升白欣对癌症化疗或放疗后白细胞减少症的疗效

为了观察升白欣对癌症患者化疗、放疗所致的白细胞减少症的疗效，作者于１９９６年７月至８月，将化疗、放疗所致白细胞减少的６８例癌症患者，随机分成升白欣治疗组（３５例）和一般升白细胞药的对照组（３３例）。结果表明，升白欣的升白细胞有效率６０．０％，明显高于对照组的２１．２％（Ｐ＜０．０１），治疗前白细胞中位值为２．６７×１０９／Ｌ±０．７９×１０９／Ｌ，治疗后升高为４．２５×１０９／Ｌ±２．２９××１０９／Ｌ。升白欣的副反应主要为发热（３４．８％）、注射部位疼痛（６５．７％）。作者认为，升白欣治疗化疗、放疗后所致白细胞减少症是有效的，有临床应用价值。     

恶性肿瘤化疗所致白细胞减少78例的治疗分析

为了观察恶性肿瘤化疗后引致白细胞减少的治疗效果,1996年7月至9月,病理确诊恶性肿瘤患者经化疗后引致的白细胞减少78例,随机分成三组:A组G-CSF组21例,B组升白欣组28例,C组一般升白细胞治疗组29例,结果表明,G-CSF总有效率85.7％,高于升白欣组的53.6％(P<0.05),明显高于一般治疗组的24.1％(P<0.01)。在三组中,G-CSF疗效最好,升白欣则次之,一般升白细胞药的治疗效果最差。     

升白欣对化疗所致白细胞和血小板减少症的临床疗效观察

目的:观察升白欣对化疗所致的白细胞、血小板减少症的疗效。方法:升白欣50U肌肉注射,每日1次,连用5～7日。结果:用药前白细胞减少症者28例,用药后25例有效,有效率89.29％。用药前血小板减少症者21例,用药后12例有效,有效率57.14％。经统计学处理均有非常显著性差异(P<0.01)。副反应主要是发热和注射局部疼痛。结论:升白欣适用于化疗所致的白细胞、血小板均低下者,特别升血小板作用较明显,且该药用量少、价格低,易于推广应用。     

升白欣治疗化疗后白细胞减少症的疗效观察

恶性肿瘤的化学治疗导致白细胞减少症常成为化疗顺利进行的一大障碍。为此，我科自1997年8月～1998年9月对收治的各种恶性肿瘤患者化疗后进行升白欣治疗观察39例，经严格设计，统计学处理。结果表明：升白欣具有明显的升白作用，且起效快，维持时间较长。     

升白欣治疗化疗后白细胞减少症的疗效观察

恶性肿瘤的化学治疗导致白细胞减少症常成为化疗顺利进行的一大障碍，为此，我科自1997年8月－1998年9月对收治的各种恶性肿瘤患者化疗后进行升白欣治疗观察39例，经严格设计，统计学处理，结果表明：升白欣具有明显的升白作用，且起效快，维持时间较长。     

惠尔血治疗肺癌化疗所致的白细胞减少的疗效观察

目的：观察麒麟啤酒株式会社生产的基因重组人粒细胞集落刺激因子—惠尔血治疗化疗所致白细胞减少的疗效。方法：用惠尔血治疗３０ 例肺癌化疗所致的白细胞减少与用一般升白细胞中药治疗３４ 例肺癌化疗所致的白细胞减少进行了对比观察。结果：１）一般升白细胞中药和惠尔血均能使化疗后白细胞下降的患者恢复至正常范围（４×１０９／Ｌ） ，但惠尔血组白细胞回升至正常范围的时间平均４．３ 天，而一般升白细胞中药则需１０．３ 天。两组相比，差异有显著性。结论：惠尔血可明显缩短白细胞降至正常值以下的持续时间，有利于化疗的顺利进行。２） 白细胞降至Ⅲ度～Ⅳ度的患者，用惠尔血治疗比一般升白细胞中药恢复正常所用的时间短，故为争取化疗时间，在Ⅲ度～Ⅳ度白细胞下降的患者最好用粒细胞集落刺激因子—惠尔血治疗。     

瑞白与惠尔血治疗化疗后白细胞减少症的疗效比较

为比较瑞白和惠尔血治疗后白细胞减少症的疗效。对182例化疗后出现Ⅲ度骨髓抑制的患者，使用不同的升血药瑞白和惠尔血，观察造血刺激因子对白细胞升高作用及毒副作用。瑞白组与惠尔血组升高白细胞所用时间无明显差异。白细胞上升后稳定时间差异无显著性。毒副反应瑞白组和惠尔血无明显差异。瑞白相对价格低，惠尔血价格昂贵，瑞金为国产药，价格低于进口药惠尔血，可根据患者的经济条件选择用药。     

升白欣防治恶性肿瘤患者化疗所致骨髓抑制的临床效果观察

升白欣防治恶性肿瘤患者化疗所致骨髓抑制的临床效果观察修元德袁胜利于爱卿张滨于洪升刘希光丁爱萍司玉峰单方方（青岛医学院附属医院肿瘤治疗研究中心，青岛２６６００３）１９９６年６月至１９９６年８月间，我们使用长春天诚药业有限公司生产的升白欣防治恶性肿瘤患者...     

升白欣治疗化疗所致白细胞减少症的临床疗效观察

升白欣是一种国产升白新药,它是应用生物工程手段从微生物中分离出来的,具有刺激机体产生多种细胞因子、调节造血功能和免疫功能的作用。我院自1996年1月至7月,运用该药治疗因化疗所致白细胞(WBC)减少患者70例,取得了较好的效果,现报告如下: 1 材料与方法 1.1 一般资料 全组70例中,男35例,女35例,年龄17岁～78岁,平均56岁。原发肿瘤为食管癌14例,胃癌14例,肺癌11例,乳腺癌8例,肠癌5例,卵巢癌3例,非霍奇金淋巴瘤9例,前列腺癌和膀胱癌各1例,多     

瑞白与惠尔血治疗化疗后白细胞减少症的疗效比较

为比较瑞白和惠尔血治疗后白细胞减少症的疗效。对 182例化疗后出现Ⅲ度骨髓抑制的患者 ,使用不同的升血药瑞白和惠尔血 ,观察造血刺激因子对白细胞升高作用及毒副作用。瑞白组与惠尔血组升高白细胞所用时间无明显差异。白细胞上升后稳定时间差异无显著性。毒副反应瑞白组和惠尔血无明显差异。瑞白相对价格低 ,惠尔血价格昂贵。瑞白为国产药 ,价格低于进口药惠尔血 ,可根据患者的经济条件选择用药     

化疗前应用重组人粒细胞集落刺激因子预防白细胞减少

 【摘要】　目的　观察重组人粒细胞集落刺激因子（rhG-CSF）预防化疗后中性粒细胞减少症的有效性和安全性。方法　采用随机对照方法，初治恶性肿瘤患者接受1个周期的化疗，其中治疗组化疗前24 h给予rhG-CSF 150 μg皮下注射1次，对照组不给予rhG-CSF。结果　入组52例肿瘤患者，分为治疗组和对照组各26例，WBC＜4.0×109／L的发生率分别为19.23 %和53.85 %（P＜0.05），白细胞减少发生率Ⅰ度分别为7.69 %和19.23 %，Ⅱ度7.69 %和15.39 %，Ⅲ度3.85 %和1.54 %，Ⅳ度0和7.69 %； 持续时间分别为1.27 d和4.04 d（P＜0.05）；抗生素使用率分别为7.69 %和26.92 %（P＜0.05）；发热性中性粒细胞减少发生率分别为3.85 %和26.92 %（P＜0.05）。rhG-CSF的毒副作用主要为骨骼肌肉疼痛、乏力、头晕等。结论　化疗前应用rhG-CSF能有效控制肿瘤化疗后白细胞减少的发生，降低肿瘤化疗后白细胞减少的程度。     

Adjuvant chemotherapy (CMF) for breast carcinoma: hematological side effects

Seventy-five patients accepted postmastectomy adjuvant CMF chemotherapy for stage II and III carcinoma of the breast. All patients, irrespective of age, were started on the same drug dosages. About 42% of the patients had leukopenia during the first two cycles; this rate was similar for patients who dropped out of the program early and those who stayed on for six or more months. Patients who developed leukopenia early are more likely to receive less than 65% of mean total CMF dosages (MTD). Otherwise, 30% of patients that never had leukopenia or had leukopenia that appeared late received more than 85% of the prescribed CMF. In our series, postmenopausal patients did not have more problem with leukopenia than premenopausal patients (thrombocytopenia occurred rarely in both groups). Among the 58 patients who had CMF for 6 months or longer, 79% had less than 85% MTD or CMF. The dosages had to be reduced for drug-related and other reasons, and leukopenia only accounted for 22% of patients who had reduced CMF dosages.     

rhG-CSF治疗30例肺癌化疗所致的白细胞减少症疗效观察

目的 :观察基因重组人粒细胞集落刺激因子 (rhG CSF ,特尔津 )对肺癌化疗所致的白细胞减少症的疗效。方法 :用rhG CSF治疗 3 0例肺癌化疗所致的白细胞减少患者 ,随机与用其他口服升白细胞药物治疗 3 0例肺癌化疗所致的白细胞减少患者 ,进行对比观察。结果 :rhG CSF和其他口服升白细胞药均能使化疗后白细胞减少症患者的白细胞数恢复至正常范围 ( 4× 10 9/L) ,但rhG -CSF组白细胞数回升至正常的时间比其他口服升白细胞药物组明显缩短 (P <0 0 0 2 ) ,且其继发性感染发生率明显降低 (P =0 0 2 99)。结论 :rhG CSF可有效治疗化疗所致的白细胞减少症 ,并能减少继发性感染机会 ,有利于化疗顺利完成     

咖啡酸治疗伊马替尼致慢性粒细胞白血病患者血小板、白细胞减少的临床观察

 【摘要】　目的　观察咖啡酸（CFA）对伊马替尼致慢性粒细胞白血病（CML）患者血小板、白细胞减少的临床疗效和患者不良反应。方法　对42例应用伊马替尼治疗后出现血小板、白细胞减少的CML患者,血小板和（或）白细胞减少时即开始应用CFA,0.2 g／次,3次／d,口服,观察治疗过程中血小板、白细胞变化情况和患者不良反应。结果　治疗血小板减少42例,其中显效21例,良效13例,无效8例,总有效率81.0 %（34／42）;治疗白细胞减少28例,其中显效15例,良效8例,无效5例,总有效率82.1 %（23／28）;治疗第2周时血小板、白细胞计数与治疗前相比差异有统计学意义（t＝2.015,P＝0.023;t＝1.913,P＝0.035 ）;CFA治疗有效患者的平均起效时间为2周。未发现治疗相关不良反应。结论　CFA治疗伊马替尼所致的CML患者血小板、白细胞减少疗效确切,无明显不良反应,是CML治疗过程中安全有效的辅助治疗药物。     

化疗诱导的白细胞减少症可预测小细胞肺癌生存

  目的  化疗是小细胞肺癌的标准治疗方式,而白细胞减少症是其常见的不良反应。本文研究旨在评估化疗诱导的白细胞减少症是否可作为预测小细胞肺癌患者疗效及生存的指标。  方法  回顾性分析了445例接受4~10个周期标准化疗的小细胞肺癌患者的病例资料,按照WHO标准将白细胞减少症分为无白细胞减少症(0级)、轻度(1~2级)及重度白细胞减少症(3~4级)。主要研究终点为总生存时间。  结果  化疗诱导的白细胞减少症与总生存时间之间明显相关,轻度白细胞减少的患者有较长的总生存期。轻度白细胞减少症的死亡危险比为0.687(95%CI:0.506~0.943),而重度白细胞减少症的死亡危险比为0.901(95%CI:0.669~1.214)。无白细胞减少的患者的中位生存时间为13个月、轻度与重度白细胞减少症的中位生存时间分别为17个月和14个月。  结论  小细胞肺癌患者化疗过程中诱发的白细胞减少程度与患者生存有关,轻度白细胞减少的患者有较长的总生存时间。      

Determinants of Myelosuppression in the Treatment of Non-small Cell Lung Cancer with Cisplatin-containing Chemotherapy

Data on 16 potential risk factors for myelosuppression were assessed in 134 patients who received either vindesine and cisplatin (VP) or mitomycin C, vindesine and cisplatin (MVP) for inoperable stage III or IV non-small cell lung cancer in a randomized trial. Determinant factors for myelosuppression were evaluated by using univariate analysis and the logistic regression model. Recursive partitioning and amalgamation (RPA) was also used to define patient subgroups frequently suffering from severe bone marrow toxicity. Overall, 33 (25%) of 134 patients experienced at least one episode of grade 4 leukopenia. In univariate analysis, age, body surface area, serum creatinine, and pretreatment hemoglobin concentration were associated with severe leukopenia. A multivariate analysis using the logistic regression method showed that only raised creatinine level was an independent predictor for grade 4 leukopenia ( P =0.049). The RPA model generated three distinct subgroups based on age, body surface area and regimen. The three subgroups were distinguished by the frequency of severe (grade 4) leukopenia (50%, 25%, and 2.4%, respectively) ( P <0.001). Grade 4 leukopenia occurred more frequently in patients in class 3 (age ≥65 years and treatment with MVP). The RPA model was useful in identifying the risk factors for myelosuppression induced by cisplatin-based chemotherapy, and in defining patient subgroups with elevated risk of toxicity.     

Association of genetic polymorphisms in SLCO1B3 and ABCC2 with docetaxel-induced leukopenia

Despite long-term clinical experience with docetaxel, unpredictable severe adverse reactions remain an important determinant for limiting the use of the drug. To identify a genetic factor(s) determining the risk of docetaxel-induced leukopenia/neutropenia, we selected subjects who received docetaxel chemotherapy from samples recruited at BioBank Japan, and conducted a case–control association study. We genotyped 84 patients, 28 patients with grade 3 or 4 leukopenia/neutropenia, and 56 with no toxicity (patients with grade 1 or 2 were excluded), for a total of 79 single nucleotide polymorphisms (SNPs) in seven genes possibly involved in the metabolism or transport of this drug: CYP3A4 , CYP3A5 , ABCB1 , ABCC2 , SLCO1B3 , NR1I2 , and NR1I3 . Since one SNP in ABCB1 , four SNPs in ABCC2 , four SNPs in SLCO1B3 , and one SNP in NR1I2 showed a possible association with the grade 3 leukopenia/neutropenia ( P -value of <0.05), we further examined these 10 SNPs using 29 additionally obtained patients, 11 patients with grade 3/4 leukopenia/neutropenia, and 18 with no toxicity. The combined analysis indicated a significant association of rs12762549 in ABCC2 ( P  = 0.00022) and rs11045585 in SLCO1B3 ( P  = 0.00017) with docetaxel-induced leukopenia/neutropenia. When patients were classified into three groups by the scoring system based on the genotypes of these two SNPs, patients with a score of 1 or 2 were shown to have a significantly higher risk of docetaxel-induced leukopenia/neutropenia as compared to those with a score of 0 ( P  = 0.0000057; odds ratio [OR], 7.00; 95% CI [confidence interval], 2.95–16.59). This prediction system correctly classified 69.2% of severe leukopenia/neutropenia and 75.7% of non-leukopenia/neutropenia into the respective categories, indicating that SNPs in ABCC2 and SLCO1B3 may predict the risk of leukopenia/neutropenia induced by docetaxel chemotherapy. ( Cancer Sci 2008; 99: 967–972)     

Surgical resection deteriorates gemcitabine-induced leukopenia in pancreatic cancer

Background Gemcitabine hydrochloride (GEM) is one of the most effective chemotherapeutic agents for pancreatic cancer; however, factors affecting GEM-induced leukopenia have not been clarified yet. In the present study, we analyzed the relationship between patients backgrounds and GEM-induced leukopenia.Methods Thirty-eight patients with pancreatic cancer were analyzed for correlation between the dose of GEM and the blood leukocyte number. Moreover, we compared leukopenia in resected and non-resected patients.Results The incidence of grade 3 or 4 leukopenia was 25% in the non-resected patients, whereas equivalent leukopenia was observed in 57% of the resected patients (P = 0.048 by the ² test). The relative decrease in blood leukocytes induced by GEM administration was more severe in resected patients (41.3 ± 9.9%), as compared to non-resected patients (52.6 ± 16.0%; P = 0.023 by t-test).Conclusion In the present study, we found that the administration of GEM to patients after surgical resection caused more severe leukopenia, as compared to findings in non-resected patients. These data suggested that more frequent monitoring of the leukocyte count and prolonged intervals between GEM administrations are necessary for resected patients with pancreatic cancer.