Case Presentation: A 45-year-old woman with type 2 diabetes mellitus (DM) and dyslipidemia presented with a 2-day history of nausea, vomiting, and epigastric pain. Two years earlier, she had an episode of pancreatitis secondary to hypertriglyceridemia (HTG; 1120 mg/dL), which was treated with gemfibrozil and atorvastatin. Her family history was significant for hyperlipidemia and type 2 DM. She denied alcohol use but admitted noncompliance with medication. Vital signs were as follows: blood pressure, 132/78 mmHg; heart rate, 90 beats/min; respiratory rate, 18 breaths/min; and body temperature, 97.9°F. Physical examination revealed moderate epigastric tenderness. Laboratory tests revealed triglyceride (TG), lipase, and glucose levels to be 3793 mg/dL, 11,911 units/L, and 361 mg/dL, respectively. Ultrasound of right upper abdominal quadrant showed no cholelithiasis or obstruction. Subsequently, a diagnosis of pancreatitis secondary to HTG was confirmed. Treatment included pain management with opioids and continuous insulin infusion at 0.05 units/kg/h, with intravenous 5% dextrose in normal saline titrated to a blood glucose level of 120–180 mg/dL for acute reduction of HTG. On day 2 of hospitalization, her TG level had dropped to 1226 mg/dL. On day 5, she was switched to subcutaneous insulin (TG, 668 mg/dL); and on day 6, she was discharged symptom free (TG, 586 mg/dL).

Discussion: Hypertriglyceridemia is the third most common cause of acute pancreatitis after alcohol and gallstone. The risk of developing acute pancreatitis is approximately 5 percent with TG > 1000mg/dL and 10-20 percent with TG > 2000mg/dL. The breakdown of TG into toxic free fatty acids is thought to be the cause of lipotoxicity during acute pancreatitis.  The treatment includes conventional treatment of acute pancreatitis, and management of serum triglyceride levels with an initial goal of <500mg/dL. While fibrates, nicotinic acid, and statins are often used to decrease the serum TG concentration, that insulin infusion acutely lowers TG levels is not common knowledge. Previous studies have demonstrated the efficacy of apheresis for acutely lowering TG levels; however, its cost and feasibility are prohibitive. Insulin decreases TG by enhancing lipoprotein lipase activity, thereby accelerating chylomicron and very low density lipoprotein metabolism to glycerol and fatty free acids. Moreover, it inhibits lipase in adipocytes, leading to an overall reduction in lipolysis. Initial rate of 0.1 to 0.3 units/kg/hour is recommended, and intravenous insulin may be more effective than subcutaneous insulin. The main adverse effect of insulin therapy is hypoglycemia, which can be avoided with 5% dextrose infusion.

Conclusions: We report a case of HTG-induced acute pancreatitis treated effectively with continuous insulin infusion, which is safe, simple, and cost-effective.  If frequent blood glucose monitoring is available, this treatment can be safely achieved even beyond the intensive care unit.