Osamu Saito1, Tomohiko Aoe, Tatsuo Yamamoto. 1. Department of Anesthesiology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Abstract
PURPOSE: Bone metastasis is one of the major causes of cancer-related pain, and not all bone cancer pain can be effectively treated. Recently, a mouse model of bone cancer pain was introduced. To test the analgesic effects of nonsteroidal antiinflammatory drugs on bone cancer pain, the authors examined the effects of oral administration of a cyclooxygenase-1 (COX-1) selective inhibitor (SC560), a COX-2 selective inhibitor (celecoxib), and a nonselective COX inhibitor (indomethacin) on bone cancer pain and compared these effects to the effect of orally administered acetaminophen and morphine. METHODS: An animal model of bone cancer pain was induced by injecting osteolytic murine sarcoma cells in the mouse femur. Drugs were administered orally 2 weeks after tumor-cell implantation, and the level of bone cancer pain was assessed 30, 60, 90, 120, and 180 min after drug administration. RESULTS: Oral administration of acetaminophen, indomethacin, and morphine, but not of SC560 or celecoxib, produced an analgesic effect on bone cancer pain. Co-administration of a subanalgesic does of morphine with acetaminophen enhanced the analgesic effect of acetaminophen. CONCLUSION: These data suggest that bone cancer pain is effectively treated by oral administration of indomethacin, acetaminophen, and morphine and that the co-administration of acetaminophen and an opioid provides a beneficial effect when treating of bone cancer pain.
PURPOSE: Bone metastasis is one of the major causes of cancer-related pain, and not all bone cancer pain can be effectively treated. Recently, a mouse model of bone cancer pain was introduced. To test the analgesic effects of nonsteroidal antiinflammatory drugs on bone cancer pain, the authors examined the effects of oral administration of a cyclooxygenase-1 (COX-1) selective inhibitor (SC560), a COX-2 selective inhibitor (celecoxib), and a nonselective COX inhibitor (indomethacin) on bone cancer pain and compared these effects to the effect of orally administered acetaminophen and morphine. METHODS: An animal model of bone cancer pain was induced by injecting osteolytic murinesarcoma cells in the mouse femur. Drugs were administered orally 2 weeks after tumor-cell implantation, and the level of bone cancer pain was assessed 30, 60, 90, 120, and 180 min after drug administration. RESULTS: Oral administration of acetaminophen, indomethacin, and morphine, but not of SC560 or celecoxib, produced an analgesic effect on bone cancer pain. Co-administration of a subanalgesic does of morphine with acetaminophen enhanced the analgesic effect of acetaminophen. CONCLUSION: These data suggest that bone cancer pain is effectively treated by oral administration of indomethacin, acetaminophen, and morphine and that the co-administration of acetaminophen and an opioid provides a beneficial effect when treating of bone cancer pain.
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