An old cause of hypercalcemia.

Document Type

Conference Proceeding

Publication Date


Publication Title

J Gen Intern Med


Learning Objective #1: Milk-alkali syndrome is an increasingly common cause of hypercalcemia due to increased calcium and vitamin D supplementation and can present with surprisingly high serum calcium levels Learning Objective #2: Review of a patient's supplement list is often neglected as not clinically relevant and should be included in a medication reconciliation CASE: Our patient was an 80-year-old female who presented to the ED with weakness of two days duration without any other systemic or localized symptoms. She had a history of atrial fibrillation, hypothyroidism, and severe aortic stenosis. Vitals were within normal limits and a neurological exam revealed decreased muscle strength with no focal neurological findings. Labs were notable for a serum calcium level of 15.7 mg/dL with an ionized calcium of 1.87 mmo/L and creatinine of 2.50 mg/dL up from a baseline of 1.4. PTH was suppressed. Vitamin D and 1,25 vitamin D were normal. Her medication regimen was discussed with her family and it was noted that she had been taking calcitriol as well as 1800mg of elemental calcium and 2000 IU of vitamin D daily for previous hypoparathyroidism diagnosed years earlier. Workup included a PTHrP within normal limits, a nuclear bone scan with no suspicious lesions and a normal SPEP/UPEP/free light chain analysis. She was noted to have a urinary tract infection and was treated with antibiotics. Her calcium and creatinine normalized within 48 hours with aggressive fluid replacement, furosemide, and calcitonin. Her calcium supplementation and calcitriol were discontinued and her calcium remained normal after 4 months of outpatient follow up. IMPACT: 90% of patient's presenting to the hospital for hypercalcemia have underlying malignancy or hyperparathyroidism. An increasing emphasis on calcium and vitamin D supplementation for the treatment of osteopenia has led to a resurgence in cases of milk-alkali syndrome. Dietary changes, acute illness, and changes in medication can precipitate severe hypercalcemia in susceptible patients. DISCUSSION: Acute hypercalcemia is common clinical entity. Values above 13mg/dl are classically attributed to malignancy with lower levels being attributed to hyperparathyroidism or vitamin D excess. Milk-alkali syndrome was originally described in patients with PUD who were treated with milk and antacids in the ERA before H2 blockers or PPIs. In the modern era, increased ingestion of calcium and vitamin D in the setting of renal failure can lead to the rapid development of hypercalcemia and metabolic alkalosis. Calciuresis then further contributes to dehydration and worsening renal failure. It was felt that in our patient, UTI with decreased oral intake precipitated acute renal failure. With the widespread use of calcium and vitamin D supplements for the prevention and treatment of osteoporosis, it is important for clnicians to recognize that milk-alkali syndrome is an increasingly common cause of hypercalcemic crisis and can present with calcium levels generally attributed to malignancy.





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