二膦酸盐相关性颌骨坏死

二膦酸盐相关性JON是二膦酸盐的一个严重并发症,有关的报道愈来愈多,已引起l临床医师的高度重视,但其病因、发病机制、临床表现和如何进行治疗、预防等尚未有统一的标准,本文就此作一综述。     

唑来膦酸治疗既往用过双膦酸盐的实体瘤骨痛的疗效观察

目的评价唑来膦酸治疗既往用过双膦酸盐的实体瘤骨转移患者骨疼痛的缓解效果和安全性。方法唑来膦酸4mg静脉注射〉15min，1次／4周，治疗既往用过和未用过双膦酸盐的骨转移实体瘤患者，记录疼痛评分，东方协作肿瘤组织（ECOG）体力状态评分和不良反应，每次用药前检测血肌酐水平。结果疼痛评分较基线下降，ECOG体力状态评分保持稳定。51例患者中，既往用过双膦酸盐28例（54．9％）。发热、乏力和恶心是最常见的不良反应，血清肌酐值无明显升高，在既往用过与未用过双膦酸盐患者间不良反应发生率无统计学意义。结论既往用过双膦酸盐静脉注射治疗的实体瘤骨转移患者，可安全的给予唑来膦酸治疗。     

双膦酸盐类药物的临床应用进展

自从1969年Fleisch报道了双膦酸盐类化合物可作用于羟基磷灰石结晶的过程，在体内、体外均具有抑制骨重吸收作用以来，至今人类已合成出双膦酸盐类化合物约300多个（不计盐及多晶型物），并有多个产品上市。是国际上药物研究的热点之一。双膦酸盐是人工合成的一类焦磷酸类似物，是近20a来发展起来的抗代谢性骨病的一类新药。主要用于治疗骨质疏松症，变形性骨炎和恶性肿瘤引起的高钙血症和骨痛症等。本文拟就双膦酸盐药物近年来的临床研究及应用进展作一简要综述。     

多发性骨髓瘤使用双磷酸盐引起颌骨坏死的探讨与护理

目的探讨双膦酸盐相关颌骨坏死的危险因素、发生率、预防、治疗和护理。方法报道2例多发性骨髓瘤（MM）患者使用双磷酸盐致颌骨坏死的临床表现、治疗经过及护理,分析其发病的危险因素、预防措施、治疗策略及护理。结果2例确诊MM患者,在联合化疗加沙利度胺的基础上,分别于使用帕米磷酸二钠治疗12个月和50个月后出现右上颌及左下颌颌骨坏死（ONJ）,1例患者发病前有拔牙史。经停用双磷酸盐,全身使用抗生素并醋酸氯已定漱口,脓肿治愈。结论静脉应用双膦酸盐可以延缓骨相关并发症,但是应该重视其应用后产生的颌骨坏死等副作用以及加强口腔护理。     

双磷酸盐相关性颌骨坏死影像学研究进展

双磷酸盐是破骨细胞抑制剂,广泛应用于治疗癌症患者骨转移,但近来有患者接受双磷酸盐类药物治疗后发生颌骨坏死的报道.本文就双磷酸盐相关性颌骨坏死的发病机制、临床表现和影像学表现做一综述.     

双膦酸盐类药物对慢性肾脏病患者血管钙化疗效的Meta分析

目的 系统评价双膦酸盐对慢性肾脏病(chronic kidney disease,CKD)患者血管钙化的影响.方法 检索PubMed、Embase、Cochrane图书馆、中国知网和万方数据库,时间从建库到2020年9月,纳入了双膦酸盐治疗慢性肾脏病患者血管钙化相关的随机对照试验(randomized controll...     

双膦酸盐治疗原发性骨质疏松症的研究进展

骨质疏松症是一种全身代谢性疾病,双膦酸盐已被证实在提高骨密度和降低骨折风险方面有显著疗效,是目前临床上治疗骨质疏松症的一线药物.本文将从几种常见双膦酸盐的作用机制、临床疗效、不良反应以及药物假期等方面展开综述,以期为临床用药选择提供参考.     

~(89)Sr、双膦酸盐及二者联合治疗肿瘤多发性骨转移的系统评价

目的系统分析~(89)Sr、双膦酸盐及~(89)Sr联合双膦酸盐(联合用药)治疗肿瘤多发性骨转移的疗效,并进行Meta分析。方法检索MEDLINE、EMBASE、The Cochrane Library、CBMdisc、CNKI,同时手检《同位素》、《肿瘤》、《中华核医学与分子影像杂志》、《中华放射肿瘤学杂志》,纳入对比分析~(89)Sr、双膦酸盐、联合用药治疗肿瘤多发性骨转移疗效的临床研究。对纳入研究进行质量评价,并应用Rev Man 5.0软件进行Meta分析。结果纳入随机对照研究7篇,半随机对照研究1篇,非随机对照研究7篇,共1 196例患者。Meta分析显示,联合用药治疗肿瘤多发性骨转移患者与分别单独使用89Sr或双膦酸盐相比,在缓解疼痛、提高患者生活质量和减少/缩小骨转移灶方面的差异有统计学意义(P0.01)。结论联合用药可更有效地缓解疼痛,提高患者生活质量和减少/缩小转移灶。     

99锝-亚甲基双膦酸盐联合钙剂治疗乳腺癌术后骨质疏松症疗效观察

目的 观察99锝-亚甲基双膦酸盐联合碳酸钙D3及活性维生素D3治疗乳腺癌术后骨质疏松症的疗效和安全性.方法 乳腺癌术后骨质疏松症患者130例均给予99锝-亚甲基双膦酸盐+碳酸钙D3+活性维生素D3治疗,比较治疗前及治疗1 a后患者骨密度值及血清钙、磷、碱性磷酸酶、骨钙素、Ⅰ型胶原交联羧基末端肽、1,25-二羟维生素D3等水平变化.结果 治疗后腰椎(L1-4)及左髋股骨颈、大转子及小转子骨密度均较治疗前增加(P＜0.05);血清骨钙素水平较治疗前增高(P＜0.05),Ⅰ型胶原交联羧基末端肽较治疗前下降(P＜0.05);血清钙、磷、碱性磷酸酶及1,25-二羟维生素D3水平与治疗前比较差异无统计学意义(P＞0.05).结论 39锝-亚甲基双膦酸盐联合碳酸钙D3及活性维生素D3治疗乳腺癌术后骨质疏松症疗效满意.     

99锝-亚甲基双膦酸盐联合钙剂治疗乳腺癌术后骨质疏松症疗效观察

目的观察99锝-亚甲基双膦酸盐联合碳酸钙D3及活性维生素D3治疗乳腺癌术后骨质疏松症的疗效和安全性。方法乳腺癌术后骨质疏松症患者130例均给予99锝-亚甲基双膦酸盐+碳酸钙D3+活性维生素D3治疗,比较治疗前及治疗1a后患者骨密度值及血清钙、磷、碱性磷酸酶、骨钙素、Ⅰ型胶原交联羧基末端肽、1,25-二羟维生素D3等水平变化。结果治疗后腰椎(L1-4)及左髋股骨颈、大转子及小转子骨密度均较治疗前增加(P<0.05);血清骨钙素水平较治疗前增高(P<0.05),Ⅰ型胶原交联羧基末端肽较治疗前下降(P<0.05);血清钙、磷、碱性磷酸酶及1,25-二羟维生素D3水平与治疗前比较差异无统计学意义(P>0.05)。结论 99锝-亚甲基双膦酸盐联合碳酸钙D3及活性维生素D3治疗乳腺癌术后骨质疏松症疗效满意。     

潜水致减压性骨坏死1例

患者男,56岁.潜水工龄32年,潜水深度一般为 10~45 m,水下作业时间>32 h/年,2001年5月潜水40 m左右,潜水约3 h,未自行减压直接出水,出水后全身麻木,四肢活动障碍,下肢活动困难.医院诊断为急性减压病.之后患者自感乏力,继而出现双下肢麻木,双侧关节活动受限.2002年7月,在当地医院行X线检查显示双股骨远端不规则高密度阴影,双股骨近端不规则囊状低密度阴影,疑为减压性骨坏死.     

Bisphosphonate‐related osteonecrosis of the jaw: data from the French national pharmacovigilance database

The aim of this study was to describe bisphosphonate‐related osteonecrosis of the jaw (BRONJ) in the French national pharmacovigilance database. BRONJ was identified with the standardized MedDRA query (SMQ) ‘osteonecrosis’ among all data from 1985 to 31 December 2014. Because this SMQ was not specific to the jaw localization, selection of cases based on anatomy was performed after data extraction. For each case, demographic and medical information was analysed, as well as data about notification (year of notification, year of occurrence, outcome, seriousness). Known associated factors for BRONJ were also documented: dentoalveolar surgery, glucocorticoids, chemotherapy, anti‐angiogenics, denosumab. Among 1404 SMQ notifications, 663 were located in the jaws and 629 were associated with bisphosphonate use. BRONJ reported in the database mainly affected women (n = 443, 71%) with an oncological indication (n = 440, 70%). BRONJ was considered as serious in 91%. Outcome was unfavourable for 92% of cases. Associated factors were identified for 70% of the patients. A peak of notification was noted in 2014 (13% of all cases), but on analysis by year of occurrence instead of by year of notification, this peak disappeared. SMQ ‘osteonecrosis’ appears to be an adequate tool to analyse BRONJ in a pharmacovigilance database.     

Bisphosphonates-associated osteonecrosis of the jaw: review on reported cases

Osteonecrosis of the jaws associated with the use of bisphosphonates (alendronate, pamidronate, risedronate et zoledronate) are described as an avascular necrosis. We have listed 184 cases of bisphosphonates-associated osteonecrosis of the maxillary in the literature. Many mechanisms are discussed in bisphosphonates-associated osteonecrosis: a disturbing bone turnover, an accumulation of bone's microdamage or an antiangiogenic effect. Other risk factors seem however to be involved: cancer, chemotherapy, glucocorticoids, infection and renal insufficiency.     

Prevalence of bisphosphonate associated osteonecrosis of the jaw within the field of osteonecrosis

Objectives Prevalence of bisphosphonate-associated osteonecrosis of the jaws within the catchment area of a university hospital maxillofacial unit and to review the outcome of treatment. Methods In a retrospective study, all patients with osteonecrosis, osteomyelitis and osteoradionecrosis treated in the period from January 2000 to March 2005 in the department for Maxillo Facial Surgery at the University of Mainz, Germany were analysed. Results Forty percent of the patients are grouped to odontogenic or surgically induced osteomyelitis. The second largest group (28%) were patients with osteoradionecrosis (ORN). Ten percent of all patients developed an osteonecrosis after treatment with bisphosphonates (BOJ). Eight percent showed osteomyelitis or sequester due to a trauma while 14% of all patients had osteomyelitis of unknown origin. All BOJ patients took bisphosphonates because of metastatic diseases of the bone (plasmocytoma, mamma carcinoma and prostate cancer) for up to 5 years. All had been administered a nitrogen-containing bisphosphonate (either pamidronat or zoledronat). Thirteen out of the 17 patients with BOJ and 14 of the 45 with ORN reported a possible trigger like previous tooth extraction, pressure denture sore or periodontal diseases. Conclusion These findings support the association of bisphosphonate therapy and osteonecrosis of the jaw. The importance of this new disease is characterised by the growing number of patients. The role of dental trigger factors and the poor surgical outcome both seem to justify a prophylactic dental care concept in high-risk patients.     

A probable case of oral bisphosphonate-associated osteonecrosis of the jaw and recovery with parathyroid hormone treatment

Introduction: Bisphosphonates are effective for treating osteoporosis, Paget's disease of bone, and malignancy-associated bone diseases. Bisphosphonate-associated osteonecrosis of the jaw (ONJ) is a rare but serious adverse effect of bisphosphonate therapy. Due to inhibitory actions on bone turnover, bisphosphonate therapy may result in the accumulation of microdamage.Case summary: A 74-year-old Korean woman (height, 150 cm; weight, 51 kg) was referred to the Department of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon, South Korea, for evaluation of pain and persistent abnormal exposure of jaw bone after extraction of teeth. She had been receiving weekly oral alendronate treatment for osteoporosis for ~5 years. The patient had the clinical features of bisphosphonate-associated osteonecrosis of the mandible, which was precipitated by teeth extraction ~14 months prior to the outpatient referral visit. At her clinical baseline visit, serum hormone concentrations and bone turnover markers were as follows: thyroid-stimulating hormone, 0.88 μIU/mL (reference range, 0.25-5.00 μIU/mL); 25-hydroxyvitamin D₃, 20.9 (9.0-37.6) ng/mL; parathyroid hormone (PTH), 57 (11-62) pg/mL; serum osteocalcin, 8.7 (12.9-55.9) ng/mL; and urine N-telopeptide 21 (26-124) nM/mM creatinine. She had multiple systemic risk factors for ONJ, including older age, type 2 diabetes mellitus, and long duration of bisphosphonate therapy. There was no mandibular lesion improvement despite repeated surgical procedures performed within a 14-month period. Bisphosphonate therapy was discontinued and PTH therapy was started. After 2 months, exposed oral mucosa had healed. After 4 months of treatment, the pain had completely subsided, and after 6 months the patient's eating and drinking habits returned. The serum concentration of osteocalcin, a bone formation marker, which was initially suppressed (8.7 ng/mL), increased 174% (15.1 ng/mL) from baseline after 6 months of treatment with PTH.Conclusions: Here we report a probable case of oral bisphosphonate-associated ONJ featuring suppressed bone turnover. Treatment with the bone formation-stimulating agent PTH was beneficial.     

Bisphosphonate-related osteonecrosis of the jaw in cancer patients: Implications for nurses

PurposeThis paper reports a review of the literature with a specific focus on osteonecrosis of the jaw. Bisphosphonate drugs are commonly used in the treatment of bone disease secondary to myeloma and solid tumours, such as breast and prostate cancer. In the past few years, an uncommon but distressing condition known as osteonecrosis of the jaw (ONJ) has been detected in patients who are having bisphosphonate treatment, particularly the intravenous (IV) preparations. Osteonecrosis of the jaw results from bone exposure in the oral cavity with subsequent death of bone tissue (necrosis).MethodThe review searched key databases including Medline, British Nursing Index, Cochrane, and meeting abstracts to ascertain the extent of literature in this field.ResultsFourty-two articles were reviewed which described the clinical manifestations of ONJ, the reported incidence and clinical cases.ConclusionThe results indicate there is an emerging body of evidence in this field and nurses delivering bisphosphonates need to familiarise themselves with the current guidance to ensure risks are minimised for patients.