Prediabetes Directly Deteriorates into Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome Triggered by Acute Pancreatitis: A Case Report Illustrating a “Chicken and Egg” Paradigm in Ketosis-Prone Diabetes

Diabetic crises occur most often in patients with type 1 diabetes and occasionally in type 2 diabetes, especially under stressful conditions. However, a diabetic crisis occurring directly from prediabetes is an unusual phenomenon.

A 45-year-old woman presented with postprandial left upper quadrant abdominal pain, nausea, and vomiting. She had a past medical history of prediabetes with impaired fasting glucose and HbA1c 6.4%. On admission, routine laboratory tests showed high anion gap metabolic acidosis (pH 6.92), anion gap 41 mmol/L, blood glucose 931 mg/dL, beta-hydroxybutyrate 28 mmol/L, and calculated effective osmolarity 322 mOsm/kg; she was diagnosed with diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS), and DKA-related abdominal pain. Later, the patient was found to have elevated lipase and amylase, and diagnosed with acute pancreatitis. Since DKA can induce abdominal pain and nonspecific lipase elevation, both of which are characteristics of acute pancreatitis, while acute pancreatitis can conversely trigger DKA, there exists a “chicken and egg” paradigm. Therefore, the differential diagnosis is discussed.

It is important to differentiate DKA from concomitant causes of abdominal pain to avoid missing the underlying etiology, which can be the trigger for DKA. During diabetic crises, treating the underlying trigger is just as important as managing metabolic derangements in order to achieve favorable outcomes; meanwhile, managing acute pancreatitis-associated hyperglycemia can promote recovery. Additionally, diabetic crisis that directly evolves from prediabetes illustrates an atypical form of diabetes called ketosis-prone diabetes; we briefly discuss its clinical characteristics, classification, and follow-up.