Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2021) 74 NCC58 | DOI: 10.1530/endoabs.74.NCC58

SFENCC2021 Abstracts Highlighted Cases (71 abstracts)

Challenging management of type II amiodarone induced thyrotoxicosis AIT

Rabia Arfan & Christine May


Churchill Hospital, Oxford, United Kingdom


Case history: 20 year old man with a complex cardiac history of Shone’s syndrome, out of hospital cardiac arrest 2015 (CRT-D implant) and multiple previous episodes of fast atrial fibrillation was admitted to hospital (28/11/2019) with 3 weeks history of intermittent palpitations and shortness of breath. His regular medications included amiodarone and bisoprolol. Examination revealed a fine tremor of outstretched hands, no obvious goitre or thyroid eye disease. Thyroid function testing (TFT) on admission revealed hyperthyroidism; TSH <0.01 munit/l (0.3–4.20), FT4 61.1 pmol/l (9–19), FT3 17.9 pmol/l (3–5.4), TFTs from 2018 were normal. Impression was of amiodarone induced thyrotoxicosis (AIT). He was commenced on carbimazole 40 mg and prednisolone 30 mg OD.

Investigations: Findings on thyroid ultrasound were suggestive of type II AIT, TSH receptor antibody were negative. The TFTs gradually started improving by 12/12/19 with FT4 47.8 pmol/l and FT3 9.0 pmol/.

Treatment: The patient was discharged with weekly TFT monitoring. Due to pre-syncpoal episode and worsening biochemistry (28/12/19 (FT4 >64.35 pmol/l, FT3 19.1 pmol/l)) he was readmitted. Prednisolone and Carbimazole were increased to 50 mg and 60 mg respectively. Diuretics were adjusted to clinical fluid status. He developed deranged liver function, felt to be due to the combination of hepatic congestion and potentially a complication for the high dose carbimazole. His thyroid uptake scan confirmed the ultrasound finding of type II AIT, the carbimazole was stopped. Due to his overall thyrotoxic state and exacerbating heart failure on steroids, a thyroidectomy was considered, but anaesthetic review deemed him a poor surgical candidate with 70% mortality risk. Other medical therapies were trialled including Colestyramine and lithium; both had to be stopped due to intolerance Lithium due to toxicity. The prednisolone was gradually reduced with improvement in patient’s fluid status and FT3 values (FT3 11.9 pmol/l). He was discharged with outpatient monitoring of thyroid function, which continued to improve. Once TFTs were normal the prednisolone was weaned and stopped. His TFTs remain normal off prednisolone.

Conclusion: This is an example of management of complex case requiring discussions both within the departmental team and with national experts seeking opinions early. This patients’ significant cardiac history meant thyroidectomy was deemed too risky but should be considered as a treatment option in AIT. The differentiation between AIT type I and II can be difficult, starting treatment for both maybe required in clinically unwell patients. Medical treatments are options but can take time to be effective and have side effects.

Volume 74

Society for Endocrinology National Clinical Cases 2021

Society for Endocrinology 

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