SAT-497 Importance of OTC Medications in Hypercalcemia

Abstract

Background: Calcium-alkali syndrome, formerly known as milk-alkali syndrome was a classic cause of hypercalcemia until newer therapies for peptic ulcer disease emerged is mostly seen today in osteoporosis prevention and secondary hyperparathyroid treatment in chronic kidney disease. Here we present the contemporary presentation as a result of the classic syndrome. Case: 57-year-old male, history of hypertension, type-2 diabetes, Hodgkin’s lymphoma in remission was admitted with lower abdominal pain and difficulty voiding. His vitals and physical exam were within normal limits. Medications included Janumet, Lipitor and Ramipril. Labs showed a white count of 15.3cells 103 /uL with a left shift and a normal hemoglobin level. Serum chemistry with BUN of 37mg/dl, creatinine at 3.86mg/dl, calcium at 15.3mg/dl, albumin level of 3.4g/dl, corrected to 15.5mg/dl, phosphorous was low at 1.6mg/dl with normal magnesium level of 1.7mg/dl. The patient had prior normal renal function and calcium levels. Lymphoma was highest on the differential for the hypercalcemia. Workup revealed intact PTH of 9.9pg/ml (Low), PTHrp at 12pg/ml (14-27), 1,25- dihydroxy vitamin D level of <8 pg/ml (Low), 25-hydroxy vitamin D at 14.9ng/ml (Low). Serum protein electrophoresis revealed elevated alpha-1 and alpha-2 proteins signifying an ongoing acute inflammation. ACE levels were low at 5U/L (9-67). TSH levels were normal. LDH levels were normal at 234U/L. Further questioning revealed that the patient took about 40 tablets of over the counter “Tums” for gastritis in the last 3 days. Tums contains 500 -1117mg elemental calcium/tablet. It has been noted that calcium absorption markedly increases in the gut with high intake of 10-15gms calcium/day despite suppressed calcitriol levels. Based on the above, the diagnosis of Milk-Alkali syndrome: modern presentation was made. The calcium was treated with aggressive hydration and counselling regarding excessive Tums usage. Removal of Tums restored normal calcium levels and renal function. The modern presentation differs from the classic in being an incidental discovery, as the patient is asymptomatic as in our case. Hypophosphatemia is common due to an absence of phosphate load unlike with milk. Hypomagnesemia could be present as the high calcium inhibits magnesium resorption. Treatment includes removal of the offending agent and isotonic saline infusion. Furosemide has been tried but it may cause hypocalcemia as the suppressed PTH is slow to respond. For the same reason bisphosphonates should be avoided. Conclusion: Calcium-Alkali-syndrome, a now uncommon classic cause of hypercalcemia presents with a reversible triad of non-PTH, noncalcitriol mediated hypercalcemia, metabolic alkalosis and renal insufficiency in the setting of excessive ingestion of calcium with an absorbable alkali. OTC medications should be included in the history to avoid missing this diagnosis.