LAUSR

We report two novel cases of hypertriglyceridaemiainduced pancreatitis induced by corticosteroid taper. Both patients had known dyslipidaemias and were later referred to the University of Michigan Lipid Management Clinic unaware of the risks of corticosteroids in their condition. These cases highlight the need to be cognisant that even short-term corticosteroids can precipitate hypertriglyceridaemia-induced pancreatitis in susceptible individuals. Characteristics of the two patients are summarised in Table 1. Patient 1 is a 41-year-old woman with underlying type-IV hyperlipidaemia who presented to the emergency department for urticaria after poison oak exposure and was discharged on a 10-day course of prednisone (60 mg × 1 d, 40 mg × 5 d and 20 mg × 1 d). Four days after beginning her corticosteroid taper, shewas hospitalised for acute-onset abdominal pain. Triglycerides (49.0 mmol/L) and lipase (7.45 μkat/L) were elevated, and computed tomography of the abdomen/pelvis confirmed acute pancreatitis. She denied recent illness or changes in diet, alcohol, medications or blood glucose. Triglycerides immediately prior to treatment were unknown; her most recent triglycerides were 2.88 mmol/L on gemfibrozil 600 mg twice daily, measured 13 days prior to her admission to the hospital. Neither the patient nor her inpatient team realised the trigger of her pancreatitis until a retrospective chart review in lipid clinic follow-up severalmonths later. Patient 2 is a 54-year-old woman with a history of type-V hyperlipidaemia and two previous episodes of hypertriglyceridaemia-induced pancreatitis, beginning at age 47. She developed a chronic obstructive pulmonary disease exacerbation and was prescribed a 7-day course of prednisone 50 mg daily. While completing her corticosteroid burst treatment (exact date of prednisone prescription unknown), she developed acute-onset abdominal pain and presented to the emergency department, where she had elevated levels of amylase (15.2 μkat/L), lipase (46.1 μkat/L) and triglycerides (72.4 mmol/L). Triglyceride levels from 2 months prior to her admission to the hospital were 7.96 mmol/L on fenofibrate nanocrystals 145 mg once daily. She endorsed recent decreased oral intake, but otherwise denied any changes in alcohol, medications or blood glucose. No linkage between corticosteroids and hypertriglyceridaemia-induced pancreatitis was considered by her inpatient team. Differential diagnosis for chylomicron syndrome precipitation in patients with underlying dyslipidaemias include poor diet and/or fat intake, alcohol use, noncompliance with medications, pregnancy and/or worsening diabetes control, systemic oestrogen use, and