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Abstract: PO1189

Hypercalcemia in a Patient with Visceral Leishmaniasis (VL) and Immune Reconstitution Inflammatory Syndrome (IRIS)

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Juarez, Lubin, Lifespan Health System, Providence, Rhode Island, United States
  • Winograd, Jacob M., Lifespan Health System, Providence, Rhode Island, United States
  • Tang, Jie, Brown University Warren Alpert Medical School, Providence, Rhode Island, United States

Hypercalcemia is a relatively common clinical problem with a wide range of etiologies. We report an unusual case of hypercalcemia due to visceral leishmaniasis triggering immune reconstitution inflammatory syndrome in a patient with AIDS.

Case Description

A 45-year-old male with history of previously treated VL complicated by a relapse now on suppressive amphotericin presented with 2 weeks of poor appetite, weight loss, and malaise. Recent history was notable for AIDS restarted on Triumeq in the preceding 2 months with slow recovery of CD4 count to 18 but robust reduction in HIV viral load. He denied other infectious symptoms. Labs were notable for AKI, calcium of 13.1, and pancytopenia. Work up revealed low PTH, low calcidiol, elevated ACE levels and high-normal calcitriol levels with bone marrow biopsy revealing non-necrotizing granulomas. Remainder of infectious work up including mycobacterium, histoplasma, and fungal cultures all remained negative. Of note, CD4 count rebounded to 354 during his month-long stay. He was ultimately diagnosed with IRIS secondary to VL leading to granulomatous hypercalcemia. Initial therapy consisted of fluids which resolved AKI and improved calcium. However, he proved to be fluid dependent as attempts at weaning would result in rise in calcium and creatinine. Definitive therapy consisted of steroids which resolved his hypercalcemia allowing him to come off fluids. Appetite improved and fatigue resolved over course of his stay with stabilization of calcium levels and creatinine returning to baseline. He was continued on suppressive Amphotericin B for VL.


Granuloma formation is a known effect of leishmania infection to combat the invading parasites. Presumably, such inflammation could lead to hypercalcemia via increased conversion of calcidiol to calcitriol. To our knowledge, this is the first case of hypercalcemia caused by VL in humans. It was likely triggered by the reconstitution of his immune system given recent re-initiation of anti-retroviral therapy and rebound of CD4 cell count. Initial management consists of fluids and bisphosphonates with definitive management consisting of steroids and amphotericin. We report this novel case of hypercalcemia in hopes of expanding the literature on the various potential manifestations of VL, particularly in the setting of IRIS and AIDS.