ATLANTA—The third-generation injectable bisphosphonate zoledronic acid (Zometa), indicated for the treatment of patients with a variety of cancers, is also approved for the treatment of hypercalcemia and may help lengthen the lives of patients with lung cancer who often have elevated levels of bone turnover, according to data presented at the American Society of Clinical Oncology annual meeting.
Many patients with cancer also suffer from hypercalcemia, because the cancer cells overstimulate osteoclasts in the bones. This results in an increased rate of bone breakdown, which releases excess calcium into the bloodstream. An intravenous (IV) infusion of zoledronic acid may help reverse that trend. The drug is currently used in patients whose cancer has metastasized to the bone. It can be administered in the outpatient setting.
Data show that when zoledronic acid is given as a slow, 15-minute IV infusion once yearly, it increases bone mineral density and reduces bone turnover in postmenopausal women. The drug is expected to be approved for osteoporosis this fall.
This bisphosphonate has been shown to suppress the biochemical markers of bone resorption in patients with bone metastases. It reduces levels of one such marker, N-telopeptide of type I collagen (NTX), in patients with advanced multiple myeloma or bone metastases from breast cancer, preventing progression of bone loss.
“Zoledronic acid is the only therapy to demonstrate efficacy in reducing or delaying bone complications across a broad range of tumor types such as breast, prostate, lung, and renal cell cancers in patients with metastatic disease when administered every 3 to 4 weeks,” said lead investigator Pierre Major, MD, of McMaster University in Hamilton, Ontario. “By decreasing these events, the drug helps preserve patients’ independence and may increase survival in some lung cancer patients.”
It was recently shown that patients with bone metastases from lung cancer who had high levels of NTX or the bone-formation marker bone-specific alkaline phosphatase were at increased risk of skeletal-related events and death compared with patients who had low levels of these markers.