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Abstract: FR-PO698

Case Study: A Report on the Efficacy of Hydroxychloroquine in Treating Hypercalcemia

Session Information

Category: Trainee Case Report

  • 402 Bone and Mineral Metabolism: Clinical


  • Hammond, Sara, Gwinnett Medical Center, Lawrenceville, Georgia, United States
  • Greenway, Parker, Georgia Nephrology, Lawrenceville, Georgia, United States
  • Paxton, William G., Georgia Nephrology, Lawrenceville, Georgia, United States

Sarcoidosis is a rare autoimmune disease resulting in the formation of non-caseating granulomas. Hypercalcemia occurs in 10 to 30 percent of sarcoidosis cases due to 1-alpha-hydroxylase over expression in granulomas.This enzyme increases 1,25-dihydroxy vitamin D levels, by conversion of 25-OH to 1,25-OH vitamin D. Hypercalcemia may be seen in any granulomatous disease. If hypercalcemia is uncontrolled it may lead to complications including nephrocalcinosis, renal lithiasis, and irreversible renal failure. Glucocorticoids are the mainstay of treatment of sarcoidosis, including the complication of hypercalcemia. Antimalarial agents such as chloroquine and hydroxychloroquine are known to impair production of 1,25-OH Vitamin D by blocking 1-alpha--hydroxylase activity. We report a case of a 56 year old caucasian female with sarcoidosis complicated by hypercalcemia successfully treated with hydroxychloroquine.

Case Description

A 56-year-old caucasian female with history of diabetes mellitus, hypothyroidism, and hypertension was referred for management of recent onset of worsening hypercalcemia. Her electrolytes were notable for serum calcium of 12.4 mg/dL (baseline 9.1-9.7), ionized calcium 1.49 mmol/L (NR 1.11-1.30), and serum creatinine of 1.7 mg/dL (baseline 0.9-1.1). Her calcium level remained elevated in spite of stopping daily Vitamin D3 supplementation and treatment with Denosumab injections. Differential diagnosis; included lymphoma and sarcoidosis: sarcoidosis was confirmed by tracheobronchial lymph node biopsy. Since pulmonary function was normal, there was a desire to avoid systemic steroid treatment. The patient was started on 200 mg hydroxychloroquine twice a day to control her hypercalcemia without the use of steroids. Within 2 months after initiation of hydroxychloroquine, calcium normalized and renal function returned to baseline. Hydroxychloroquine was then decreased to once a day and calcium remained normal over a period of greater than 2 years.


This case uses hydroxychloroquine as a steroid sparing alternative in the treatment of hypercalcemia. This case demonstrates the efficacy of hydroxychloroquine in the treatment of hypercalcemia, by directly inhibiting the 1-alpha-hydroxylase activity. Based on this mechanism of action it should be considered as a treatment strategy in any disease resulting in 1-alpha hydroxylase overproduction.