SAT-610 The Double Impact : A Rare Case of Amioradone-Induced Thyrotoxicosis and Amidaorone-Induced Isolated Hyperbilirubinemia

Background: Amiodarone-induced thyrotoxicosis (AIT) with concomitant amiodarone-induced isolated hyperbilirubinemia is rare, making it a diagnostic and therapeutic challenge. We report a case illustrating the complexities involved in managing such a patient. Clinical Case: A 24 year old male with underlying cyanotic congenital heart disease and supraventricular arrhythmias on oral amiodarone (200mg/d) presented with a one month history of progressive jaundice, lethargy and palpitations. Initial tests were consistent with thyrotoxicosis: FT4 > 100 pmol/L (9-19.05 pmol/L), TSH < 0.01 uIU/mL (0.35-4.94 uIU/mL) with isolated conjugated hyperbilirubinemia 250umol/L (3.4-20.5 umol/L). Thyroid autoimmunity was negative. Thyroid ultrasound showed a normal thyroid with generalized hypovascularization, scintigraphy revealed mild tracer uptake indicating Type 2 amiodarone-induced thyrotoxicosis (AIT)/mixed AIT. Amiodarone was discontinued and he was started on high doses of thionamides, glucocorticoids and beta-blockers. Unfortunately his hyperthyroidism worsened (FT4 191 pmol/L, TSH < 0.01 uIU/mL) and his TB increased to 832 umol/L. Carbimazole was discontinued and a rapid blockade was attempted with Lugol's solution, lithium and cholestyramine. Liver biopsy was consistent with amiodarone hepatic toxicity (Mallory denk bodies, canalicular cholestasis, cellular fibrosis). Because of refractoriness to medical treatment and high surgical risk, 6 cycles of plasmapharesis was given with methimazole. Despite improvement of his thyroid function (FT4 29.26 pmo/L,TSH 0.02 uIU/mL), his TB worsened (718 umol/L). Methimazole was stopped temporarily and N-acetylcysteine infusion was given however with little effect. He subsequently developed severe nosocomial sepsis with multiorgan involvement. Continuous veno-venous hemofiltration combined with resin adsorption was started for removal of inflammatory cytokines(1), however despite aggressive medical therapy, our patient finally succumbed to overwhelming sepsis on D49 of admission. Conclusion: Our case demonstrates the potential severity of amiodarone toxicity and the complexities of management especially in a double pathology such as our patient. Isolated hyperbilirubinemia is a rare feature of amiodarone toxicity. To our knowledge this is the first ever report of such a case. The anticipation of such events is complicated by the lack of a consistent relationship between toxicity and dose, duration of therapy, cumulative dose, or serum and tissue concentrations. Plasmapheresis and dialysis with resin adsorption may provide a transient therapeutic alternative before definitive surgery. References: 1. Blood hemoperfusion with resin adsorption combined continuous veno-venous hemofi ltration for patients with multiple organ dysfunction syndrome. Lu-yi Liu et al. World J Emerg Med 2012;3(1):44-48