Butter Blood

Abstract

Acute pancreatitis induced by hypertriglyceridemia is a rare but well-established complication, though the exact pathogenesis remains unclear. Estimated rates account for 1-4% of acute pancreatitis cases with noticeable rising risk as serum levels increase (triglycerides > 1000 carry 5% risk; triglycerides > 2000 carry 10-20% risk). Occurrence is more commonly associated in those with acquired disorders (such as diabetes mellitus, hypothyroidism, obesity, pregnancy, medication-induced, nephrotic syndrome) than in those with inborn errors of lipoprotein metabolism (such as familial combined hyperlipidemia, familial hypertriglyceridemia). Therapeutic measures in such patients include standard pancreatitis management, along with lipidlowering oral agents, low-molecular weight heparin, and insulin in those who are diabetic. In situations where these measures fail to improve patient clinic course, plasma exchange is used to expedite removal of triglycerides (TG). Here, we present a case of a noncompliant, insulin-dependent diabetic patient found to have hypertriglyceridemia-induced pancreatitis. Case: A 40-year-old African American male with poorly-controlled, insulin-dependent diabetes presented to our facility with complaints of abdominal pain accompanied with nausea and vomiting. Laboratory examination was consistent with severe pancreatitis and mild ketoacidosis (Table 1). Abdominal CT scan confirmed the clinical diagnosis of severe pancreatitis of the pancreatic head and uncinate process with inflammation of the adjacent duodenum (Image 1-2). The appearance of latescent serum accompanied with lipemic serum pointed toward a diagnosis of pancreatitis secondary to hypertriglyceridemia.Figure 1Figure 2Figure 3As our patient did not carry a familial history of genetic abnormalities of lipoprotein metabolism, we attributed the hypertriglyceridemia secondary to his poorly-controlled diabetes and diabetic ketoacidosis. The patient was treated with gemfibrozil, atorvastatin, IV fluids, bowel rest, and insulin infusion. Improvement of his triglyceride level coincided with improvement in blood sugars and abdominal pain. Plasmapharesis was not undertaken in this patient given improvement with conventional therapies.