Plasmapheresis in Treatment of Severe Hypertriglyceridemia Induced Acute Pancreatitis

Abstract

Hypertriglyceridemia induced pancreatitis (HTGP) is the third most common causes of acute pancreatitis (AP) after alcohol and gallstones. The commonly used treatment for HTGP is either intravenous (IV) insulin or heparin along with fenofibrates. A 34 year old obese Hispanic female with past medical history of hyperlipidemia (HPL) presented to the emergency room with a chief complaint of 3 days history of progressively worsening severe epigastric pain radiating to her lower back, associated with nausea and vomiting. She had no prior similar episodes. Her personal, family, medication and social history was unremarkable except occasional alcohol drinking of the standard one to two drinks every month, but prior to this ER visit she reported drinking more than 3 standard drinks per day for the past 2 days. Relevant laboratory tests revealed mild hyponatremia of 130 mEq/L, lipase of 1039 U/L, with a normal calcium, blood glucose (BG) and liver function tests, but the serum was abnormally milky white in appearance. The lipid panel revealed triglycerides (TG) > 3000 mg/dl. An abdominal ultrasound showed non-obstructive cholelithiasis with a common bile duct size of 7 mm. She was managed conservatively with AP treatment guidelines, but due to severe hypertriglyceridemia (SHTG) and symptoms she underwent one session of plasmapheresis with albumin replacement. The TG subsequently trended down to 349 mg/dl and she was advanced on a low fat diet and Fenofibrate. Follow-up TG after 1 month was 80 mg/dl. HTGP is clinically evident when levels are > 1000mg/dl and is classified as SHTG and very severe HTG for levels > 2000 mg/dl. The goal of the treatment is lowering the TG levels to < 250 mg/dl and identifying the underlying cause. Patients with HTGP have higher chances of recurrent AP than pancreatitis from other causes. There is evidence of improvement in symptoms as well as lowering TG levels with IV insulin in patients with HTGP and marked hyperglycemia, but in patients with normal BG levels treatment of HTGP is not very well defined. Our patient was treated with plasmapheresis leading to a significant improvement in her TG levels, clinical and laboratory parameters in a relatively short time leading to a shorter hospital stay. Currently there are no guidelines for the use of plasmapheresis in treatment of HTGP. Plasmapheresis seems to be an effective method for the treatment of HTGP and an important area of future research, especially in patients with severe AP and normal BG levels.