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Endocrine Abstracts (2023) 91 WC6 | DOI: 10.1530/endoabs.91.WC6

University Hospital Limerick, Limerick, Ireland


55-year-old man referred to the medical assessment unit by GP with weight loss and tachycardia. His past medical history was significant for myocarditis, long-QT syndrome, out of hospital cardiac arrest and an in-situ ICD. On examination the patient was tremulous, sweaty and tachycardic but otherwise well. An ECG demonstrated sinus tachycardia and routine blood tests were unremarkable. A clinical diagnosis of thyrotoxicosis was made and confirmed biochemically with TSH<0.01 (0.03–4.2)mU/l and FT4>100 (10.5–22.8) pmol/l. The patient had no family history of thyroid dysfunction, no recent iodinated contrast, no clinical signs suggestive of Grave’s disease and no goitre, lymphadenopathy or tenderness on neck examination. His medical history was significant for exposure to Amiodarone therapy, although this had been stopped approximately 12 months before his current presentation. The patient was assessed for thyroid autoimmunity, TPO antibodies <15 (0-34)kU/land TRAb was sent to an external lab with a reporting time of approximately 2 weeks. The patient was commenced on beta blockade for symptom control and Carbimazole. A presumed diagnosis was made of Amiodarone Induced Thyrotoxicosis (AIT), likely type-2 relating to remote amiodarone exposure. Radiological investigations were expedited to aid in the diagnosis. An ultrasound of then thyroid revealed ‘Heterogenous appearance to both thyroid lobes with multiple microcystic change present suggestive of thyroiditis no significant increase in vascularity. No large discrete nodule identified’. This was followed by a pertechnate scan of the thyroid showing ‘Absent thyroid uptake. In the setting of thyrotoxicosis and the given the appearance of diffuse thyroiditis on recent ultrasound. If the patient is on amiodarone, this appearance may relate to amiodarone induced thyrotoxicosis, most commonly type-2 in the setting of absent uptake’. The radiological findings were most in keeping with AIT type-2, specifically an absence of a nodular thyroid, reduced vascularity and absent uptake on nuclear medicine scan, as such the patient was commenced on prednisolone 40 mg daily. The patient’s clinical course is outlined in table 1. TRAb was negative. The patient responded very well to therapy and remains under follow-up in the endocrine clinic.

Table 1: Clinic follow-up
Diagnosis4 weeks8 weeks16 weeks
TSH mU/l<0.01<0.01<0.0115.9
FT4 pmol/l>100.089.920.012.9
FT3 pmol/l18.317.34.65.1
TherapyStart Prednisolone 40 mg Carbimazole 40 mgContinue Prednisolone 40 mg Carbiamzole 40 mgDose reduce to Prednisolone 10 mg Carbimazole 10 mgSlow taper Prednisolone Stop Carbimzole

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