The Troublesome Triad: Hypertriglyceridemia-Induced Acute Pancreatitis in Diabetic Ketoacidosis

Abstract Background: Diabeticketoacidosis (DKA) is an acute metabolic derangement that can triggerhypertriglyceridemia-induced acute pancreatitis (HTGAP). While DKA classicallypresents in patients with Type 1 Diabetes Mellitus (DM1), previous literaturedescribes HTGAP in DKA as the initial presentation of Type 2 Diabetes Mellitus(DM2). The following case illustrates the diagnostic complexities of thisenigmatic triangle. Clinical Case: Apreviously healthy, 28-year-old Hispanic male with a family history of DM2presented to the ED complaining of a sharp epigastric 10/10 pain radiating tothe right flank for one day that evolved into nausea with intractablenonbilious, nonbloody vomiting. He recently immigrated from Mexico City and hasnot seen a physician since childhood. He denied any tobacco, alcohol, norillicit substance use. Oninitial exam, he was afebrile and hemodynamically stable with dry mucosa,epigastric tenderness with voluntary guarding, but no evidence of jaundice,scleral icterus, nor abdominal distention. Pertinent initial labs foundglucosuria and ketonuria with a normal CBC, but his CMP was delayed as hisblood was lipaemic requiring serial dilutions that found hyperglycemia (415mg/dL, n <140), decreased carbon dioxide (17 mmol/L, n:23–29), a high aniongap (18 mmol/L, n<12), elevated ALT (154 u/L, n:4–36). Additional testingfound severely elevated triglycerides (4,427 mg/dL, n<150 mg/dL), elevated lipase(536 u/L, n<160), elevated Beta-hydroxybutyrate (5.30 mg/dL, n<2.81), andan elevated HgA1C (10.1%, n<5.7). These findings confirmed the diagnosis ofDKA with concerns for underlying HTGAP. CT abdomen showed hepatic steatosis andperipancreatic inflammation, confirming the diagnosis. Hewas admitted to the ICU, received aggressive IV fluid resuscitation with 5%dextrose in half normal saline while on an insulin infusion, with morphine andondansetron to control his pain and nausea. His abdominal pain resolved as histriglycerides trended down and anion gap closed. He was transitioned to an oraldiet with subcutaneous insulin prior to discharge on insulin and fenofibrate. At 1 month follow up, he reported medication compliance and denied anyrecurrence. Conclusion: While DKA rarely triggers HTGAP in <4% of pancreatitis cases, HTGAP willexacerbate DKA as the pancreatic inflammation leads to acute beta celldysfunction causing insulin deficiency, propagating lipolysis. A serumtriglyceride level >1000 mg/dL is required for diagnosis of HTGAP, and thedegree of elevation is associated with the severity of pancreatitis. Reference: Timilsina, S, et al. (2019). Triad of Diabetic Ketoacidosis,Hypertriglyceridemia, and Acute Pancreatitis: Severity of Acute PancreatitisMay Correlate with the Level of Hypertriglyceridemia. Cureus, 11(6), 4930–4934.