ODP136 A Rare Case of Necrotizing Myopathy after Statin Use

INTRODUCTION: Statin associated necrotizing autoimmune myopathy is an extremely rare side effects of stain use. The incidence is approximately 2-3/100,000 Patients treated with statins. It usually associated with significant proximal muscle weakness, strikingly elevated creatine kinase (CK) levels and persistent symptoms despitestatin discontinuation. Here, we present a case with necrotizing myopathy after statin use as a reminder to clinicians for appropriately suspicious of this phenomenon while on treatment of statins. Clinical case: A 35 year old male with a past medical history of Autism, Type 2 Diabetes Mellitus, Hyperlipidemia, and Hypertension was brought to emergency room for right leg pain. Family states he had difficulty walking for a few weeks and had a fall from couch a week ago. Initial Vitals showed HR at 134 bpm, temp 35.9, BP 157/85 mmHg, RR 19 breaths/min. Labs showed Creatinine. 3.29 mg/dL, CO2 24 mmol/L, Na 141 mmol/L, K 4.2 mmol/L, Ca 9.5 mg/dL, glucose 265 mg/dL, AST/ALT 914/919 units/L, CK>14,000 units/L, WBC 9.2 thou/mcL, Hb 12.6 g/dL, TSH 9.42 mcIU/mL, Free T3 1.41 pg/mL, Free T4 0.95 mcg/dL. Urinalysis showed large blood with RBC of 1. Myoglobin>8750 mcg/L. Neuro motor exam showed strength 4/5 in bilateral lower extremities. His home medications including atorvastatin 20 mg nightly for 2 years, metformin and olmesartan, which all had been held. He was treated for rhabdomyolysis with aggressive hydration and Creatinine was improving. However, CK continued trending up to 42,915 units/L on day 5 with unreleased symptoms of lower extremity weakness. Neurology was consulted. Differential diagnosis of myopathy were suspected. His CK was continue to trend up to 45,585 units/L on day 10. Decision was made to have muscle biopsy with pathology showed: necrotizing myopathy without any clear evidence of inflammation. Although some autoimmune necrotizing myopathy may not show inflammation like those seen with HMG-CR antibodies or signal recognition antigen antibodies. Autoantibodies against 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (HMGCR Ab) was above 550. Following the biopsy, he received IV Solu-medrol 1g daily×4 doses, and then PO Prednisone 80 mg daily and then tapered down to 40 mg daily. He was also promptly started on IVIG 400 mg/kg/day for 5 days and methotrexate 7.5 mg weekly. His CK started to improve, down to 5815 units/L three weeks later. No significant improvement of strength. CONCLUSION: Our case demonstrates that the appropriate diagnosis of statin induced necrotizing autoimmune myopathy with muscle biopsy and HMGCR Ab. We also wanted to alert future clinicians to have an early suspicious of such rare side effect and initiate treatment as early as possible which may bring the maximum benefit for patients. Presentation: No date and time listed