed again (TSH <0.02 mU/l, fT4 53.6 pmol/l) and carbimazole 40 mg daily was recommenced.

‘One-Stop’ clinics are encouraged on the NHS but may lead to increased clinical risk. This patient’s TFTs immediately prior to the RAI therapy was 3 months out-of-date by the time he was seen in the Thyroid Clinic. It is postulated that he was biochemically hyperthyroid at the time of his RAI treatment and this then precipitated a radiation thyroiditis. Political expediency should not be a substitute for clinical safety.