MON-774 - When GLP-1 RA Side Effects Tip the Scale: Nausea-Driven Milk-Alkali Syndrome

Introduction:
Milk-alkali syndrome (MAS) is characterized by the triad of hypercalcemia, metabolic alkalosis, and renal dysfunction from excessive calcium and absorbable alkali ingestion. With increased calcium absorption and reduced renal calcium excretion, a cycle of hypercalcemia and volume contraction occurs. We present a case of severe life-threatening hypercalcemia with acute kidney injury (AKI) after ingesting significant amounts of calcium carbonate for nausea triggered by tirzepatide use.


Case:
A 71-year-old female with history of Sjogren’s syndrome on chronic prednisone, primary biliary cholangitis, GERD, hypothyroidism, prediabetes, and osteopenia presented to the emergency room due to symptomatic hypercalcemia.

The patient has prescribed Tirzapetide, however, she takes it intermittently going 2-3 months without a dose. The patient reported she took a dose of Tirzapetide prior to a holiday party three days prior to admission. The next day and day after she had significant nausea and acid reflux symptoms. For this, she took 7-10 Tums for two days prior to admission. She also continued her 600 mg of calcium supplement daily and a vitamin D supplement daily for osteopenia.

Laboratory data were notable for corrected calcium of 15.7 (8.4-10.2) mg/dL, PTH 5 (15-88) pg/mL, vitamin D 25-OH 73 (≥30) ng/mL, phosphorous of 4.2 (2.4-4.8) mg/dL, bicarbonate 29 (23-32) mmol/L, creatinine of 2.10 (0.6-1.2) mg/dL and eGFR of 25 (≥60) mL/min/1.73m2.

Additional work up for PTH independent hypercalcemia was performed. The patient had no evidence of multiple myeloma and vitamin A (retinol) was normal at 0.61 (0.3-1.20) mg/L. She was noted to have low vitamin D 1,25-(OH)2 to 13.7 (19.9-79.3) pg/mL and very mildly elevated PTHrP of 3.8 (0-3.4) pmol/L likely due to renal dysfunction.

She was treated with IV fluids which promptly returned her calcium to normal range. Upon discharge she was advised to stop all calcium and vitamin D supplementation. Her calcium remains in normal range a week later, and creatinine has slowly improved to 1.1 (0.6-1.2) mg/dL.



Discussion:
This case highlights the potential risk of milk-alkali syndrome due to gastrointestinal side effects of GLP-1 RA, specifically tirzepatide-induced nausea prompting excessive calcium carbonate antacid use. It is important to educate patients on side effects such as nausea, especially when dosing intermittently. Our patient was self-treating her nausea with over-the-counter calcium carbonate antacids while already taking calcium and vitamin D supplements of osteopenia. This combination plus reduced PO intake makes one vulnerable to MAS. Quick recognition and treatment with IV fluids and discontinuation of all calcium sources typically results in complete resolution as shown in our patient.

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