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Humoral hypercalcemia in Hodgkin's disease. Clinical and laboratory evaluation
J O Jacobson1, F R Bringhurst, N L Harris
1Hematology/Oncology Unit, Massachusetts General Hospital, Boston 02114.
Insights
Humoral hypercalcemia in Hodgkin's disease (HD) primarily affects middle-aged men with bulky intraabdominal tumors. It is likely caused by tumor-produced 1,25(OH)2D3 and another factor, leading to bone resorption.
Area of Science:
- Endocrinology
- Oncology
- Pathology
Background:
- Humoral hypercalcemia is a rare complication of Hodgkin's disease (HD).
- Understanding its pathogenesis is crucial for patient management.
Observation:
- Three middle-aged men with symptomatic hypercalcemia were diagnosed with bulky intraabdominal HD.
- None had bone involvement or hyperparathyroidism.
- Elevated 1,25(OH)2D3 levels were observed in two patients at diagnosis.
Findings:
- Genomic blot analysis excluded T-cell or B-cell origin for HD in two cases.
- In vitro assays demonstrated tumor medium stimulated bone resorption, partly independent of 1,25(OH)2D3.
- These cases align with previously reported patients with HD and humoral hypercalcemia.
Implications:
- Humoral hypercalcemia in HD predominantly affects middle-aged males with intraabdominal disease.
- The mechanism involves tumor-related production of 1,25(OH)2D3 and a secondary factor.
- Further research is needed to elucidate the exact pathway and identify the second factor.
Abstract:
To provide further understanding of humoral hypercalcemia in Hodgkin's disease (HD) the authors describe the clinical features and laboratory investigation of three patients recently treated at Massachusetts General Hospital. All were middle-aged men who presented with symptomatic hypercalcemia which led to a diagnosis of bulky intraabdominal HD. None had evidence of bone involvement or hyperparathyroidism. In the two cases tested 1,25(OH)2D3 was elevated at the time of diagnosis. These characteristics are remarkably similar to those of ten patients with HD and probable humoral hypercalcemia described in the literature. The diagnosis of HD was supported in Cases 1 and 3 by genomic blot analysis which showed no evidence of T-cell or B-cell tumor origin. In an in vitro assay, primary tumor medium from Case 1 stimulated dose-dependent bone resorption which was not entirely ascribable to 1,25(OH)2D3. The authors conclude that humoral hypercalcemia in HD predominantly affects males of middle age, that intraabdominal bulky disease is common, and that hypercalcemia appears to be mediated by tumor related production of 1,25(OH)2D3 in concert with a second factor.
