SAT-763 - Hypercalcemic Crisis and Stercoral Colitis: A Severe Case of Milk-Alkali Syndrome

Background: Milk-alkali syndrome (MAS) is characterized by hypercalcemia, metabolic alkalosis, and acute kidney injury (AKI) due to excessive intake of calcium or alkali. While renal complications are well-documented, severe gastrointestinal complications secondary to hypercalcemia are less recognized.

Case: A 59-year-old woman presented with a two-week of constipation, abdominal upset, and headache. She expressed ingesting two bottles of calcium carbonate over 10 days for acid reflux. At admission, her lab showed a total calcium of 18.6 mg/dL, creatinine of 5.3 mg/dL, arterial pH of 7.53, and ionized calcium of 1.91 mmol/L. An abdominal X-ray showed a heavy stool burden without obstruction. A CT scan of the abdomen and pelvis confirmed fecal impaction with stercoral colitis and showed bilateral medullary nephrocalcinosis with non-obstructive nephrolithiasis.
Her past medical history was negative for thyroid or parathyroid disease, chronic kidney disease, or cancer. The patient was admitted to the ICU. She was given normal saline, IV calcitonin, pamidronate, and soap sud enema. Within 36 hours, her calcium improved to 12.5 mg/dL, and creatinine to 4.68 mg/dL. Further workup showed a 25-hydroxyvitamin D of 35.7 ng/mL, PTH of 21 pg/mL, PTHrP of < 2 pmol/L, and 1,25-dihydroxyvitamin D of 10 pg/mL.

Discussion: This case demonstrated MAS precipitated by recent high-dose calcium carbonate intake. The exposure history of calcium carbonate, along with the endocrine profile of inappropriately normal PTH, low 1,25-dihydroxyvitamin D, normal 25-hydroxyvitamin D, and negative PTHrP, confirms a non-PTH-mediated mechanism consistent with MAS and argues against primary hyperparathyroidism, PTHrP-mediated malignancy, and vitamin D intoxication.

Management includes directly stopping calcium carbonate and starting isotonic saline to restore intravascular volume and promote calciuresis. Calcitonin can be used for a rapid but short-lived reduction in serum calcium. Antiresorptive agents such as pamidronate are typically reserved for cases in which malignancy is suspected or when hypercalcemia does not respond to initial therapy, as prolonged hypocalcemia may occur once the exogenous calcium source is removed.

Conclusion: In patients with severe hypercalcemia, patients should be asked about calcium carbonate and other supplement use. A pattern of inappropriately normal PTH, low 1,25-dihydroxyvitamin D, and metabolic alkalosis is strongly suggestive of milk-alkali syndrome. This case also shows that, in addition to causing kidney injury, severe hypercalcemia can lead to significant gastrointestinal hypomotility, such as stercoral colitis. Stopping calcium/alkali intake and providing adequate fluid resuscitation usually causes improvement.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*