MON-151 Hypertriglyceridemia and Acute Pancreatitis Leading to Ketoacidosis in a Patient with Type 2 Diabetes

Introduction: We describe a case of type 2 diabetes presenting with acute pancreatitis (AP), hypertriglyceridemia, and diabetic ketoacidosis (DKA). Clinical Case: A 34-year-old Caucasian male presented to the emergency room with worsening intractable nausea and vomiting for 2 days. Medical problems included obesity, hypertension, hyperlipidemia, and fatty liver disease. He had a history of polysubstance use (denied recent alcohol intake) and noncompliance with self-care and was a known carrier for hemochromatosis. He gave a history of 30-lb weight loss over the past 6 weeks with associated polydipsia, polyuria, and abdominal pain. Six days prior to admission, the patient had been seen by his primary care physician for headache, nausea and vomiting, found to have a hemoglobin A1c of 13.5% (n=4.2-5.8%) and was started on metformin for newly-diagnosed T2DM. Physical exam revealed him to be afebrile, tachycardic (heart rate 145 bpm), and with a BP of 146/98 mmHg. Laboratory tests were significant for sodium 125 mmol/L (n=135-145mmol/L), potassium 4.0 mmol/L (n=3.5-5.1 mmol/L), anion gap 25 mmol/L (n=2-14 mmol/L), glucose 330 mg/dL (n=70-99 mg/dL), creatinine 1.5 mg/dL (n=0.5-1.3 mg/dL), lipase 268 U/L (n=8-78 U/L), triglyceride 1619 mg/dl (n<150 mg/dL), and negative alcohol and cardiac markers. Urine testing was positive for ketones with a negative drug screen. Arterial blood gas showed a pH of 7.27 (n=7.35-7.45), pCO2 19 mmHg (n= 35-45 mmHg), and pO2 111 mmHg (n=80-100 mmHg). CT of the abdomen revealed inflammation surrounding the pancreatic head, consistent with pancreatitis. The patient was admitted to the intensive-care unit for DKA and AP. He was treated with intravenous fluids and required an insulin drip for 72 hours before transitioning to subcutaneous insulin with resumption of oral nutrition as the pancreatic inflammation and gastrointestinal symptoms resolved. He was discharged on basal-bolus insulin therapy and lipid-lowering medications. Conclusion: Both DKA and AP are serious medical conditions with a high mortality rate when these two disorders occur simultaneously. Treatment requires aggressive fluid resuscitation with replacement of electrolytes and initiation of insulin. Identifying the potential trigger is key to preventing future occurrences. In the case presented, it is likely that primary hypertriglyceridemia, worsened by elevated glucose levels, was the etiologic factor for the onset of AP, which in turn precipitated DKA. However, it is also possible, though less likely, that uncontrolled hyperglycemia, glucose toxicity, and relative insulin deficiency led to increased production of very-low-density lipoprotein (VLDL) in the liver and its reduced clearance from the plasma, thus predisposing to hypertriglyceridemia. Close monitoring and appropriate therapy are required to control the latter and prevent future recurrences of AP and possibly DKA.