Craniopharyngioma and Severe Hypercalcemia: Metabolic Derangements from Local Invasion
Michael Limia1, Caroline Thomas1, Matthew Gorris2, Cynthia Burns2
1Wake Forest School of Medicine, 2Endocrinology, Atrium Health Wake Forest Baptist
Objective:
To describe the presentation and etiology of hypercalcemia secondary to osseous invasion in a patient with recurrent craniopharyngioma.
Background:
Craniopharyngioma is a benign, yet locally destructive tumor that has the potential to cause pituitary invasion. Although this invasion has been associated with numerous metabolic abnormalities, hypercalcemia remains a rare complication with multiple potential etiologies.
Results:
Our case involves a 29-year-old male with a history of panhypopituitarism secondary to recurrent craniopharyngioma, previously treated with multiple resections and gamma knife radiosurgery. He presented at the emergency department with symptoms of dehydration and fatigue, after outpatient lab work revealed hypercalcemia. Subsequent lab work in the ED and inpatient unit demonstrated an elevated corrected calcium of 17.34, low PTH of 3, low vitamin D, and normal PTHrP levels. CT imaging did not reveal any malignancies, and further testing excluded vitaminosis A, hyperthyroidism, and multiple myeloma as potential causes. His hypercalcemia was successfully treated with aggressive IV fluids, furosemide, calcitonin, and zoledronic acid. Upon discharge, CT and MRI confirmed a substantial increase in the size of his craniopharyngioma, with invasion into adjacent bone. Consequently, he underwent a left maxillectomy, and post-operative MRI showed a marked reduction in tumor size, accompanied by subsequent lab work revealing a consistent reduction in serum calcium levels.
Conclusions:
Our case demonstrates a rare metabolic presentation of craniopharyngioma: hypercalcemia secondary to osseous invasion. This process involves the direct invasion of the tumor into the bone, resulting in the release of calcium into the bloodstream. In response to these elevated calcium levels, the body compensates by reducing the secretion of PTH. This reduction attempts to lower serum calcium levels by indirectly decreasing the activation of osteoclasts and the production of 1,25 OH vitamin D. This case serves as a pertinent reminder to consider metabolic derangements when providing care for patients with locally invasive cancers.