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Endocrine Abstracts (2019) 63 P406 | DOI: 10.1530/endoabs.63.P406

ECE2019 Poster Presentations Thyroid 1 (70 abstracts)

Exacerbation of thyrotoxicosis following radioiodine therapy in benign thyroid diseases: can it be predicted?

Ahmed Hanafy 1 , Simon Holmes 2 , Jason Britton 2 & Olivia Pereira 2


1Leeds Teaching Hospitals NHS Trust, Leeds, UK; 2The Mid Yorkshire Hospitals NHS Trust, Wakefield, UK.


Introduction: Radioactive iodine (RAI) is an effective and widely used treatment for thyrotoxicosis. Post-radioiodine thyrotoxicosis is a well-known side effect of RAI. This is usually mild and easily controlled mostly with beta blockers but sometimes needs anti-thyroid drugs (ATD).

Aim of the study: To assess the incidence and predictors of post-radioiodine thyrotoxicosis.

Methods: Retrospective analysis of 86 patients who had RAI treatment in 2017 for hyperthyroidism in Mid-Yorkshire Hospitals, UK. Thyroid function tests were checked at diagnosis, immediately before RAI treatment and 4-6 weeks following RAI treatment. Post-radioiodine thyrotoxicosis was defined by undetectable TSH and high free T4 level 4–6 weeks after RAI. Multiple logistic regression analysis was conducted to assess for the presence of any predictor of post-radioiodine thyrotoxicosis.

Results: Mean age was 52.53 years and 73% were female. Thyrotoxicosis was caused by Graves’ disease in 65.1% of the patients. 93.1% were pre-treated with antithyroid drugs prior to RAI. Mean TSH, free T4 and free T3 prior to RAI treatment was 1.36 mu/L, 17.29 pmol/L and 5.96 pmol/L, respectively. RAI dose of 385 MBq was given in 72.1% while 539 MBq was given in 27.9%. Post-radioiodine thyrotoxicosis occurred in 20 (23.3%) patients. Mean free T4 and free T3 was 44.73 pmol/L and 15.09 pmol/L, respectively. Two (2.3%) patients showed classic radiation thyroiditis (thyrotoxicosis with neck pain and tenderness). In 8 (9.3%) patients, this was associated with thyrotoxic symptoms (none of them developed thyroid storm). In 7 (8.14%) patients, free T4 was 2 times above the upper limit of normal (free T4 >50 pmol/L) and Carbimazole (median dose 35 mg) was restarted to control thyrotoxicosis. Six months following RAI, 13 (65%) patients become hypothyroid. On the other hand, 6 (30%) patients remained thyrotoxic. Multiple logistic regression analysis showed that none of the independent variables (age, sex, cause of thyrotoxicosis, free T4 at diagnosis, TSH receptor antibody titre, goitre size, highest dose of Carbimazole, duration between diagnosis and RAI treatment, RAI dose and immediate restart of ATD following RAI) was significantly associated with post-radioiodine thyrotoxicosis (P value >0.05 for all independent variables). However, TSH receptor antibody was measured in only 44% of patients.

Conclusion: Exacerbation of thyrotoxicosis following radioiodine treatment is common and usually easy to control. However, it cannot be predicted. Patients need to be prepared for the likelihood of requiring antithyroid medications post radioiodine.

Volume 63

21st European Congress of Endocrinology

Lyon, France
18 May 2019 - 21 May 2019

European Society of Endocrinology 

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