Abstract #1407180: Drug Induced Acute Pancreatitis Secondary to Ezetimibe

Abstract

Drug induced acute pancreatitis (DIAP) is a rare clinical entity with incidence of <2% in general population. Most cases are typically mild and have excellent prognosis but prompt diagnosis and cessation of offending drug is important to avoid adverse outcomes. A 58-year-old female former smoker with history of COPD and hyperlipidemia presented to the hospital with sudden onset abdominal pain radiating to the back associated with nausea and vomiting for 12 hours. On arrival vitals were normal and physical examination showed epigastric tenderness with negative murphy’s sign. Labs showed normal CBC and CMP with elevated serum lipase (2469 U/L – Normal 16 - 61 U/L) concerning for acute pancreatitis. CT abdomen and pelvis showed normal biliary tract. US of the abdomen showed no evidence of gall stone or biliary sludge. Serum lipid panel showed total cholesterol of 193, HDL of 66, LDL of 111 and triglyceride of 87. Serum Calcium was normal. Detailed history revealed no alcohol but that patient recently started ezetimibe 10 mgs daily 8 weeks prior to present due to history of statin intolerance. Her only other medication was inhaled Albuterol taken as needed. Immune panel include IgG-4 was negative. Patient was diagnosed with drug induced acute pancreatitis secondary to ezetimibe, and was managed conservatively cessation of ezetimibe, pain meds and bowel rest. Her overall condition improved in 48 hours and diet was progressed. She was discharged with outpatient follow up. Serum lipase dropped to 74 U/L prior to discharge. Drug induced pancreatitis account for ∼ 5% of all cases of pancreatitis. There is limited data on the exact mechanism by which drugs can induce pancreatitis as most evidence is bases on case reports or meta-analysis. On the basis of these case reports drugs are classified from class I-IV depending on the probability to cause pancreatitis. Some proposed mechanisms include immunologic reactions, direct toxic effect, accumulation of a toxic metabolite, ischemia, intravascular thrombosis, and an increased viscosity of pancreatic juice. Though most cases are mild the identification of the offending drug is crucial to prevent ongoing damage and recurrence. However, in most instances the diagnosis of drug induced pancreatitis and identification of offending drug can be challenging due to the presence of multiple agents. Current proposed criteria for identification include: 1) Pancreatitis develops during treatment with the drug, 2) Other likely causes of pancreatitis are not present 3) Pancreatitis resolves upon discontinuation of the drug and 4) Pancreatitis usually recurs upon re-administration of the drug. Our patient fulfilled 3 of the above criteria which suggest Ezetimibe induced Pancreatitis. Prior to this case there is one more case reported cases of Ezetimibe induced Pancreatitis but in both the cases there is no re-challenge of Ezetimibe which makes it a Class IV drug to cause pancreatitis.