My Heartburn is Better but I am confused: A Rare Case of Calcium Carbonate-Induced Severe Hypercalcemia

Fadi Samaan, MD 1, Subhash Paudel, MD 2, Hadeel Zainah, MD 3, 1Rhode Island Hospital ,Providence , RI (Lifespan), North Street, RI; 2Rhode Island Hospital ,Providence ,RI (Lifespan); 3, Current affiliation: Kent County Hospital, Warwick, Rhode Island/Previous affiliation: The MIriam Hospital, Providence, RI

Meeting: Hospital Medicine 2018; April 8-11; Orlando, Fla.

Abstract number: 830

Categories: Adult, Clinical Vignettes, Hospital Medicine 2018

Keywords: ,

Case Presentation: A 54 year-old male with history of stroke, hypertension, chronic kidney disease stage III, gastroesophageal reflux, diabetes mellitus, peripheral vascular disease, and alcohol abuse (sober for 3 months), presented with acute change in mental status, generalized weakness, and difficulty ambulating. Vitals showed blood pressure of 134/ 86 mmHg, pulse of 95/min, temperature of 97.8 °F and normal oxygen saturation. He was mumbling incoherently, unable to follow commands to complete neurological exam. Cardiopulmonary exam was normal. Laboratory workup revealed sodium of 129 mEq/L, CO2 of 33 mEq/L, albumin of 3.9 g/dL, calcium of 16.8 mg/dL, ionized calcium of 8 mg/dL (4.2-5.2 mg/dL), and creatinine of 2.92 mg/dL (baseline 1.8 mg/dL). Brain computed tomography (CT) was negative. Family denied the use of vitamin D, calcium supplements or thiazide diuretics. Symptoms were attributed to life-threating hypercalcemia and he was admitted to the intensive care unit. He received aggressive hydration and salmon calcitonin therapy. Further results showed: 25-hydroxy vitamin D 11.6 ng/mL (30-100 ng/mL), 1-25 hydroxy vitamin D <8 pg/mL (18-72 pg/mL), and PTH <5 pg/mL (14-72 pg/mL). Vitamin A, TSH and cortisol levels were normal. The severity of hypercalcemia triggered malignancy workup. Chest and abdominal CT showed esophageal thickening. Esophagogastroduodenoscopy showed severe esophagitis, the biopsy was negative for malignancy. Serum and urine protein electrophoresis/immunofixation, serum free light chain ratio, and PSA were normal. The etiology of hypercalcemia was still unclear and upon further questioning specifically about over-the-counter heartburn medications, the wife reported excessive consumption of antacids (8-10 tablets/day), which turned out to contain calcium carbonate (1000 mg, elemental calcium 400 mg/tablet). Encephalopathy improved slowly with correction of calcium. Subsequently, calcium dropped to 6.7 mg/dL (corrected calcium 7.7 mg/dL), and repeat PTH was 122 pg/mL. Calcium carbonate and calcitriol were started with improvement in calcium level.

Discussion: Severe hypercalcemia is usually due to malignancy and sarcoidosis. High calcium carbonate intake alone is a rare cause of hypercalcemia, however, excessive consumption with concomitant chronic kidney disease could cause life-threatening hypercalcemia. Our patient had an unusually high intake of calcium carbonate equivalent to 3000-4000 mg of elemental calcium a day, which he did not report initially. This created a diagnostic dilemma especially in the absence of hyperparathyroidism, malignancy or other causes of hypercalcemia. Careful questioning about nonprescription medications helped to diagnose this unusual cause of hypercalcemia.

Conclusions: Hospitalists should recognize calcium-containing antacids as an uncommon cause of severe hypercalcemia especially in renal impairment. Thus, we emphasize the importance of obtaining a detailed history of nonprescription medications.

To cite this abstract:

Samaan, F; Paudel, S; Zainah, H. My Heartburn is Better but I am confused: A Rare Case of Calcium Carbonate-Induced Severe Hypercalcemia. Abstract published at Hospital Medicine 2018; April 8-11; Orlando, Fla. Abstract 830. Accessed February 25, 2020.

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