SUN-866 - A Metabolic Storm: Hypercalcemia, Hypertriglyceridemia Pancreatitis, and DKA Revealing Occult Primary Hyperparathyroidism

Background
Primary hyperparathyroidism (PHPT) is a common cause of hypercalcemia and is often asymptomatic or incidentally identified [1,2]. In acute settings, hypercalcemia may be misattributed to dehydration, particularly in diabetic ketoacidosis (DKA), where hemoconcentration and acidosis can transiently elevate calcium levels [3,4]. However, severe or persistent hypercalcemia with inappropriately elevated parathyroid hormone (PTH) should prompt evaluation for endocrine pathology [1]. We present a case of PHPT unmasked during sequential metabolic crises.

Case Presentation
A 51-year-old female with hypertension presented with acute abdominal pain and was diagnosed with pancreatitis due to severe hypertriglyceridemia (~1800 mg/dL). Labs showed elevated lipase and transaminases; imaging revealed edematous pancreatitis with peripancreatic fluid. She required ICU care with insulin infusion and was transitioned to fibrate therapy with improvement. Her corrected calcium was at the upper limit of normal (~10.8 mg/dL) at discharge. Two weeks later, she returned with altered mental status and severe DKA (glucose ~1000 mg/dL) with acute kidney injury and marked hypercalcemia (~14 mg/dL). She required intubation. Despite fluids and DKA management, hypercalcemia persisted. Workup showed elevated PTH (~95 pg/mL), suppressed PTHrP, and low vitamin D, consistent with PTH-mediated hypercalcemia suggestive of PHPT [1,5]. Urinary calcium was detectable. She improved, was extubated, and discharged on insulin with persistent but improved hypercalcemia and endocrinology follow-up.

Discussion
This case highlights a diagnostic pitfall: attributing hypercalcemia in DKA solely to dehydration. While mild elevations may occur, severe hypercalcemia with elevated PTH is not explained by DKA and suggests PHPT [3,4,6]. Subtle hypercalcemia during initial admission indicates PHPT likely predated both presentations. Although pancreatitis was attributed to hypertriglyceridemia, PHPT is associated with pancreatitis via calcium-mediated enzyme activation [7,8]. Hypercalcemia can also impair insulin secretion, reduce sensitivity, and promote dehydration, worsening hyperglycemia [9]. These factors likely contributed to clinical deterioration. This case underscores the importance of evaluating hypercalcemia in DKA when severe or persistent. Early recognition of PTH-dependent hypercalcemia enables timely diagnosis of PHPT and prevention of recurrent metabolic complications, with consideration of definitive management [1,10].

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