Abstract

Introduction: Hypertriglyceridemia (HTG) is a common etiology of acute pancreatitis (AP) after gallstones and alcohol and accounts for 1-4% of all cases. Both primary and secondary causes of lipoprotein metabolism may be associated with HTG-induced pancreatitis. It is important to recognize this disease entity for timely management and to prevent life threatening complications. Methods: We retrospectively reviewed all electronic patient records with a discharge diagnosis of “acute pancreatitis” and “hypertriglyceridemia” based on ICD codes between November 2010 and April 2013. All patients with triglyceride levels >1000 mg/dL were included. Patients with etiologies other than HTG were excluded from the study. Results: A total of 22 encounters involving 20 patients were identified with a mean age of 40.3 years. Fifteen out of 20 patients had a past diagnosis of DM, and 4 were newly diagnosed. Mean HbA1c was 12, indicating poor control. Initial Ranson score ranged from 0 to 3 (Median 1.54). All patients were treated with intravenous fluid replacement, nasogastric suction, morphine for pain control, and were administered weight-based insulin. Sixteen out of 22 admissions required medical intensive care unit (MICU) care, out of which 3 were mechanically intubated for ARDS. The mean length of hospital stay was 18.8 days. Seven out of 22 encounters needed therapeutic plasmapharesis (PE). Overall, patients in PE group suffered more complications, had longer hospital stay, and required more surgical intervention. All patients were commenced on oral therapy for hypertriglyceridemia either with fenofibrate or gemfibrozil prior to discharge. Conclusion: Hypertriglyceredemia is an important cause of acute pancreatitis, and triglyceride levels should be routinely tested. Diabetic ketoacidosis was the most common presentation. Serum levels of triglycerides do not correspond with the severity of pancreatitis. Insulin therapy with or without dextrose is the mainstay of therapy. Plasmapharesis can be used as an adjunctive therapy in clinically severe pancreatitis or in patients who did not show significant drop in triglyceride levels after 24 hours of insulin therapy.Table 1: Plasmapharesis vs Nonplasmapharesis

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