Hypercalcemia due to giant cell myocarditis: a case report
Ami M Patel1, Mariell Jessup, John Tomaszewski
1Drexel University College of Medicine, Philadelphia, Pennsylvania.
Insights
Giant cell myocarditis, a rare granulomatous disease, can cause hypercalcemia through excess vitamin D production. Steroid therapy and heart transplant resolved the condition in this unique case.
Area of Science:
- Endocrinology
- Cardiology
- Nephrology
Background:
- Granulomatous diseases are an uncommon cause of hypercalcemia.
- Pathogenesis involves endogenous 1,25-dihydroxyvitamin D production by activated macrophages in granulomatous lesions.
Observation:
- The first reported case of hypercalcemia associated with giant cell myocarditis is presented.
- A patient with giant cell myocarditis developed progressive heart failure, cardiorenal syndrome, and subsequently hypercalcemia with elevated 1,25-vitamin D and suppressed PTH levels during stage 4 chronic kidney disease.
Findings:
- Hypercalcemia in this patient was attributed to extrarenal calcitriol production linked to giant cell myocarditis.
- Other potential causes of hypercalcemia, including vitamin D intoxication and multiple myeloma, were ruled out.
- Treatment with low-dose steroids normalized calcium levels, which remained stable after heart transplantation.
Implications:
- This case highlights giant cell myocarditis as an unusual cause of hypercalcemia.
- It underscores the importance of considering extrarenal 1,25-dihydroxyvitamin D production in granulomatous diseases.
- The findings suggest a potential therapeutic role for steroids in managing such cases.
Abstract:
Granulomatous diseases are a rare cause of hypercalcemia. The pathogenesis is presumed to be from endogenous production of 1,25-dihydroxyvitamin D by activated macrophages in granulomatous lesions, which harbor the 1α-hydroxylase enzyme. Herein the first case of hypercalcemia associated with giant cell myocarditis, an unusual type of granulomatous process, is reported. In this case, a patient with giant cell myocarditis had development of progressive heart failure and cardiorenal syndrome that required biventricular support. One year later, hypercalcemia associated with a relatively high 1,25-vitamin D level and a concomitantly suppressed parathyroid hormone level developed in the presence of stage 4 chronic kidney disease. Her other workup of hypercalcemia was unrevealing for vitamin D intoxication and multiple myeloma. Computed tomography of her chest showed no signs of hilar lymphadenopathy. Her calcium levels returned to normal with low-dose steroid therapy and have remained normal following a successful heart transplant. This case illustrates an unusual cause of hypercalcemia thought to be due to extrarenal calcitriol production associated with giant cell myocarditis.
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