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Abstract Disclosure: A.T. Wahba: None. A.A. Shibli-Rahhal: None. A 40-year-old man presented with 2 weeks of palpitations, weight loss, decreased appetite and malaise. The symptoms were preceded by neck pain for 1-2 weeks that improved spontaneously. He was in atrial fibrillation at 126 bpm, but otherwise clinically stable. He had a mildly tender enlarged thyroid with no palpable nodules, and the rest of his exam was negative. A chest CT with IV contrast ruled out pulmonary embolism. His TSH was 0.01 µIU/mL (N:0.27-4.20), free T4 7.77 ng/dL (N: 0.80-1.80) and free T3 of 29.7 (N: 2.6-4.4 pg/ml), obtained prior to contrast administration. TSI antibody was negative and thyroid ultrasound showed diffuse enlargement with heterogeneous echotexture and reduced vascularity on doppler images. Thyroid uptake and scan could not be obtained due to iodinated contrast exposure. The patient’s medical history was notable for nonischemic cardiomyopathy (EF 50%), cardiac arrest with implantable cardiac defibrillator, and paroxysmal atrial fibrillation. He was previously treated with amiodarone for 2 years, and it was stopped 2 months before presentation. Other relevant medical problems included subclinical hypothyroidism diagnosed within the previous year and an uncomplicated acute COVID-19 infection 1 month prior to presentation.Given his cardiac history and high Burch-Wartofsky score, he received PTU 200 mg Q4h, hydrocortisone 100mg Q8h and propranolol for 3 days. As his FT3 level declined to 9.8 pg/ml, he was transitioned to methimazole 40 mg daily, propranolol and prednisone 40 mg daily and discharged with outpatient follow up. The atrial fibrillation worsened again 1 week later, and his FT3 increased to 20.2 with a FT4 7.77. He was put back on PTU 200 mg TID, prednisone and propranolol were continued and cholestyramine 2g BID was added. 1 week later, his FT4 and FT3 were unchanged. The tests were performed using a different assay and the results were consistent. Two sessions of plasma exchange (PLEX) did not yield a significant response, so thyroidectomy was eventually performed. Pathology showed morphologic findings consistent with type 2 amiodarone-induced thyrotoxicosis. While pathology showed amiodarone-induced changes, the patient’s hyperthyroidism occurred after a COVID-19 infection and was associated with neck pain, pointing to severe viral thyroiditis. De novo thyroid hormone production has been reported following COVID-19 infection, but the minimal improvement in thyroid hormone levels with thionamide therapy suggests that de novo secretion had little contribution to this patient’s hyperthyroidism. Presentation: 6/3/2024
Wahba et al. (Tue,) studied this question.