Endocrine Abstracts

Introduction: Amiodarone, a drug with high iodine content, is commonly associated with thyroid dysfunction. There are two well-recognized forms of amiodarone induced thyrotoxicosis. Thyrotoxicosis due to iodine excess leading to increased thyroid hormone synthesis is referred to as Amiodarone induced thyrotoxicosis type 1 (AIT type 1) whilst thyrotoxicosis due to direct toxic effect (thyroiditis) is known is amiodarone induced thyrotoxicosis Type 2 (AIT type 2). The aim in both is to achieve euthyroidism, achieved by thionamides in AIT type 1 and glucocorticoid in AIT Type 2. Mixed or uncertain cases are treated with combination trial of both. The table from European thyroid association guideline highlights comparison.

Case: A 70-year-old male, with background of hypertension and atrial fibrillation, presents with 6-week history of palpitation,1.5 stone weight loss and syncope. He has been on amiodarone since 14 years, with previous failed cardioversions. Thyroid function tests on presentation showed thyrotoxicosis TSH:< 0.01 munit/l,T4:64.35 pmol/l,T3:17.2 pmol/l. All historic TFT were normal. TRAB was < 0.4 IU/l, TPO < 35IU/ml. He also had exertional dyspnoea and was in decompensated heart failure with bilateral limb edema. He was noted to have goitre but no thyroid eye disease. He was initiated on carbimazole 40 mg od. He proceeded to have a doppler ultrasound scan which showed increased vascularity indicating AIT 1. He was reviewed by cardiology team who stopped amiodarone and echocardiogram showed EF >55%. His TFT slowly improved within 2 weeks of initiation of carbimazole, TSH <0.01 munit/l, T4 50.2 pmol/l, T3: 9.4pmnol/l. His case was discussed in MDT and the plan is to offer definitive treatment once euthyroidism achieved.

Discussion: The above case is unique as the presentation is 14 years post initiation of amiodarone with no underlying autoimmune thyroid dysfunction. Normally the effect of amiodarone on thyroid is seen as early as few weeks post-initiation and up to several months post-discontinuation due to long half-life. There was also reluctance in initiating combined therapy with prednisolone due to concern of worsening heart failure with fluid retention. Doppler ultrasound proved the most useful diagnostic aid.