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J Nucl Med. 2004 Aug;45(8):1358-65.

Radiopharmaceutical therapy for palliation of bone pain from osseous metastases.

Pandit-Taskar N1, Batraki M, Divgi CR.

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Abstract

Bone metastasis occurs as a result of a complex pathophysiologic process between host and tumor cells leading to cellular invasion, migration adhesion, and stimulation of osteoclastic and osteoblastic activity. The process is mediated by parathyroid hormones, cytokines, and tumor-derived factors. Several sequelae occur as a result of osseous metastases and resulting bone pain can lead to significant debilitation. Pain associated with osseous metastasis is thought to be distinct from neuropathic or inflammatory pain. Several mechanisms-such as invasion of tumor cells, spinal cord astrogliosis, and sensitization of nervous system-have been postulated to cause pain. Pharmaceutical therapy of bone pain includes nonsteroidal analgesics and opiates. These drugs are associated with side effects, and tolerance to these agents necessitates treatment with other modalities. Bisphosphonates act by inhibiting osteoclast-mediated resorption and have been increasingly used in treatment of painful bone metastasis. While external beam radiation therapy remains the mainstay of pain palliation of solitary lesions, bone-seeking radiopharmaceuticals have entered the therapeutic armamentarium for the treatment of multiple painful osseous lesions. (32)P has been used for >3 decades in the treatment of multiple osseous metastases. The myelosuppression caused by this agent has led to the development of other bone-seeking radiopharmaceuticals, including (89)SrCl, (153)Sm-ethylenediaminetetramethylene phosphonic acid ((153)Sm-EDTMP), (179m)SnCl, and (166)Ho-Labeled 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetramethylenephosphonate ((166)Ho-DOTMP). (89)Sr is a bone-seeking radionuclide, whereas (153)Sm-EDTMP is a bone-seeking tetraphosphonate; both have been approved by the Food and Drug Administration for the treatment of painful osseous metastases. While both agents have been shown to have efficacy in the treatment of painful osseous metastases from prostate cancer, they may also have utility in the treatment of painful osseous metastases from breast cancer and perhaps from non-small cell lung cancer. This article illustrates the salient features of these radiopharmaceuticals, including the approved dose, method of administration, and indications for use. We conclude with recommended guidelines for therapy and follow-up.

PMID: 15299062[Indexed for MEDLINE] Free full text

Following your answer, I add two articles regarding 153Sm and 223Ra .

Improving the dose-myelotoxicity correlation in radiometabolic therapy of bone metastases with Sm-153-EDTM

DOI 10.1007/s00259-013-2552-2

Massimiliano Pacilio, Guido Ventroni, Chiara Basile......Lucio Mango

Abstract

(153)Sm-ethylene diamine tetramethylene phosphonic acid ((153)Sm-EDTMP) is widely used to palliate pain from bone metastases, and is being studied for combination therapy beyond palliation. Conceptually, red marrow (RM) dosimetry allows myelotoxicity to be predicted, but the correlation is poor due to dosimetric uncertainty, individual sensitivity and biological effects from previous treatments. According to EANM guidelines, basic dosimetric procedures have been studied to improve the correlation between dosimetry and myelotoxicity in (153)Sm-EDTMP therapy. RM dosimetry for 33 treatments of bone metastases from breast, prostate and lung tumours was performed prospectively (with (99m)Tc-MDP) and retrospectively, acquiring whole-body scans early and late after injection. The (153)Sm-EDTMP activity was calculated by prospective dosimetry based on measured skeletal uptake and full physical retention, with the RM absorbed dose not exceeding 3.8 Gy. Patient-specific RM mass was evaluated by scaling in terms of body weight (BW), lean body mass (LBM) and trabecular volume (TV) estimated from CT scans of the L2-L4 vertebrae. Correlations with toxicity were determined in a selected subgroup of 27 patients, in which a better correlation between dosimetry and myelotoxicity was expected. Skeletal uptakes of (99m)Tc and (153)Sm (Tc% and Sm%) were well correlated. The median Sm% was higher in prostate cancer (75.3 %) than in lung (60.5 %, p = 0.005) or breast (60.8 %, p = 0.008). PLT and WBC nadirs were not correlated with administered activity, but were weakly correlated with uncorrected RM absorbed doses, and the correlation improved after rescaling in terms of BW, LBM and TV. Most patients showed transient toxicity (grade 1-3), which completely and spontaneously recovered over a few days. Using TV, RM absorbed dose was in the range 2-5 Gy, with a median of 312 cGy for PLT in patients with toxicity and 247 cGy in those with no toxicity (p = 0.019), and 312 cGy for WBC in those with toxicity and 232 cGy in those with no toxicity (p = 0.019). ROC curves confirmed the correlations, yielding toxicity absorbed dose thresholds of 265 cGy for PLT and 232 cGy for WBC. The best predictor of myelotoxicity and blood cells nadir was obtained scaling the RM absorbed dose in terms of the estimated TV. It seems clear that the increase in skeletal uptake due to the presence of bone metastases and the assumption of full physical retention cause an overestimation of the RM absorbed dose. Nevertheless, an improvement of the dose-toxicity correlation is easily achievable by simple methods, also leading to possible improvement in multifactorial analyses of myelotoxicity.

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