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In response to “Hypertriglyceridemia-induced recurrent acute pancreatitis: A case-based review”, we report a similar case of familial hypertriglyceridemia-induced acute pancreatitis in which we used a slightly different treatment approach.
A 42-year-old female with history of newly diagnosed Type V hypertriglyceridemia and diabetes mellitus type 2 presented to our institution with 10/10 mid-epigastric abdominal pain with associated non-bloody/non-bilious emesis, and decrease oral intake for the following 3 days. She ran out of her omega-3 fatty acids and fenofibrate the week prior and did not get refills.
On admission, patient was afebrile, heart rate of 120, blood pressure of 95/76, saturating 97% on room air. Her admission labs were significant for blood sugar of 207 mg/ dl, lipase of 300 u/l. Otherwise complete blood count and complete metabolic prolife were unremarkable. A fasting lipid panel was drawn which revealed total cholesterol 257 mg/dl, low-density lipoprotein (LDL) cholesterol 76 mg/dL, high-density lipoprotein (HDL) cholesterol 22 mg/dL, very-low-density lipoprotein (VLDL) cholesterol 667 mg/dL, and triglycerides of greater than 5000 mg/dl.
Similarly to the patient in Kota et al., we started the patient on fenofibrate 160 mg once daily, omega-3 acid ethyl esters 4 g once daily along with other standard pancreatitis treatment including intravenous fluids, bowel rest, and narcotics. Additionally, in the acute setting we started the patient on an insulin infusion at 0.1 units/kg/hour even though the patient did not have evidence of profound hyperglycemia or evidence of a ketoacidosis state. Dextrose was co-administered to prevent hypoglycemia and keep patient's blood glucose between 150 and 200 mg/dl. Furthermore, we started the patient on IV heparin at 600 units/h. As the case in our center, and many other centers, lipid apheresis was not readily available. We rechecked her lipid profile the next day and her triglycerides improved to 923. Clinically, the patient continued to gradually improve with these interventions. On the day of discharge, the patient's triglycerides were 423.
Although, no concrete guidelines exist as to the treatment of hypertriglyceridemia induced pancreatitis, it has been demonstrated that insulin infusion are effective in lower triglycerides. It is proposed that insulin increases lipoprotein lipase activity which degrades chylomicrons thus reducing serum triglycerides. However, the role of heparin remains controversial as it has been shown to transiently increase endothelial release of lipoprotein lipase, but in the long term may lead to heparin degradation resulting in an actual overall depletion of lipoprotein lipase. Nonetheless as demonstrated in our case and other in similar reports, such as Berger et al., heparin and insulin combination infusion therapy can be used successfully to treat hypertriglyceridemia-induced pancreatitis. This holds especially true in instances where lipid apheresis is not readily available.