Acetaminophen induced pancreatitis is uncommon and the mechanism of injury is not well understood. To date, only six cases have been reported. A 46 year old Hispanic woman presented with 4 weeks of worsening abdominal pain. The pain was located in the bilateral flanks, described as constant, and associated with chills. For this pain she took 1300 mg of acetaminophen every 4 hours in addition to acetaminophen PM with minimal relief. Eventually the pain migraited to the right upper quadrant. She had a medical history of obesity s/p gastric bypass, biliary colic s/p cholecystectomy, seizures, and hypertension. Initial evaluation revealed normal vital signs; however, several laboratory abnormalities were found: AST/ALT = 3472/1223, lipase of 4664, and serum Acetaminophen level of 69.8. CT of abdomen and pelvis demonstrated pyelonephritis, hepatomegaly, and acute pancreatitis. She was admitted to ICU and treated with NAC therapy for acetaminophen hepatotoxicity, intravenous hydration, and antibiotics for pyelonephritis. Evaluation of common causes of pancreatitis (e.g. ethanol, choledocolithiasis, hypertriglyceridemia) was negative. Medication list was reviewed and no common offending agents were appreciated. Tesitng for infectious etiologies such mumps and salmonella were negative. Her serum calcium was within normal limits. Given her negative workup, it was determined that although rare, the most likely cause seemed to be acetaminophen toxicity. The patient's pancreatitis improved with cessation of acetaminophen and concurrent treatment of drug toxicity, as evidenced by resolution of abdominal pain and down trending lipase levels (4664 on admission, down to 440 two days later). A repeat CT 2 weeks later confirmed nearly resolved pancreatitis. Our proposed mechanism of action is hepatic inflammation/damage leads to inflammation (e.g. seeding) of surrounding organs. Data from a 2015 large cohort study demonstrated patients with acute acetaminophen hepatic toxicity exhibit a 2.4 fold higher risk of acute pancreatitis within the first year of follow up (1). Our case shows treatment of acetaminophen toxicity may mollify associated pancreatitis. Further research is needed concerning the mechanisms of acetaminophen toxicity given the drug's widespread availability and complications.1411_A.tif Figure 1: CT Scan of the Abdomen and Pelvis at time of Admission. In this figure above we can see acute peripancreatic inflammation. The arrow points towards an area of possible necrosis, underscoring the severity of this pancreatitis1411_B.tif Figure 2: AST/ALT/Lipase (IU/L) over a period of time. The figure above shows that treatment of the patient's liver failure coincided concurrent down trending of her lipase levels, and clinical resolution of her pancreatitis