99Tc-亚甲基二膦酸盐的临床应用研究进展

99Tc-亚甲基二瞵酸盐(99Tc-MDP)可以抑制炎性反应,发挥抗炎、抗风湿作用;能抑制前列腺素的合成,具有明显镇痛作用.此外,99Tc-MDP还可通过调节人体自身免疫及调节骨代谢而发挥作用.临床上99Tc-MDP主治类风湿性关节炎、强直性脊柱炎、甲亢伴浸润性突眼等自身免疫性疾病,对癌转移痛、股骨头坏死及骨质疏松也有较好疗效.     

89SrCl2与153Sm-乙二胺四亚甲基膦酸治疗骨转移癌的对比研究

目的 对比研究89SrCl2和153Sm-乙二胺四亚甲基膦酸(153Sm-EDTMP)治疗骨转移癌疗效.方法 120例骨转移患者随机分为89SrCl2治疗组和153Sm-EDTMP治疗组,分别为69例和51例,89SrCl2剂量为1.11～2.22 MBq/Kg,153Sm-EDTMP剂量为25.9～37.0 MBq/kg,3～6月复查SPECT,对止痛效果、转移灶变化及不良反应进行比较分析.结果 89SrCl2组总有效率、显效、有效、无效分别为92.8%、69.6%、23.3%、7.2%;153Sm-EDTMP组的总有效率、显效、有效、无效分别为94.2%、66.7%、27.5%、5.8%,两组比较的差异无统计学意义(X2=4.98,P>0.05);89SrCl2治疗组骨转移病灶Ⅰ级(变淡,缩小或消失,无新增病灶出现)为56.5%,153Sm-EDTMP组为54.9%,两组比较的差异无统计学意义(X2=4.81,P>0.05);骨髓抑制情况(白细胞和血小板中任一项降低)分别为40.8%和59.2%,两组比较的差异有统计学意义(X2=7.45,P<0.05).结论 153Sm-EDTMP和89SrCl2控制乳腺癌、前列腺癌及大多数肺癌骨转移疼痛有效,可根据经济条件选择相应药物.89SrCl2疗效持久,相对骨髓抑制较小,更安全可靠,可作为早期骨转移患者的首选药物.     

^89SrCl2与^153Sm-乙二胺四亚甲基膦酸治疗骨转移癌的对比研究

目的对比研究^89SrCl2和^153Sm-乙二胺四亚甲基膦酸（^153Sm-EDTMP）治疗骨转移癌疗效。方法120例骨转移患者随机分为SOSrCl2治疗组和^153Sm-EDTMP治疗组,分别为69例和51例,^89SrCl2剂量为1．11-2．22MBq／kg,^153Sm-EDTMP剂量为25．9～37．0MBq／kg,3-6月复查SPECT,对止痛效果、转移灶变化及不良反应进行比较分析。结果^89SrCl2组总有效率、显效、有效、无效分别为92．8％、69．6％、23．3％、7．2％;^153Sm-EDTMP组的总有效率、显效、有效、无效分别为94．2％、66．7％、27．5％、5．8％,两组比较的差异无统计学意义（χ^2=4．98,P〉0．05）;^89SrCl2治疗组骨转移病灶Ⅰ级（变淡,缩小或消失,无新增病灶出现）为56．5％,^153Sm-EDTMP组为54．9％,两组比较的差异无统计学意义（χ^2=4．81,P〉0．05）;骨髓抑制情况（白细胞和血小板中任一项降低）分别为40．8％和59．2％,两组比较的差异有统计学意义（r=7．45,P〈0．05）。结论^153sm-EDTMP和^89SrCl2控制乳腺癌、前列腺癌及大多数肺癌骨转移疼痛有效,可根据经济条件选择相应药物。^89SrCl2疗效持久,相对骨髓抑制较小,更安全可靠,可作为早期骨转移患者的首选药物。     

^99Tc-亚甲基二膦酸盐对胶原诱导性关节炎大鼠滑膜及软骨凋亡相关因子的影响

目的探讨^99Tc-亚甲基二膦酸盐（MDP）对胶原诱导性关节炎（CIA）大鼠的疗效,以及对滑膜和软骨细胞凋亡相关因子bcl-2、bax的影响。方法设立正常对照组;采用皮下注射法用牛Ⅱ型胶原和不完全弗氏佐剂诱导CIA大鼠模型,分为模型对照组（尾静脉注射生理盐水）、^99Tc-MDP组（每天1次尾静脉注射^99Tc-MDP,按体质量0．04μg ^99Tc／kg）和甲氨蝶呤（MTX）组（按体质量每周1次尾静脉注射MTX 1mg／kg）,采用关节炎指数（AI）评价各CIA组大鼠关节炎程度,免疫组织化学染色法检测滑膜及软骨细胞bcl-2和bax表达;应用SPSS13．0软件对实验数据进行统计学处理。结果（1）^99Tc-MDP和MTX均能减轻CIA大鼠关节炎程度,降低AI评分,改善CIA大鼠关节滑膜炎的病理学变化。（2）与正常对照组[bcl-2：（7．56±1．18）％,bax：（6．14±1．71）％]比较,CIA模型对照组滑膜bcl-2和bax表达明显升高[（39．30±0．53）％、（27．37±2．45）％;q=46．27,24．57,P均〈0．001];与模型对照组比较,^99Tc-MDP组和MTX组滑膜细胞bcl-2水平降低[（30．24±2．09）％、（27．25±3．33）％;q=13．20,17．56,P均〈0．001],bax表达有所增加但差异无统计学意义,bcl-2／bax比值明显降低。（3）在软骨细胞中,CIA模型对照组bcl-2和bax表达[（20．20±2．78）％、（36．40±1．67）％]显著高于正常对照组[（9．91±4．09）％、（6．71±3．50）％;q=10．51,37．01,P均〈0．001];与模型对照组比较,^99Tc-MDP组和MTX组bcl-2增高[（26．58±2．52）％、（27．06±1．92）％;q=6．53,7．01,P均〈0．001],而bax水平降低[（24．26±2．75）％、（23．53±0．74）％;q=15．12,16．04,P均〈0．001],bcl-2／bax比值增高。结论凋亡相关因子bcl-2和bax的异常表达与CIA的发生发展密切相关。^99Tc-MDP能够减轻CIA大鼠关节炎程度,调节滑膜和软骨细胞b     

免疫基因介入疗法治疗大鼠转移性肝癌的实验研究

目的观察经动脉插管导入肿瘤坏死因子α(TNF-α)和白介素2(IL-2)重组腺病毒对转移性大鼠肝癌模型的治疗作用.材料和方法用293细胞扩增人TNF-α和IL-2重组腺病毒,并测定病毒滴度;9组大鼠于胃十二指肠动脉分别注人Ad.lacZ(2×109pfu/m1),采用X-Gal染色方法检测lacZ基因在各个脏器的表达;Walker256乳癌细胞感染人TNF重组腺病毒后,观察其体外增殖能力、皮下致瘤性的变化及进行肿瘤局部病理学检查;瘤体局部注射TNF重组腺病毒,观察荷瘤大鼠的肿瘤生长情况及生存期;取大鼠乳腺癌细胞株(Walker256)转染至肝脏的荷瘤大鼠动物模型,分为hTNF组,人IL-2(hlL-2)组,hTNF+hlL-2组,病毒对照组(lacZ组)和培养液对照组进行治疗,观察大鼠生存期.结果所制备的人TNF-α和IL-2重组腺病毒滴度为2×l09Dfu/ml和2.1×l09pfu/ml;实验组于12h取材,经染色lacZ基因在肝脏中即有表达,而此时脾、肺、肾等内脏器官尚未见表达,21d该基因在肝脏仍有表达,而在其他脏器如脾、肺及肾表达仅维持14d;转染基因瘤株体外增殖能力和皮下致瘤性显著下降,瘤体周围有大量淋巴细胞及单核细胞浸润;肿瘤局部注射Ad.hTNF能显著抑制Walker256的生长,并延长荷瘤大鼠的生存期;单独注射TNF-α或IL-2重组腺病毒能有效延长转移性肝癌大鼠的存活期;这两种重组腺病毒单独使用时,治疗效果之间无显著性差异;联合应用这两种重组腺病毒比单一使用TNF-α或IL-2重组腺病毒能更有效地延长荷瘤大鼠的存活期.结论经肝动脉插管注射目的基因重组腺病毒,是基因治疗肿瘤的一种较为有效的途径,为细胞因子基因的临床应用打下了基础.     

锝亚甲基二膦酸盐注射液治疗距骨骨软骨损伤的临床研究

目的:总结锝亚甲基二膦酸盐注射液(~(99m)Tc-MDP)对距骨骨软骨损伤(OLT)的治疗效果。方法:收集45例OLT的MRI、SPECT-CT资料,根据病程分期对32例符合保守治疗患者的治疗效果进行回顾性分析,依据美国足与踝关节外科协会(AOFAS)踝与后足功能评分标准及视觉模拟评分法(VAS)评定患者的临床疗效。结果:所有患者MRI见距骨滑车关节面不规则条状、带状异常长T_1、长T_2信号,连续或不连续,部分呈地图样或囊变影,Ⅰ期5例,Ⅱ期13例,Ⅲ期14例,Ⅳ期8例,Ⅴ期5例;SPECT-CT治疗前后病灶核素浓聚范围缩小,显效11例,有效18例,无效3例。AOFAS评分显著高于治疗前(P0.05);VAS评分显著低于治疗前(P0.05)。随访临床疗效优良率为73.33%。结论:MRI对OLT诊断明确,~(99m)Tc-MDP注射液治疗OLT效果良好。     

hNIS基因转染介导Hela细胞移植瘤放射性核素显像和治疗的实验研究

目的 利用131I对转染hNIS基因的宫颈癌Hela-NIS（＋）细胞移植瘤进行显像及治疗实验研究,评价hNIS基因转染介导131I治疗宫颈癌的可行性.方法 （1）利用Hela-NIS（＋）细胞和未转染hNIS的Hela细胞分别建立荷宫颈癌裸鼠模型,进行131I及99TcmO4-显像,观察移植瘤的显影情况,并计算移植瘤部位与对侧相同部位的T/B比值.（2）通过腹腔注射法观察比较74,111和148 MBq131I对荷Hela-NIS（＋）宫颈癌裸鼠移植瘤的抑制作用,另设不行任何治疗的对照组.用SPSS 13.0软件,样本均数间差异行t检验.结果 （1）成功构建荷Hela-NIS（＋）裸鼠移植瘤与荷Hela裸鼠移植瘤模型.131I显像示荷Hela-NIS（＋）裸鼠移植瘤部位明显放射性浓聚,注射后8 h T/B比值最高达17.34,而未转染hNIS基因的荷Hela裸鼠移植瘤部位始终未见明显的放射性浓聚.99TcmO4-显像示荷Hela-NIS（＋）裸鼠移植瘤部位在注射后25 h内持续放射性浓聚.（2）经不同剂量的131I治疗后2～3周起,各治疗组荷Hela-NIS（＋）裸鼠移植瘤生长开始受到抑制,移植瘤体积有不同程度缩小.111MBq组和148 MBq组的移植瘤抑制率差异无统计学意义（t=0.13～2.17,P＞0.05）,但二者均明显高于74 MBq组的移植瘤抑制率（t=2.74～5.75,P＜0.05）.对照组荷Hela-NIS（＋）裸鼠移植瘤持续生长.结论 荷Hela-NIS（＋）宫颈癌裸鼠移植瘤可明显聚集131I及99TcmO4-,且在较长时间内持续清晰显影;131I体内治疗效果显著.     

原发性腹膜砂粒体癌~(99)Tc~m-亚甲基二膦酸盐SPECT-CT全身骨显像一例报告

患者女,78岁,原发性腹膜砂粒体癌术后9月,左上腹部疼痛2月,行~(99)Tc~m-亚甲基二膦酸盐~(99)Tc~m-methylene-diphosphonate,~(99)Tc~m-MDP)前后位全身骨显像示:脊柱侧弯,第10胸椎骨质代谢轻度增高,其余骨骼未见异常;腹盆腔内可见多处不规则团块状非均匀性显像剂分布异常增高影,经局部断层和X线定位示:显像剂分布异常增高区为肠管外腹膜内软组织.     

大鼠骨癌痛模型的制备及电压依赖性钠通道Nav1.8在其背根神经节的表达研究

目的 建立大鼠骨癌痛模型并观察电压依赖性钠通道Nav1.8在其背根神经节(DRG)的表达,以探讨Nav1.8在癌症性疼痛中的作用.方法 在雌性SD大鼠左胫骨内注射Walker256细胞(103/μl、104/μl、105/μl)后1、3、5、7、10、14天观察机械痛敏阈值和CO2激光热痛敏阈值的变化,与对照组大鼠进行比较,分析癌痛组大鼠出现痛阈降低的时间.于接种细胞后14天取双侧胫骨做病理切片观察肿瘤生长情况.RT-PCR检测癌痛组及对照组大鼠L5～L6DRG Nav1.8基因的表达.结果 所有接种Walker256细胞的大鼠均可见胫骨内实质性肿瘤的膨胀性生长和严重的骨质重构.各癌痛组大鼠分别于第7～14天出现进行性加重的疼痛行为学改变,其左侧(癌痛侧)DRG Nav1.8的表达明显升高(P＜0.05),对侧的表达与对照组之间无明显差异.结论 胫骨内注射Walker256细胞的大鼠在产生浸润性生长的骨肿瘤同时,可伴进行性的痛觉过敏,是骨转移瘤相关疼痛研究可靠的动物模型.Nav1.8基因在骨癌痛模型大鼠DRG中的表达水平上调,提示该通道可能参与骨癌痛的发生过程.     

光动力疗法对荷瘤小鼠血清中TNF-α含量影响的实验研究

目的探讨光动力疗法（PDT）抑瘤效应的免疫机制,以及PDT联合肿瘤局部注射卡介苗（BCG）的治疗效果。方法建立小鼠Heps肝癌移植瘤模型72只,随机分为对照组、PDT组、BCG组和联合组,每组18只。观测各组移植瘤体积的变化。采用酶联免疫吸附实验（ELISA）,测定各组PDT治疗后2、24 h和7 d荷瘤小鼠血清中肿瘤坏死因子（TNF）-α的变化。结果 1.各治疗组治疗后7 d的移植瘤体积较对照组均明显缩小（P〈0.01）。治疗后7 d联合组的肿瘤体积较PDT组明显缩小（P〈0.05）。2.ELISA结果显示,治疗后2、24 h和7 dPDT组和联合组荷瘤小鼠血清中TNF-α的含量均明显高于对照组和BCG组（P〈0.01）,联合组荷瘤小鼠血清中TNF-α的含量明显高于PDT组（P〈0.05）。结论 PDT可增强荷瘤小鼠全身的免疫力,肝癌移植瘤体积明显缩小。PDT联合局部注射BCG的疗效优于单用PDT和单用BCG。     

A Walker 256 tumor-induced osteogenic small animal model for the evaluation of [99mTc] diphosphonate radiopharmaceuticals

A mammalian model has been developed for the in vivo evaluation of bone imaging agents. The model is based upon the quantification of a discrete, initial secondary periosteal osteogenesis induced in cortical bone immediately adjacent to an intramuscularly implanted Walker 256 tumor in Fisher 344 rats. Evaluation of the model consists of a histopathological examination of the periosteal bone formation, biodistribution studies on 99mTc-MDP and 99mTc-HMDP commercial kit preparations, and biodistribution studies on two 99mTc-HEDP component fractions isolated after anion exchange chromatographic separations from an investigative "carrier added" preparation. Reversed phase HPLC separations of the 99mTc-MDP and 99mTc-HMDP commercial kit preparations illustrate distinct differences in chemical composition between the two bone agents.     

Effects of increasing doses of samarium-153-ethylenediaminetetramethylene phosphonate on axial and appendicular skeletal growth in juvenile rabbits

INTRODUCTION: Targeted radiotherapy using samarium-153-ethylenediaminetetramethylene phosphonate (153 Sm-EDTMP) is currently under investigation for treatment of osteosarcoma. Osteosarcoma often occurs in children, and previous studies on a juvenile rabbit model demonstrated that clinically significant damage to developing physeal cartilage may occur as a result of systemic 153 Sm-EDTMP therapy. The aim of this study was to evaluate the late effects of 153 Sm-EDTMP on skeletal structures during growth to maturity and to determine if there is a dose response of 153 Sm-EDTMP on growth of long bones. METHODS: Female 8-week-old New Zealand white rabbits were divided into three treatment groups plus controls. Each rabbit was intravenously administered a predetermined dose of 153 Sm-EDTMP. Multiple bones of each rabbit were radiographed every 2 months until physeal closure, with subsequent measurements made to assess for abbreviated bone growth. Statistical analyses were performed to determine the differences in bone length between groups, with significance set at P<.05. RESULTS: Significant differences in lengths of multiple bones were detected between the high-dose group and other treatment groups and controls at each time interval. A significant difference in lengths of the tibias was also noted in the medium-treatment group, compared to controls. Mean reduction of bone length was first detected at 4 months and did not increase significantly over time. CONCLUSIONS: These data suggest that clinically significant bone shortening may occur as a result of high-dosage administration of 153 Sm-EDTMP. Further investigation regarding the effects of bone-seeking radiopharmaceuticals on bone growth and physeal cartilage is warranted.     

Radiopharmaceutical therapy for palliation of bone pain from osseous metastases.

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.     

Samarium-153-EDTMP: pharmacokinetic, toxicity and pain response using an escalating dose schedule in treatment of metastatic bone cancer.

Samarium-153 emits medium-energy beta particles and an imageable gamma photon with a physical half-life of 46.3 hr. When chelated to ethylenediaminetetramethylenephosphonic acid (EDTMP), it is remarkably stable in vitro and in vivo. In this study, we administered escalating amounts of 153Sm-EDTMP, from 0.1 to 1.0 mCi/kg (3.7-37 MBq/kg), to 22 patients with painful metastatic bone cancer. A complete concordance was found when the scintigrams of 153Sm-EDTMP were compared qualitatively to 99mTc-HDP bone images. Moreover, the skeletal uptake of the 153Sm-EDTMP related to the number of metastatic sites (r = 0.65; p = 0.001) showed an inverse proportion to the plasma radioactivity at 30 min following injection (r = -0.79; p = 0.0001) and was unaffected by the administered (mCi/kg), (r = 0.33; p = 0.13). Myelotoxicity was observed in 10 of the 29 treatment courses and leukopenia occurred in two. Thrombocytopenia occurred in patients who had low pretreatment platelet counts, albeit within the normal range (p = 0.001), most suffered from prostate cancer (p = 0.007) and retained a higher percentage of the 153Sm-EDTMP in their skeleton (p = 0.057). In four patients an exacerbation of the pre-existing pain ("flare reaction") was recorded. Pain palliation occurred in 65% of the treated patients (mean: 3.8 mo, range: 1-11 mo). Retreatment in first time responder patients was quite effective. Our preliminary results indicate that 153Sm-EDTMP is a promising radiotherapeutic agent for palliative treatment of metastatic bone cancer pain, and further study is necessary to ascertain its optimal dose, efficacy and toxicity.     

Bone uptake studies in rabbits before and after high-dose treatment with 153Sm-EDTMP or 186Re-HEDP.

The aim of this animal study was to measure the bone uptake of (99m)Tc-hydroxymethylene diphosphonate (HDP) before and after high-dose treatment with (153)Sm-ethylenediaminetetramethylenephosphonate (EDTMP) or (186)Re-(tin)1,1-hydroxyethylidene diphosphonate (HEDP) to prove or disprove post-therapeutic alterations of bone uptake of radiolabeled bisphosphonates. METHODS: Quantitative bone scanning using 100 MBq (99m)Tc-HDP was performed on 12 rabbits before and 8 wk after radionuclide therapy with 1,000 MBq of either (153)Sm-EDTMP or (186)Re-HEDP. Whole-body images were acquired at 3 min, 3 h, and 24 h after injection, and the activities for the whole body, urinary bladder, and soft tissue were measured by region-of-interest technique. From these data, bone uptake was calculated as initial whole-body activity minus urinary excretion and remainder soft-tissue activity. RESULTS: In animals treated with (153)Sm-EDTMP (n = 6), no differences could be proven for the bone uptake of (99m)Tc-HDP at 24 h after injection before and after therapy (51.1% +/- 5.5% vs. 48.0% +/- 6.1%, P > 0.05). There were also no significant differences for the remainder soft-tissue activities and the urinary excretion rates before and after therapy. Similar results were obtained in rabbits treated with (186)Re-HEDP: Bone uptake (44.8% +/- 6.7% vs. 40.4% +/- 4.9%, P > 0.05) and urinary excretion revealed no significant differences before and after treatment. CONCLUSION: No significant impairment of bone uptake of (99m)Tc-HDP could be observed 8 wk after high-dose radionuclide bone therapy. Because both the biokinetic data obtained for (186)Re-HEDP and (153)Sm-EDTMP and the myelotoxic effects were quite similar in rabbits to those in patients, it seems justifiable to expect the same result (i.e., no significant alteration of bone uptake of radiolabeled bisphosphonates) in patients undergoing a second radionuclide therapy within 2-3 mo after standard treatment with (186)Re-HEDP or (153)Sm-EDTMP.     

Effects of 153Sm-ethylenediaminetetramethylene phosphonate on physeal and articular cartilage in juvenile rabbits.

Previous studies reported that the radiopharmaceutical (153)Sm-ethylenediaminetetramethylene phosphonate ((153)Sm-EDTMP) is an effective component of multimodality therapy for the treatment of primary bone tumors. Therefore, (153)Sm-EDTMP may prove to be an integral component of therapy for the treatment of juvenile osteosarcoma. The purpose of this study was to determine the effects of intravenous administration of (153)Sm-EDTMP on the developing physeal and articular cartilage of healthy, juvenile rabbits. METHODS: Sixteen healthy 8-wk-old male New Zealand White rabbits were assigned to 1 of 2 groups: treatment (n = 12) and control (n = 4). (153)Sm-EDTMP was administered to the treatment group at 37 MBq/kg (1 mCi/kg). The animals were sacrificed at 16 wk of age, and the physeal cartilage of multiple bones was evaluated by use of histologic, immunohistochemical, and histomorphometric analyses. The overall changes in the lengths of the radius and the tibia between control and treatment groups were calculated and compared. Measurement data were combined for each group, and means +/- SEMs were determined. RESULTS: Significant differences in radial bone growth were present between the groups. Histologically, the physes of the treatment group were disrupted and chaotic in appearance. Significant differences in the immunoreactivity of type X collagen and matrix metalloproteinase-13 were seen between the groups, as these markers were positively expressed in the zone of hypertrophy of the control rabbits. CONCLUSION: Clinically significant damage to the developing physeal cartilage may occur as a result of the intravenous administration of (153)Sm-EDTMP at the dose studied.     

SPECT显像评价骨肿瘤治疗剂^153Sm—EDTMP在骨转移灶的保留率

本文报道了用１５３Ｓｍ－ＥＤＴＭＰ治疗骨转移癌３２例，用ＳＰＥＣＴ显像法动态连续观察转移灶和正常骨胳各时相的保留率，发现骨转移灶和正常骨对１５３Ｓｍ－ＥＤＴＭＰ的清除在４８小时以前有显著性差异，而在４８小时以后无显著性差异。资料又证明骨转移癌病人的尿液和１５３Ｓｍ－ＥＤＴＭＰ原液纸层析测定其Ｒｆ值是完全相同的。表明１５３Ｓｍ－ＥＤＴＭＰ以骨中清除是以原形物的方式入血，入血的１５３Ｓｍ－ＥＤＴＭＰ又被代谢活跃的转移灶再摄取，结果致转移灶的放射性活度增加，而正常骨代谢低于转移灶，再摄取的量极少，因而两者在４８小时以前有差异，而４８小时以后清除到血中的量减少，再摄取减少，故无差别     

Uptake and localization of99mTc-methylene diphosphonate in mouse osteosarcoma

The localization of^99mTc-methylene diphosphonate (^99mTc-MDP) in mouse osteosarcoma was studied using a skeletal scintigraphic method and macro- and microautoradiographic methods. On the skeletal scintigraph, the tumor showed a high uptake of^99mTc-DMP and its concentration was about 20 times as high as the value seen in the muscular tissue. The macroautoradiography showed high activity in the tumor bone region and little activity in the nonossified region. On the microautoradiography, the activity of^99mTc-MDP was localized in the mineralized matrix of tumor bone and was almost nil in the nonmineralized matrix (osteoid) and the tumor cells. These findings indicate that the mineralization of the tumor bone matrix plays an important role in^99mTc-MDP uptake in osteosarcoma.