OBJECTIVE: To present a case of hypercalcemia associated with Castleman disease. METHODS: The details of case presentation, evaluation, diagnosis, and treatment are reviewed in a 25-year-old woman with severe hypercalcemia, joint pain, conjunctival injection, and lymphadenopathy. RESULTS: Endocrinopathies such as primary hyperparathyroidism were ruled out. Infectious and rheumatologic laboratory evaluations revealed normal results. On a whole-body scan, the patient was noted to have diffusely increased osseous uptake in conjunction with increased periarticular uptake, consistent with a metabolic superscan. After extensive evaluation, the patient underwent a right axillary lymph node biopsy and was found to have multicentric Castleman disease. She was treated with high-dose corticosteroids and eventually immunomodulators to help control her disease. CONCLUSION: To the best of our knowledge, this is the first published case report demonstrating hypercalcemia in association with Castleman disease. The pathologic mechanism is likely bone turnover mediated by cytokines such as interleukin-6.
OBJECTIVE: To present a case of hypercalcemia associated with Castleman disease. METHODS: The details of case presentation, evaluation, diagnosis, and treatment are reviewed in a 25-year-old woman with severe hypercalcemia, joint pain, conjunctival injection, and lymphadenopathy. RESULTS:Endocrinopathies such as primary hyperparathyroidism were ruled out. Infectious and rheumatologic laboratory evaluations revealed normal results. On a whole-body scan, the patient was noted to have diffusely increased osseous uptake in conjunction with increased periarticular uptake, consistent with a metabolic superscan. After extensive evaluation, the patient underwent a right axillary lymph node biopsy and was found to have multicentric Castleman disease. She was treated with high-dose corticosteroids and eventually immunomodulators to help control her disease. CONCLUSION: To the best of our knowledge, this is the first published case report demonstrating hypercalcemia in association with Castleman disease. The pathologic mechanism is likely bone turnover mediated by cytokines such as interleukin-6.