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IntroductionDiabetic 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.Case ReportA 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.ConclusionIt 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.

Introduction and importance hypercalcemia of malignancy is a severe complication of malignancy and associated with poor prognosis. Four mechanisms are implicated in this metabolic disorder, including excess parathyroid-related peptide secretion, focal osteolysis secondary to bone metastasis or multiple myeloma, excess calcitriol production, and ectopic parathyroid hormone production. Humoral hypercalcemia of malignancy secondary to isolated PTHrP or calcitriol overproduction is known; however, hypercalcemia of malignancy due to simultaneous PTHrP and calcitriol overproduction is less well known. Case presentation we report a case of a 63-year-old male who was diagnosed with poorly differentiated esophageal squamous cell carcinoma with simultaneous PTHrP and calcitriol overproduction. Clinical discussion while hypercalcemia of malignancy secondary to simultaneous PTHrP and calcitriol secretion has been reported in other solid cancers, this is the first case of humoral hypercalcemia of malignancy secondary to simultaneous PTHrP and calcitriol secretion associated with esophageal cancer. This phenomenon deserves increased recognition as it has both diagnostic and therapeutic consequences. We discuss the current testing algorithm and its limitations in determining the etiology of hypercalcemia of malignancy since it may miss the diagnosis of simultaneous PTHrP and calcitriol production. Conclusion we propose a revised testing algorithm for hypercalcemia of malignancy, which may improve the identification of simultaneous overproduction of PTHrP and calcitriol. This new algorithm can better characterize the mechanisms of hypercalcemia of malignancy and more appropriately guide treatment.