Acute Pancreatitis Secondary to Severe Hypertriglyceridemia: Where Do We Stand with Intensive Insulin Therapy? 1261

• Published in: The American journal of gastroenterology Vol. 113; no. Supplement; p. S725
• Main Authors: Munir, Ahmed, Iqbal, Sadat, Inayat, Faisal, Hussain, Qulsoom, Khan, Zarak H., Zafar, Fahad, Lodhi, Hanan T., Hurairah, Abu
• Format: Journal Article
• Language: English
• Published: New York Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins 01-10-2018
• Subjects: Gallstones; Gastroenterology; Insulin; Pancreatitis; Triglycerides
• ISSN: 0002-9270; 1572-0241
• DOI: 10.14309/00000434-201810001-01261

Hypertriglyceridemia is the third most common cause of acute pancreatitis (AP) after alcohol and gallstones. With an increased reporting of hypertriglyceridemia-induced pancreatitis, it is crucial to include hypertriglyceridemia in the differential when working up AP. 39 years old gentleman with past medical history of gout, pre-diabetes and hyperlipidemia presented with a 4 day history of abdominal pain and increased urination. He had some associated nausea but denied any vomiting. On presentation the patient was diaphoretic, febrile to 101.2° F and tachycardic to 114/min with epigastric tenderness. On routine labs, he was hyperglycemic and had an elevated lipase with a triglyceride level of 5047 mg/dl. An abdominal CT done soon after confirmed acute pancreatitis with no evidence of gallstones (Figure 1 and 2). He was admitted to the medical ICU to initiate an insulin drip to lower his triglycerides and blood glucose while the pancreatitis was treated supportively with IV hydration. After 12 days of intensive insulin therapy, the triglyceride level trended down to less than 500 mg/dl and he started Fenofibrate therapy after he resumed enteral feeds. Hypertriglyceridemia accounts for roughly 1-36% of cases of AP. It is hypothesized that excessive triglycerides (>1,000mg/dl) circulating as chylomicrons may obstruct capillaries in the pancreas causing local damage and exposing the triglycerides to pancreatic lipases. Their subsequent degradation to free fatty acids and free radicals causes further parenchymal damage and start a vicious cycle. Decrease in triglycerides can be expedited by Plasmapheresis or an alternative approach of enhancing the catabolic activity of Lipoprotein Lipase by IV heparin and/or insulin. Once the TG level falls below 500, oral lipid lowering therapy agents can be started and used for long term management. Initiation of IV heparin and/or insulin therapy may be used as an alternative in correctng hypertriglyceridemia especially for center that lack access to plasmapharesis. 1. Kohli RS, Bleibel W, Shetty A, Dhanjal U. Plasmapheresis in the treatment of hypertriglyceridemic pancreatitis with ARDS. Dig Dis Sci. 2006 Dec;51(12):2287-91. 2. Mikhail N, et al. Treatment of severe hypertriglyceridemia in nondiabetic patients with insulin. Am J Emerg Med. 2005 May;23(3):415-7. 3. Jain D, Zimmerschied J. Heparin and insulin for hypertriglyceridemia-induced pancreatitis: case report. ScientificWorldJournal. 2009 Nov 1;9:1230-2.