Myelopathy from Waldenström's macroglobulinemia: improvement after Rituximab therapy

Approximately 20% of patients with Waldenström's macroglobulinemia (WM) have neurological complications; primarily peripheral neuropathies and symptoms related to a hyperviscosity syndrome. We report a rare case of a patient presenting with a slowly progressive myelopathy due to WM who had a marked response to Rituximab therapy.     

The role of complement in the mechanism of action of rituximab for B-cell lymphoma: implications for therapy

Rituximab, a genetically engineered chimeric monoclonal antibody specifically binding to CD20, was the first antibody approved by the U.S. Food and Drug Administration for the treatment of cancer. Rituximab significantly improves treatment outcome in relapsed or refractory, low-grade or follicular B-cell non-Hodgkin's lymphoma (NHL). However, there are also some challenges for us to overcome: why approximately 50% of patients are unresponsive to rituximab in spite of the expression of CD20, and why some responsive patients develop resistance to further treatment. Although the antitumor mechanisms of rituximab are not completely understood, several distinct antitumor activities of rituximab have been suspected, including complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), apoptosis, and direct growth arrest. To counteract resistance to rituximab therapy, several strategies have been developed to: (a) augment the CDC effect by increasing CD20 expression, heteroconjugating rituximab to cobra venom factor and C3b, and inhibiting membrane complement regulatory protein, especially CD59, function; (b) enhance the ADCC effect through some immunomodulatory cytokines and CR3-binding beta-glucan; and (c) reduce the apoptotic threshold or induce apoptotic signaling on the tumor. Extensive studies indicate that rituximab combined with these approaches is more effective than a single rituximab approach. Herein, the mechanism of action of and resistance to rituximab therapy in B-cell NHL, in particular, the involvement of the complement system, are extensively reviewed.     

利妥昔单抗联合二线化疗药物治疗老年人复发或难治性淋巴瘤

目的 研究利妥昔单抗联合二线化疗药物对老年人复发和难治性非霍奇金淋巴瘤(NHL)的治疗效果及安全性.方法 采用利妥昔单抗联合二线化疗药物治疗复发和难治性NHL患者12例.结果 12例共治疗38个周期,总有效(CR+PR)8例,有效率66.7%,临床收益(CR+PR+SD)11例,收益率91.3%.1年无进展生存率和总生存率分别为41.0%和50.0%.不良反应以自细胞和血小板减少最为常见,但均可耐受.结论利妥昔单抗联合二线化疗方案治疗老年人复发和难治性NHL安全有效,且能耐受.     

小剂量利妥昔单抗联合糖皮质激素治疗儿童落叶型天疱疮一例疗效观察

患儿男,9岁,头皮红斑、糜烂伴瘙痒1个月,泛发全身1周。皮损组织病理：表皮内颗粒层下方水疱形成,疱内见大量棘层松解细胞,真皮浅层小血管周围淋巴细胞及嗜酸性粒细胞浸润。直接免疫荧光检查示表皮细胞间IgG、补体C3呈网状沉积,IgM、IgA阴性。酶联免疫吸附实验检测血清抗Dsg1抗体阳性（157.00 U/ml）。诊断：落...     

含利妥昔单抗方案治疗晚期套细胞淋巴瘤临床分析

目的 探讨含利妥昔单抗化疗方案治疗晚期套细胞淋巴瘤(MCL)患者临床疗效及预后。方法 回顾性分析2011年7月至2021年7月丹东市第一医院收治的42例晚期MCL患者的临床资料,化疗方案中均包括利妥昔单抗。采用MCL国际预后指数(MIPI)评估患者预后,ECOG评分评估患者功能状态,评估治疗疗效、疾病控制率(DCR)、客观缓解率(ORR)及不良反应发生率,采用Kaplan-Meier法评估无进展生存期(PFS)及总生存期(OS),应用Cox回归对筛选的临床特征、分子病理、治疗反应以及预后因素进行分析。结果 42例患者中位发病年龄为70岁,其中男性31例、女性11例。27例接受利妥昔单抗联合CHOP方案化疗,6例接受利妥昔单抗联合苯达莫斯汀方案化疗,9例接受利妥昔单抗联合伊布替尼方案化疗。42例晚期MCL的客观缓解率为42.8%,疾病控制率为61.9%,中位OS为63个月(95%CI:50.030～75.930),中位PFS为18个月(95%CI:6.645～29.355)。皮疹和间质性肺炎为最常见的不良反应。结论 晚期MCL患者应用含利妥昔单抗方案治疗具有较好的近期疗效,不良反应可耐受...     

利妥昔单抗治疗温抗体自身免疫性溶血性贫血的疗效评价

目的评价利妥昔单抗治疗温抗体自身免疫性溶血性贫血(WAIHA)的临床疗效。方法选择2012年1月10日至2013年12月30日在我院被诊断为WAIHA的160例患者为研究对象,随机分为试验组(80例)和对照组(80例)。试验组接受375 mg/m2利妥昔单抗,1次/周,连续4周,对照组接受同等体积的生理盐水进行治疗。随访12个月后进行数据统计分析。结果试验组的完全缓解率(65%)高于对照组(35%),1年复发率(10%)低于对照组(50%),两组比较差异有统计学意义(P<0.05)。结论利妥昔单抗治疗WAIHA可以提高患者的完全缓解率,降低患者的复发率。     

美罗华治疗32例弥漫型大B细胞性非何杰金氏淋巴瘤

目的 评价美罗华治疗弥漫型大B细胞性非何杰金氏淋巴瘤DLBCL的临床效果及不良反应。方法 用同期对照的前瞻性研究方法,将68例弥漫型大B细胞性NHL患者分为研究组(美罗华组)和对照组,前组32例用CHOP方案(环磷酰胺、阿霉素、长春新碱和强的松)联合美罗华治疗;后组36例单用CHOP方案。每4周循环1个疗程,3～6疗程后作评价。将两组患者按国际淋巴瘤预后因子指数(IPI)分为中低危组和高危组,分析其疗效与预后。全部患者6个疗程后停止治疗,随访观察生存情况。结果 美罗华组完全缓解率(CR)达56.3％,总有效率87.5%;对照组分别为13.9％、63.9%,两组疗效差异有统计学意义(P<0.001)。美罗华组6、12、24、36月总的生存率分别为96.9％、87.5％、71.9％和65.6％,对照组分别为91.7％、80.6％、58.3％和41.7％(P>0.05)。美罗华组中中低危组的CR及部分缓解率(PR)分别为68.4％、26.3％,高危组分别为38.5%、38.5％(P<0.01);对照组中低危组的CR及PR分别为15.8％、68,4％,高危组则分别为11.8％、29.4％(P<0.001)。结论 美罗华联合CHOP方案治疗DLBCL的疗效显著,3年生存率高,不良反应较单纯化疗少,可作为该病目前的首选方案。