What question did this study set out to answer?

To highlight an unusual presentation of Mycobacterium infection characterized by symptomatic hypercalcemia in a lung transplant patient.

May 20, 2026

C68-09 Symptomatic Hypercalcemia Secondary to Mycobacterium Intracellulare (mac) Infection in a Lung Transplant Patient

Key Points

To highlight an unusual presentation of Mycobacterium infection characterized by symptomatic hypercalcemia in a lung transplant patient.
Descriptive case study of a 66-year-old female lung transplant recipient
Assessment included clinical examination, laboratory results, CT imaging, and bronchoalveolar lavage
Management involved intravenous fluids, calcitonin, and multiple anti-MAC medications.
The patient presented with severe hypercalcemia and acute kidney injury caused by Mycobacterium infection.
Despite treatment with ethambutol, rifabutin, azithromycin, inhaled amikacin, and isoniazid, the infection progressed.
Ultimately, the patient succumbed to pneumonia and respiratory failure linked to multi-drug resistant MAC infection.

Abstract

Abstract Introduction The decision to treat MAC requires balancing treatment-related toxicities with patient symptoms and disease burden, which can be challenging in solid organ recipients. We present an unusual case of aggressive MAC infection presenting as symptomatic hypercalcemia. Case Description History: The patient is a 66-year old female who had received a bilateral lung transplant for pleuroparenchymal fibroelastosis five years prior. She presented with lethargy and confusion. Previous maintenance immunosuppression included tacrolimus, mycophenolate, prednisone and belatacept. Vital signs and physical exam were unremarkable except for cognitive slowing. Clinical course: Laboratory results revealed severe hypercalcemia and acute kidney injury. CT imaging demonstrated lower lobe consolidations and tree-in-bud infiltrates. Bronchoalveolar lavage cultures were 3+ AFB-positive and grew MAC. Hypercalcemia was managed with intravenous fluids and calcitonin. MAC therapy was commenced with ethambutol, rifabutin, and azithromycin. Sensitivity testing subsequently revealed MAC resistance to macrolides and fluoroquinolones. Despite adding inhaled amikacin and isoniazid, the patient’s MAC infection continued to progress. She eventually succumbed to worsening pneumonia and respiratory failure. Conclusion This case illustrates an unusual form of MAC infection with symptomatic hypercalcemia. Elevated 1-25-Vit-D supports that hypercalcemia was driven by granulomatous disease . Of note, the patient’s explant surgical pathology showed caseating granuloma, and early post-transplant surveillance were positive for MAC. Given lack of clinical symptoms or radiographic abnormalities and out of concern for treatment-related toxicities, the patient did not receive early MAC therapy, and she remained asymptomatic for five years. She eventually developed an unusually aggressive form of multi-drug resistant MAI infection. Risk factors for this include previous colonization with MAC, prior exposure to macrolides for prevention of chronic lung allograft dysfunction and potential over-immunosuppression with the addition of belatacept. Infection with multi-drug resistant MAC infers a substantial risk of treatment failure and mortality, especially in immunocompromised hosts. This abstract is funded by: None

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