Prolonged insulin infusion failed to reduce triglyceride levels below 500 mg/dL (peak 2007 mg/dL) in a patient with hypertriglyceride-induced pancreatitis, though abdominal pain resolved.
Case Report (n=1)
Prolonged insulin therapy may be insufficient to rapidly lower severe hypertriglyceridemia in some cases of hypertriglyceride-induced pancreatitis, highlighting a potential role for early plasmapheresis.
Abstract Hypertriglyceride-induced pancreatitis (HTGP) accounts for 1 in 35 cases of pancreatitis. It is often associated with obesity and diabetes. Hypertriglyceridemia is often defined by triglyceride levels greater than 500 mg/dL. Pancreatitis is defined by two of three Atlanta criteria including abdominal pain, elevated pancreatic enzymes, or imaging consistent with pancreatitis. The etiology of HTGP remains unclear, but it is believed to be due to a positive feedback loop in which triglycerides are converted to fatty acid in the setting of elevated serum lipase from acute pancreatitis. Triglyceridemia from underlying dyslipidemia or diet, with subsequent pancreatitis leads to lipotoxicity which may result in further pancreatic injury, which increases the release of pancreatic digestive enzymes. While pancreatitis does not cause hypertriglyceridemia directly, triglyceride levels may rise as an inflammatory response to pancreatitis. Poorly controlled diabetes or diabetic ketoacidosis (DKA) are additional triggers that induce or worsen HTGP. A 71 year old female with a past medical history of type 2 diabetes and hyperlipidemia presented with acute epigastric pain radiating to her back. CT abdomen revealed a dilated pancreatic duct of 7 mm. Labs showed elevated serum and urine ketones, elevated anion gap, and mild metabolic acidosis on venous blood gas. The patient was started on an insulin infusion for DKA and admitted to the intensive care unit for close monitoring. Although the anion gap closed by hospital day two, she continued to have epigastric abdominal pain and could not tolerate oral intake. Initial triglyceride levels were elevated at 1871 mg/dL and radiographic imaging was reread and found to be consistent with pancreatitis. Insulin drip, at 0.3 units/kg/hour, was continued for an additional 11 days. Despite this, the patient’s triglyceride levels did not fall below 500 mg/dL, and her peak triglyceride level was 2007 mg/dL. The patient left against medical advice prior to being able to obtain plasmapheresis from nephrology for her triglyceridemia. Despite persistent hypertriglyceridemia, the patient’s abdominal pain resolved, and she tolerated a low-fat diet. Infusion of insulin is preferred to treating HTGP as it is less invasive than plasmapheresis and may improve triglyceride clearance and the toxic free fatty acids. Although plasmapheresis can reduce triglyceride levels by 50-80 percent, current evidence shows no significant difference in mortality or complications between those who received plasmapheresis versus control. This case highlights the potential role of early plasmapheresis consideration in patients with HTGP. This abstract is funded by: None
Thota et al. (Fri,) conducted a case report in Hypertriglyceride-induced pancreatitis (n=1). Insulin infusion was evaluated on Triglyceride levels. Prolonged insulin infusion failed to reduce triglyceride levels below 500 mg/dL (peak 2007 mg/dL) in a patient with hypertriglyceride-induced pancreatitis, though abdominal pain resolved.