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A case of hypercalcemia associated with Castleman disease
Terri Washington1, Avni Vora, Dan Mihailescu
1Department of Internal Medicine, University of Illinois Chicago, Chicago, IL, USA. twashi@att.net
Insights
This case report details severe hypercalcemia in a patient with Castleman disease, a rare lymphoproliferative disorder. The findings suggest a link between Castleman disease and elevated calcium levels, potentially mediated by inflammatory cytokines.
Area of Science:
- Endocrinology
- Oncology
- Rheumatology
Background:
- Castleman disease is a rare lymphoproliferative disorder with diverse clinical presentations.
- Hypercalcemia is a significant metabolic disturbance that can be associated with various underlying conditions.
Observation:
- A 25-year-old woman presented with severe hypercalcemia, joint pain, conjunctival injection, and lymphadenopathy.
- Initial evaluations ruled out common causes of hypercalcemia, including primary hyperparathyroidism, infections, and rheumatologic conditions.
- Whole-body bone scan revealed a metabolic superscan pattern, indicating increased bone turnover.
Findings:
- Biopsy confirmed multicentric Castleman disease as the underlying diagnosis.
- This is the first reported case of hypercalcemia associated with Castleman disease.
- The hypercalcemia is hypothesized to be driven by cytokine-mediated bone turnover, particularly interleukin-6.
Implications:
- This case expands the known clinical spectrum of Castleman disease.
- It highlights the importance of considering Castleman disease in the differential diagnosis of unexplained hypercalcemia.
- Understanding the cytokine-driven mechanism may inform future therapeutic strategies for managing hypercalcemia in Castleman disease.
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.
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