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From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia
Published on: October 19, 2014
[Hipercalcemia and non-Hodgkin's lymphomas. Report of three patients (author's transl)]
Insights
Hypercalcemia, a serious complication, occurred in 3% of non-Hodgkin's lymphoma patients, causing significant issues like renal failure. Early detection and management are crucial for these patients.
Area of Science:
- Oncology
- Nephrology
- Endocrinology
Background:
- Non-Hodgkin's lymphoma (NHL) is a significant hematologic malignancy.
- Hypercalcemia is a known but infrequent complication in patients with lymphoproliferative disorders.
Observation:
- Three out of 140 NHL patients developed hypercalcemia during their clinical course.
- Symptomatic hypercalcemia presented as renal failure and metabolic encephalopathy.
- Elevated alkaline phosphatase and bone disease were noted in affected patients.
Findings:
- Serum calcium levels ranged from 14.8 to 16.6 mg/100 ml.
- Serum phosphate and tubular reabsorption of phosphate remained normal.
- Prednisone, calcitonin, and forced diuresis provided transient relief; indomethacin was ineffective.
Implications:
- Hypercalcemia in NHL patients is associated with a poor prognosis.
- Pathogenesis may involve osteoclastic activator factors, excluding prostaglandins and PTH-like mechanisms.
- This highlights the need for vigilant monitoring of calcium levels in lymphoma patients.
Abstract:
Three out of 140 patients with non-hodgkin's lymphoma treated in a Department of Internal Medicine showed hypercalcemia during their clinical course. Hypercalcemia was symptomatic in two patients causing renal failure in one of them and a metabolic encephalopathy in the other. In the third case hypercalcemia was a casual finding. Serum calcium levels varied between 14.8 and 16.6 mg/100 ml; serum phosphate and tubular reabsorption of phosphate were normal. Alkaline phosphatase were high in the three cases. Bone disease was present in two cases. Transient responses were obtained with the administration of prednisone and calcitonin associated to forced diuresis. Indomethacin was ineffective. Pathogenesis of hypercalcemia could be related to the release of an osteoclastic activator factor. The role of prostaglandins and the presence of PTH-like mechanisms were discarded in our cases by indirect methods. The poor prognosis of patients with non-hogkin's lymphoma and hypercalcemia in stressed.

