骨相关性浆细胞瘤的临床特征及其影响因素分析
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摘要
目的分析骨相关性浆细胞瘤(BRP)的临床特征及其影响因素。方法收集229例多发性骨髓瘤(MM)患者的临床资料,包括基本临床特征、临床检验检查结果。根据影像学检查结果将患者分为BRP组(n=40)和普通MM组(n=189)。分析BRP组和普通MM组患者的临床特征,以及MM患者发生BRP的影响因素。结果BRP组和普通MM组患者的Durie-Salmon(DS)分期和国际分期体系(ISS)分期比较,差异均有统计学意义(P﹤0.05)。普通MM组和BRP组患者的β-胶原降解产物(β-CTX)、红细胞沉降率(ESR)、血尿素氮(BUN)、肌酐(Cr)、尿酸(UA)水平比较,差异均有统计学意义(P﹤0.05)。多因素Logistic回归分析结果显示,β-CTX升高是MM患者发生BRP的独立保护因素(P﹤0.05,OR=0.050)。结论β-CTX升高可作为MM患者发生BRP的独立保护因素。
Objective To explore the clinical features of bone-related plasmacytoma(BRP) and to investigate the influence factors. Method The clinical data of 229 patients with multiple myeloma(MM) were collected, including general data and clinical laboratory test results. According to the characteristics of imaging, subjects were divided as BRP group(n=40) and common MM group(n=189). The clinical features of BRP group and common MM group patients were analyzed, besides, the factors influencing the occurrence of BRP in MM patients were investigated. Result The DurieSalmon(DS) stage and International Staging System(ISS) stage in BRP group and common MM group differed significantly(P<0.05). Evident differences were noted regarding the β-collagen degradation product(β-CTX), erythrocyte sedimentation rate(ESR), blood urea nitrogen(BUN), creatinine(Cr), and uric acid(UA) level between common MM group and BRP group patients, showing statistically significant differences(P<0.05). Multivariate logistic regression analysis showed that incresed β-CTX was an independent protective factor in the development of BRP among MM patients(OR=0.050, P<0.05). Conclusion Increased β-CTX can be an independent protective factor for the occurrence of BRP in MM patients.
Objective To explore the clinical features of bone-related plasmacytoma(BRP) and to investigate the influence factors. Method The clinical data of 229 patients with multiple myeloma(MM) were collected, including general data and clinical laboratory test results. According to the characteristics of imaging, subjects were divided as BRP group(n=40) and common MM group(n=189). The clinical features of BRP group and common MM group patients were analyzed, besides, the factors influencing the occurrence of BRP in MM patients were investigated. Result The DurieSalmon(DS) stage and International Staging System(ISS) stage in BRP group and common MM group differed significantly(P<0.05). Evident differences were noted regarding the β-collagen degradation product(β-CTX), erythrocyte sedimentation rate(ESR), blood urea nitrogen(BUN), creatinine(Cr), and uric acid(UA) level between common MM group and BRP group patients, showing statistically significant differences(P<0.05). Multivariate logistic regression analysis showed that incresed β-CTX was an independent protective factor in the development of BRP among MM patients(OR=0.050, P<0.05). Conclusion Increased β-CTX can be an independent protective factor for the occurrence of BRP in MM patients.
引文
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[24]王晶,耿爽,钟玉萍,等.髓外浆细胞瘤循环浆细胞的检测[J].中华血液学杂志, 2016, 37(4):337-339.
[25]张文娟,景红梅,克晓燕,等. 12例骨孤立性浆细胞瘤的临床特点与预后回顾性分析[J].中国癌症杂志, 2008, 18(12):933-936.
[2] Touzeau C, Moreau P. How I treat extramedullary myeloma[J]. Blood, 2016, 127(8):971-976.
[3] Rajkumar SV, Dimopoulos MA, Palumbo A, et al. International Myeloma Working Group updated criteria for the diagnosis of multiple myeloma[J]. Lancet Oncol, 2014, 15(12):e538-e548.
[4] BladéJ, Lust JA, Kyle RA. Immunoglobulin D multiple myeloma:presenting features, response to therapy, and survival in a series of 53 cases[J]. J Clin Oncol, 1994, 12(11):2398-2404.
[5] Wu P, Davies FE, Boyd K, et al. The impact of extramedullary disease at presentation on the outcome of myeloma[J].Leuk Lymphoma, 2009, 50(2):230-235.
[6] Usmani SZ, Heuck C, Mitchell A, et al. Extramedullary disease portends poor prognosis in multiple myeloma and is over-represented in high-risk disease even in the era of novel agents[J]. Haematologica, 2012, 97(11):1761-1767.
[7] Varga C, Xie W, Laubach J, et al. Development of extramedullary myeloma in the era of novel agents:no evidence of increased risk with lenalidomide-bortezomib combinations[J]. Br J Haematol, 2015, 169(6):843-850.
[8] BladéJ, Fernández de Larrea C, Rosi?ol L, et al. Soft-tissue plasmacytomas in multiple myeloma:incidence, mechanisms of extramedullary spread, and treatment approach[J].J Clin Oncol, 2011, 29(28):3805-3812.
[9]陈海飞,傅卫军,王东星,等. 40例多发性骨髓瘤伴髓外病变患者的临床特征分析[J].中华血液学杂志, 2007, 28(10):655-658.
[10] Kyle RA, Gertz MA, Witzig TE, et al. Review of 1027 patients with newly diagnosed multiple myeloma[J]. Mayo Clin Proc, 2003, 78(1):21-33.
[11] Booth SL, Centi A, Smith SR, Gundberg C. The role of osteocalcin in human glucose metabolism:marker or mediator[J]. Nat Rev Endocrinol, 2013, 9(1):43-55.
[12] Zoch ML, Clemens TL, Riddle RC. New insights into the biology of osteocalcin[J]. Bone, 2016, 82:42-49.
[13] Bataille R, Chappard D, Marcelli C, et al. Recruitment of new osteoblasts and osteoclasts is the earliest critical event in the pathogenesis of human multiple myeloma[J].J Clin Invest, 1991, 88(1):62-66.
[14] Jakob C, Sterz J, Liebisch P, et al. Incorporation of the bone marker carboxy-terminal telopeptide of type-1 collagen improves prognostic information of the International Staging System in newly diagnosed symptomatic multiple myeloma[J]. Leukemia, 2008, 22(9):1767-1772.
[15] Weinstock M, Ghobrial IM. Extramedullary multiple myeloma[J]. Leuk Lymphoma, 2013, 54(6):1135-1141.
[16] Goulard M, Dosquet C, Bonnet D. Role of the microenvironment in myeloid malignancies[J]. Cell Mol Life Sci,2018, 75(8):1377-1391.
[17] Alsayed Y, Ngo H, Runnels J, et al. Mechanisms of regulation of CXCR4/SDF-1(CXCL12)-dependent migration and homing in multiple myeloma[J]. Blood, 2007, 109(7):2708-2717.
[18] Zhang Y, Moschetta M, Huynh D, et al. Pyk2 promotes tumor progression in multiple myeloma[J]. Blood, 2014, 124(17):2675-2686.
[19] Billecke L, Penas EM, May AM, et al. Similar incidences of TP53 deletions in extramedullary organ infiltrations,soft tissue and osteolyses of patients with multiple myeloma[J]. Anticancer Res, 2012, 32(5):2031-2034.
[20] Charles JF, Aliprantis AO. Osteoclasts:more than‘bone eaters’[J]. Trends Mol Med, 2014, 20(8):449-459.
[21] An G, Acharya C, Feng X, et al. Osteoclasts promote immune suppressive microenvironment in multiple myeloma:therapeutic implication[J]. Blood, 2016, 128(12):1590-1603.
[22] Thiele B, Kloster M, Alawi M, et al. Next-generation sequencing of peripheral B-lineage cells pinpoints the circulating clonotypic cell pool in multiple myeloma[J]. Blood,2014, 123(23):3618-3621.
[23] Vij R, Mazumder A, Klinger M, et al. Deep sequencing reveals myeloma cells in peripheral blood in majority of multiple myeloma patients[J]. Clin Lymphoma Myeloma Leuk, 2014, 14(2):131-139.e1.
[24]王晶,耿爽,钟玉萍,等.髓外浆细胞瘤循环浆细胞的检测[J].中华血液学杂志, 2016, 37(4):337-339.
[25]张文娟,景红梅,克晓燕,等. 12例骨孤立性浆细胞瘤的临床特点与预后回顾性分析[J].中国癌症杂志, 2008, 18(12):933-936.