SAT-507 Pneumocystis Carinii Pneumonia: A Rare Cause of Granulomatous Hypercalcemia

Pneumocystis Carinii pneumonia (PCP) is a well-known complication of immunosuppression. Scattered case reports have linked PCP and its ability to induce a granulomatous response to hypercalcemia. PCP related hypercalcemia appears to be resistant to standard therapy. We report a case of hypercalcemia that preceded PCP and continued to worsen during the course of infection. A 63y man with renal transplant for polycystic kidney disease one year prior, presented with a three week history of fatigue, cough and chills. Patient was hypoxic and CT of the thorax revealed diffuse ground glass opacities. He was started on empiric therapy for PCP with intravenous methylprednisolone, clindamycin, and primaquine. Laboratory studies revealed a serum calcium of 12 mg/dl (baseline 9.2mg/dl, reference range 8.6-10.4 mg/dl) and creatinine of 3.23 mg/dl, which rose from a baseline value of 1.6 mg /dl. The patient’s bronchoalveolar lavage confirmed PCP. Endocrinology was consulted for evaluation of hypercalcemia. Further investigations revealed a suppressed PTH of 15 pg/ml from a baseline of 97 pg/ml (reference range 15-65pg/ml) post-transplant, 25-hydroxyvitamin D level of 30 ng/ml (reference range >20 ng/ml ), and 1,25-dihydroxyvitamin D(1,25D) level was elevated (>156 pg/ml; reference range 20-79 pg/ml). A diagnosis of 1,25D mediated hypercalcemia was made, intravenous fluids started and high dose steroids continued. Serum calcium levels improved transiently but subsequently rose to a peak level of 13.5 mg/dl. Ketoconazole 200 mg every 8hrs was started to reduce 1,25D production. Serum calcium remained high despite a reduction in 1,25D level (33 pg/ml). Bisphosphonates therapy was considered unsafe because of decreased GFR. Therefore, denosumab 30mg was administered, which resulted in decrease in serum calcium level to 10.3 mg/dl by day 19. Improvement of hypercalcemia correlated with improvement of PCP and renal function. Patient was discharged home after completing the 21 day course of treatment for PCP. Five weeks later, serum calcium stayed normal with an elevated PTH of 153 pg/ml and 1,25D level of 20 pg/ml. Hypercalcemia heralding PCP infection has been reported in the literature. Elevated calcium of 10.6 mg/dl was present one month prior to our patient’s hospitalization around the time of onset of his symptoms. Of the 19 cases of hypercalcemia due to PCP infection, 5 had hypercalcemia that preceded PCP infection by few weeks. The gold standard for diagnosis of PCP involves identification of the organism in induced sputum or bronchoalveolar lavage specimen. Measurement of serum 1,3-β-d-Glucan, which has high sensitivity, may be used as a screening tool in the right clinical setting such as our patient with immunosuppression and hypercalcemia to diagnose PCP at an earlier stage. We believe that hypercalcemia in a patient with immunosuppression should alert the possibility of PCP infection.