Therapy Of Bone Pain Due To Osteoblastic Metastases

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The treatment of cancer-induced bone pain involves analgesics, with or without radiation and chemotherapy. The pattern of analgesic use is generally based on the World Health Organization's (WHO's) three-step approach to pain relief, beginning with nonsteroidal inflammatory medications, followed, if necessary, by level II drugs (relatively weak opiates). If these are insufficient, more potent opiate analgesics such as morphine are employed. Opiates have often distressing side effects, including sedation, nausea, and constipation, so that the dose of these should be as low as possible to maintain the patient's overall quality of life. In an attempt to lower these doses of analgesics, radiation and chemotherapy are employed. Radiation is usually given with teletherapy, either in a single dosage of 8 Gy or in fractionated dosages of about 30 Gy. These two radiother-apeutic approaches have equal initial efficacy, but the latter has a longer lasting effect in most patients. This form of treatment is often employed for a single painful site but cannot be repeated if the pain recurs. Hemibody radiation has been successfully employed in the past and has a success rate for pain palliation equal to that of other radiation modalities. Recognition of its gastrointestinal and hematologic side effects has reduced hemibody or wide field radiation utilization significantly in the United States.

An effect of appropriate chemotherapy can be to reduce bone pain, as has been documented for mitoxantrone in prostate cancer and the taxanes in breast cancer in up to 30% of patients. Another sort of "chemotherapy" is the use of the bisphosphonates to treat bone pain. Oral and intravenous bisphosphonates have been shown to reduce bone pain, especially in osteolytic cancers, as well as to reduce the risk of pathologic fracture and treat hypercalcemia. Nitrogen-containing bisphosphonates inhibit farnesyl diphosphate synthase, an enzyme involved in osteoclast cholesterol biosynthesis. This leads to a reduction in the lipid geranylger-anyldisphosphate which prenylates guanosine triphosphatases (GTPases) required for normal cytoskeletal organization and vesicular traffic in the osteoclast. In addition, bisphosphonates modulate the expression of bcl-2, leading to caspase-dependent osteoclast apoptosis. This multifaceted osteoclast inhibition and destruction lead to reduced bone turnover, and increased bone mass and mineralization. As bisphosphonates are not radioactive, and therefore require no special licensure or handling, and one infusion of the newer bisphosphonates is effective for up to four weeks, medical oncologists often favor these drugs which can be given in the office. For at least one of these bisphosphonates, pamidronate, no inhibition of subsequent skeletal uptake by the therapeutic tetraphosphonate samarium-153 (Sm-153) lexidronam (to be discussed next) has been found.

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