ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 P1228 | DOI: 10.1530/endoabs.63.P1228

Radioactive Iodine (RAI) Treatment for Benign Thyroid Disease: A UK District General Hospital Perspective

Joseph Gerard Timmons1, Babu Mukhopadhyay2 & Graham McCurrach3


1University Hospital Hairmyres, East Kilbride, Glasgow, UK; 2University Hospital Hairmyres, East Kilbride, Glasgow, UK; 3University Hospital Monklands, Airdrie, UK.


Aim: To determine patient outcomes following radioactive iodine (I131) therapy in a UK district general hospital for the treatment of benign thyroid disease.

Methods: A record of all patients at University Hospital Hairmyres (Scotland, UK) undergoing radioactive iodine therapy for benign thyroid disease was kept. Patients were identified using a unique community health index (CHI) number. A retrospective case note review was then carried out for these patients. Patients treated between 2012 and 2016 were included. This ensured a minimum 2 year post radioactive iodine follow-up for all patients included in the review (maximum 6 years follow-up). Retrospective review was undertaken as per Royal College of Physicians (UK) guidelines. Age, gender, indication for RAI therapy, prescribed dosage of RAI, outcome of treatment, post RAI hypothyroidism and the incidence of worsened thyroid eye disease were recorded. GP prescribing records and bloods were examined to identify any further cases of hypothyroidism not immediately identified on case note review.

Results: A total of 37 patients were identified. 32/37 were female. 5/37 were male. Age at time of treatment ranged from 26 to 79 years with a mean age of 55.4 years. 24/37 were given RAI due to Grave’s Disease refractory to medical management. 13/37 were treated with RAI for toxic multinodular goitre (TMG). Prescribed radioactive iodine dose ranged from 200 to 600 MBq. Dosage was 400 MBq in 32/37 patients, while 4/37 patients were prescribed 600 MBq. One patient was prescribed 200 MBq of RAI. 35/37 patients were successfully treated following first RAI treatment. 2/37 patients – both with a diagnosis of Grave’s Disease - required further treatment for hyperthyroidism following RAI therapy. 26/37 were rendered hypothyroid following RAI. 11/37 were euthyroid at follow-up (minimum 2 years). 4/37 patients had a recorded flair of thyroid eye disease.

Conclusion: RAI is a safe and effective treatment for refractory hyperthyroidism not managed with medical therapy. The majority of patients in our cohort 35/37 were successfully treated with one dose of RAI. 400 MBq was an effective dose for the majority of patients. Hypothyroidism is a common outcome following RAI therapy and patients should be counselled to this effect.

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