MON-781 - MAC Attack: Granulomatous Hypercalcemia Due to Disseminated Mycobacterium Avium Complex (MAC) in HIV-Associated Immune Reconstitution Inflammatory Syndrome (IRIS)

Background:
Hypercalcemia caused by granulomatous diseases such as sarcoidosis, tuberculosis, and Mycobacterium avium-complex (MAC) is a well-recognized entity. It is thought to result from macrophage mediated conversion of 25-hydroxy vitamin D to 1,25-dihydroxy vitamin D. We present a patient with newly diagnosed HIV and MAC who, following initiation of antiretroviral therapy (ART) developed immune reconstitution inflammatory syndrome (IRIS) precipitating hypercalcemia due to granulomatous inflammation.


Case Presentation:
A 30-year-old African American male presented with abdominal pain, hematochezia and three months of unintentional weight loss, admitted for hemorrhagic shock secondary to acute blood loss anemia. On admission, corrected calcium was 9.1 mg/dL (8.6-10.3 mg/dL). Colonoscopy revealed a 15 cm circumferential rectal mass causing partial obstruction, and biopsy confirmed squamous cell carcinoma. During his hospitalization, he was newly diagnosed with acute HIV infection (CD4 count 7 /uL; and HIV RNA 570796 copies/mL) and initiated on ART. One week after ART initiation, he became febrile. Computer tomography of the chest showed multiple 3-6 mm centrilobular pulmonary nodules, and cultures confirmed disseminated MAC infection, and he was started on azithromycin. Hospital course was complicated by acute onset hypercalcemia, with corrected calcium 12.3 mg/dL (8.6-10.3 mg/dL). Further work-up showed suppressed PTH (3 pg/mL; ref 12-88), normal 25-hydroxy vitamin D (50 ng/mL; ref >20), normal 1,25-hydroxy vitamin D (38 pg/mL; ref 19.9-79.3) and low PTH-related peptide (PTHrP) (9 pg/mL; ref 11-20). Hypercalcemia persisted despite intravenous fluids and calcitonin. Given the context of disseminated MAC and IRIS, a granulomatous etiology was suspected. Prednisone 40 mg daily was initiated, leading to normalization of calcium within three days.


Discussion:
This case illustrates steroid responsive hypercalcemia in the setting of disseminated MAC infection. Uniquely, hypercalcemia arose in the context of initiation of ART, highlighting the role of macrophage activation and 1-α-hydroxylase activity. Normal serum 1,25-dihydroxy vitamin D does not exclude a granulomatous mechanism, as increased local tissue production may drive hypercalcemia. This case emphasizes the importance of considering granulomatous hypercalcemia in immunocompromised patients experiencing IRIS and demonstrates the effectiveness of corticosteroid therapy in this context.

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