Abstract: TH-PO0248
From Heartburn to Hospitalization: A Case of Milk-Alkali Syndrome
Session Information
- Bone and Mineral Metabolism: Clinical Reports and Practice
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Pal, Aman, Albany Medical Center, Albany, New York, United States
- Khan, Muhammad Riaz, Albany Medical Center, Albany, New York, United States
- Abid, Sidrah, Albany Medical Center, Albany, New York, United States
- Mehta, Swati, Albany Medical Center, Albany, New York, United States
- Hongalgi, Krishnakumar D., Albany Medical Center, Albany, New York, United States
Introduction
Milk-alkali syndrome (MAS) was initially associated with the "Sippy regimen", a cocktail of milk and bicarbonates for peptic ulcer disease. Although the incidence of MAS declined with the use of acid-suppressive therapy, it has resurged in recent decades due to increased use of over-the-counter calcium and alkali supplements. This paper highlights MAS as an underrecognized cause of hypercalcemia and outlines the management challenges it poses compared to other etiologies of hypercalcemia.
Case Description
A 72-year-old female presented with acute confusion and nonsensical speech following a fall. Collateral history revealed a 10-day history of worsening epigastric pain and poor oral intake, which she attributed to her reflux disease. In an attempt to self-treat, she consumed approximately 25 tablets daily of calcium carbonate (tums) 500 mg. Labs revealed severe hypercalcemia (corrected calcium >19 mg/dL), metabolic alkalosis (bicarbonate 34 mmol/L), hypokalemia (2.8 mmol/L), hypomagnesemia (1.0 mg/dL), suppressed PTH (19 pg/mL), normal PTH-related peptide (<2 pmol/L) normal calcitriol (<7 pg/mL), normal creatinine (1.12 mg/dL), and a negative immunofixation. Her clinical presentation was consistent with MAS, and she was treated with intravenous fluids, calcitonin, and zoledronic acid. Her mental status improved alongside the normalization of her calcium levels and improved oral intake. However, rebound hypocalcemia became the primary barrier to discharge, necessitating intravenous calcium supplementation and delaying her transition to outpatient care.
Discussion
MAS is typically linked to intake >4g/day of elemental calcium, though it can occur with <2g/day when risk factors like, chronic kidney disease, vitamin D supplements, diuretics, or renin-angiotensin system blockers are present. In this case, MAS resulted from 25 daily Tums tablets, equating to 5g of elemental calcium. Early diagnosis is crucial. Unlike malignancy-related hypercalcemia, rebound hypocalcemia is common in MAS, making bisphosphonates inappropriate. This case highlights MAS as a reversible but underrecognized cause of hypercalcemia and encephalopathy, with treatment often complicated by overcorrection and prolonged hospitalization.