# Late Onset Hypercalcemia in an HIV Patient as a Manifestation of Immune Reconstitution Inflammatory Syndrome (IRIS)

## TL;DR

An HIV patient developed late-onset hypercalcemia due to immune reconstitution inflammatory syndrome (IRIS) triggered by a granulomatous infection.

## Contribution

This case highlights IRIS as a novel cause of hypercalcemia in HIV patients with granulomatous infections.

## Key findings

- Hypercalcemia occurred in an HIV patient with Mycobacterium avium-intracellulare (MAI) infection.
- Normal levels of vitamin D metabolites were unexpectedly found to be the cause of hypercalcemia.
- Treatment with steroids successfully managed the hypercalcemia linked to IRIS.

## Abstract

Hypercalcemia in human immunodeficiency virus (HIV) patients can be challenging due to various underlying mechanisms. 1,25- dihydroxycholecalciferol (1,25 (OH)2 vitamin D)-mediated hypercalcemia due to increased activity of extrarenal 1-alpha hydroxylase is one of the well-known mechanisms of hypercalcemia described in HIV patients. Mycobacterium avium-intracellulare (MAI) is a granulomatous disease that can cause hypercalcemia due to ectopic production of alpha -1 hydroxylase and result in increased levels of 1,25 (OH)2 vitamin D. Herein, we present a case of “late-onset” hypercalcemia in a patient with HIV/AIDS and MAI infection in the setting of suspected immune reconstitution inflammatory syndrome (IRIS). The hypercalcemia workup showed an inappropriately average level of 1,25 (OH)2 vitamin D while the rest of the workup was unrevealing. Unusually normal levels of vitamin D metabolites were the driving mechanism of hypercalcemia in this case. The late presentation of hypercalcemia was likely due to IRIS unmasking an underlying granulomatous infection, and this consideration led to the successful treatment of the patient with steroid administration. This case emphasizes the importance of considering IRIS in evaluating hypercalcemia that presents late in the course of granulomatous infections in HIV patients.