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Hypercalcemia and elevated serum 1,25-dihydroxyvitamin D3 in a patient with Hodgkin's lymphoma
Insights
This study details a patient with Hodgkin's disease experiencing hypercalcemia due to elevated 1,25-dihydroxyvitamin D3. Treatment with steroids normalized calcium and vitamin D levels, suggesting tumor-produced vitamin D caused the condition.
Area of Science:
- Endocrinology
- Oncology
- Internal Medicine
Background:
- Humoral hypercalcemia of malignancy is a complex endocrine-paraneoplastic syndrome.
- Elevated 1,25-dihydroxyvitamin D3 (calcitriol) is a known, albeit rare, cause of hypercalcemia in lymphoid malignancies.
Observation:
- A 74-year-old woman presented with fatigue, weight loss, and hypercalcemia.
- Physical examination revealed enlarged inguinal lymph nodes, and biopsy confirmed lymphocyte-depleted Hodgkin's disease.
- Markedly elevated serum 1,25-dihydroxyvitamin D3 levels were detected.
Findings:
- Treatment with corticosteroids effectively normalized serum calcium and 1,25-dihydroxyvitamin D3 levels.
- Calcitonin treatment was ineffective in managing the hypercalcemia.
- Despite chemotherapy, a subsequent hypercalcemic episode recurred with elevated 1,25-dihydroxyvitamin D3 levels.
Implications:
- The findings strongly suggest that the humoral hypercalcemia in this patient was mediated by tumor production of 1,25-dihydroxyvitamin D3.
- This case highlights the importance of considering vitamin D-mediated hypercalcemia in patients with Hodgkin's disease.
- Further research into the mechanisms of vitamin D production by tumors is warranted.
Abstract:
A 74-year-old woman was hospitalized because of decreased appetite, fatigue, and weight loss. The laboratory examination revealed hypercalcemia, a slightly increased serum creatinine level, and a markedly elevated serum level of 1,25-dihydroxyvitamin D3. The most important finding the physical examination revealed was enlarged inguinal lymph nodes. A biopsy disclosed lymphocyte-depleted Hodgkin's disease. After steroids, but not after calcitonin, both the elevated calcitriol concentration and serum calcium normalized. In spite of intensive chemotherapy, a further episode with hypercalcemia occurred and increased 1,25-dihydroxyvitamin D3 serum levels were observed. According to the available evidence it seems probable that the humoral hypercalcemia in this patient resulted from production of 1,25-dihydroxyvitamin D3 in the tumor.