7661 Therapeutic Plasma Exchange as a Bridge Therapy to Total Thyroidectomy in Treatment-Resistant Amiodarone-Induced Thyrotoxicosis

Abstract

Abstract Disclosure: M. Maher: None. R. McEvoy: None. V. Farnan: None. D.J. Tansey: None. S. McKenna: None. J. O'Connell: None. R. McQuillan: None. M. Griffin: None. J. Lyne: None. C. Magee: None. C. Traynor: None. A. Hudson: None. M.W. O'Reilly: None. A. Agha: None. M. Sherlock: None. C.M. Moran: None. Background: Amiodarone-induced thyrotoxicosis (AIT) is challenging to manage where conventional medical treatment fails. We report our experience using therapeutic plasma exchange (TPE) to prepare for salvage thyroidectomy. Clinical Cases: A 53-year-old man was diagnosed with AIT type 2 (FT4 45.3pmol/L, RR 12-22; TSH 0.02mU/L, RR 0.27-4.20) whilst on amiodarone, on a background of lamin A/C cardiomyopathy. He remained thyrotoxic despite carbimazole, prednisolone, iodine solution and cholestyramine. TFTs following 4 TPE sessions showed an improvement in TSH (0.03mU/L) and total T4 (129nmol/L, RR 63-151), despite rising FT4 (91.5pmol/L) and FT3 (12.56pmol/L, RR 2.43-6.01).A 47-year-old man was diagnosed with TRAb-negative AIT type 1 (FT4 51.2pmol/L, TSH 0.03mU/L) on a background of atrial fibrillation treated with amiodarone. He became progressively more thyrotoxic despite carbimazole, prednisolone, lithium and cholestyramine. Following 4 TPE sessions, TFTs demonstrated a reduction in FT4 (42.9pmol/L) and FT3 (10pmol/L, RR 3.1-6.8), along with normalisation of total T4 (155nmol/L, RR 66-181).A 56-year-old female was diagnosed with AIT type 2 (FT4 33.9pmol/L, TSH 0.02mU/L), whilst on amiodarone for ventricular fibrillation. She became rapidly and progressively more thyrotoxic despite carbimazole, prednisolone, iodine solution and cholestyramine (FT4 >100pmol/L). After 5 TPE sessions, TFTs showed a persistently elevated FT4 (>100pmol/L), FT3 (13.1pmol/L), and total T4 (318nmol/L). Lastly, a 65-year-old gentleman was diagnosed with AIT type 2 (FT4 >100pmol/L, FT3 18.4pmol/L, Total T4 >320nmol/L, TSH <0.01mU/L) on a background of atrial fibrillation that had been treated with amiodarone. FT3 showed a modest reduction (8.2pmol/L) following treatment with carbimazole and prednisolone; however, FT4 remained >100pmol/L. The patient developed acute decompensated heart failure and underwent TPE as a bridge to emergency thyroidectomy. Following 3 TPE sessions, TFTs demonstrated a reduction in FT4 (67.3pmol/L) and Total T4 (223nmol/L). All 4 patients underwent uneventful thyroidectomy and were subsequently rendered euthyroid with thyroxine. Heparin was administered during TPE in all cases. Conclusion: TPE is beneficial as a bridge to thyroidectomy in treatment-resistant AIT. Our cases demonstrate that the biochemical response is variable. Given the possibility for heparin to cause displacement of bound thyroid hormones, Total T4 may be a better biochemical indicator of response than free thyroid hormone(s) for patients on TPE. Presentation: 6/2/2024