Black, Meghan

Abstract Amiodarone is known to cause thyroid dysfunction, due to both direct cytotoxicity and high iodine content. Due to its lipophilic properties, amiodarone gets stored in the adipose tissue and may induce delayed amiodarone-induced thyrotoxicosis (AIT), months after discontinuation. We present the case of a 60-year-old man admitted with new-onset atrial fibrillation. He had a history of ventricular tachycardia, treated with amiodarone that was discontinued 14 months earlier. On admission, thyrotropin was undetectable, with markedly elevated free thyroxine and total triiodothyronine. He had no previous history of thyroid dysfunction or recent exposure to iodinated contrast. Additional history revealed that the patient had been taking tirzepatide 10 mg weekly resulting in a 54-kg weight loss over the previous 12 months. With this information, a spot urine iodine/creatinine (Cr) was measured and found to be significantly increased at 2323 µg/g Cr (SI: 2075 µmol/mol Cr) (normal reference range <584 µg/g Cr, [SI: <521 µmol/mol Cr]). He was treated with prednisone and methimazole with eventual resolution of hyperthyroidism. Delayed AIT should be considered in the differential diagnosis of new-onset thyrotoxicosis in patients previously treated with amiodarone who experience significant weight loss.

Abstract This is a case of a 26-year-old male patient, with relapsing Hodgkin lymphoma, treated with nivolumab and brentuximab-vedotin, who was admitted with hyperglycemia and severe insulin resistance requiring approximately 2000 units of intravenous insulin per day. He had no prior diagnosis of diabetes. He was eventually diagnosed with massive cytokine release and hemophagocytic lymphohistiocytosis that led to multi-organ failure and death. The mechanisms behind the hyperglycemia with severe insulin resistance remain unclear but are possibly related to hyperinflammation and immune dysregulation resulting from massive cytokine release. Nivolumab among other immunotherapeutic agents, brentuximab-vedotin, and lymphoid malignancies are rare but known risk factors for massive cytokine release and hemophagocytic lymphohistiocytosis.