Endocrine Abstracts

Multiple myeloma is a hematologic malignancy characterized by osteolytic bone destruction which follows the increased osteoclastic resorption of bone that is not accompanied by increased bone formation. This can lead to bone pain, diffuse osteopenia, focal lytic lesions, pathologic fractures, spinal cord compression, and hypercalcemia, so it is evident that osteolytic bone disease is a major cause of morbidity and mortality in patients with multiple myeloma. Long-term monthly infusions of pamidronate as an adjunct to chemotherapy or as a maintenance therapy can reduce skeletal events and may improve the survival of patients.

Hypercalcemia is mainly caused by interleukin-6 and tumor necrosis factor. Myeloma cells activate genes that both stimulate bone resorption via osteoclast activation and prevent new bone creation by inhibiting osteoblasts. Pamidronate is a second-generation bisphosphonate, which inhibits bone resorption. Bisphosphonate bind strongly to hydroxyapatite crystals in the bone matrix, preferentially at the sites of increased bone turnover and inhibit the formation and dissolution of the crystals. Pamidronate does not interfere with bone mineralization at therapeutic doses.

A standard daily infusion dose of pamidronate for the treatment of hypercalcemia in patients with normal renal function is 60–90 mg over 2–4 h every 3–4 weeks for 2 years. Pamidronate appears to reduce calcium levels for prolonged periods of time, and hypocalcemia, which would increase PTH levels, might be an adverse complication. Some studies showed that intravenous pamidronate can aggravate secondary hyperparathyroidism, but for 2-year period, pamidronate is a safe and effective treatment for the correction of hypercalcemia. Here we present a female patient with multiple myeloma who has been receiving pamidronate for more than 5 years and developed secondary hyperparathyroidism.