目的:观察地榆升白片对非小细胞肺癌化疗后外周血细胞的影响，以了解地榆生白片对骨髓的保护作用。方法:将63例非小细胞肺癌患者随机分为观察组和对照组。观察组（33例）采用地榆升白片加NP方案治疗，对照组（30例）单用NP方案化疗，观察两组外周血象变化情况及集落刺激因子(G-CSF)用量。结果:观察组Ⅲ度及Ⅳ度骨髓抑制发生率9.09％，显著低于对照组（对照组为30.0%，χ2=4.467，Plt;0.05）；观察组外周血WBC、PLT、Hb治疗结束后1月与治疗前相比，差异无统计学意义，Pgt;0.05；对照组外周血WBC、PLT、Hb治疗结束后1月较治疗前明显下降，其中WBC、PLT差异有统计学意义，Plt;0.05。观察组和对照组人均集落刺激因子（惠尔血150 μg）用量分别为（0.58±1.99）支和（1.93±3.62）支差异有统计学意义(t=2.501，Plt;0.05)。结论:地榆升白片可预防肺癌患者化疗药物引起的骨髓抑制，提高外周血WBC和PLT水平，减少集落刺激因子的用量，值得推广。
目的 观察消化道肿瘤患者服用甲羟孕酮（medroxyprogesterone acetate, MPA）对化疗后骨髓抑制的影响。 方法 2008年11月-2009年8月，将接受化疗的消化道肿瘤患者共100例随机分为治疗组(MPA加化疗组，54例)及对照组(单纯化疗组，46例)，2周期化疗后评价骨髓抑制状况和生活质量变化。 结果 治疗组和对照组化疗后白细胞、血红蛋白和血小板Ⅰ~Ⅱ度骨髓抑制发生率没有差异（Pgt;0.05），但治疗组Ⅲ~Ⅳ度骨髓抑制发生率低于对照组，KPS评分改善率高于对照组（Plt;0.05）。未见明显不良反应。 结论 MPA可有效减轻化疗后骨髓抑制。
ObjectiveTo suggest the importance of taking notice of oral chemotherapy drugs in cancer patients, and the importance of drug-use evaluation in patients with insufficient kidney functions, by reporting one death case caused by multiple organ failure because of myelosuppression after oral tegafur, gimeracil and oteracil potassium (S-1) capsules for 10 days in a patient with insufficient kidney functions. MethodsThrough the analysis of one patient who died of multiple organ failure due to degree-Ⅳ myelosuppression and the related literature review, we discussed the necessity of individualized administration of clinical chemotherapy. ResultsThe patient had grade-Ⅱ renal insufficiency before chemotherapy and did not undergo dihydropyrimidine dehydrogenase (DPYD) gene test. Myelosuppression occurred 10 days after oral chemotherapy drugs. The white blood cells, neutrophils and platelets decreased progressively, and then developed into degree-Ⅳ suppression. Finally the patient died of multiple organ failure. Conclusions Genetic variation and renal insufficiency may cause differences in drug metabolism. The reduced urinary excretion of guimet pyrimidine (CDHP), the inhibitors of dihydropyrimidine dehydrogenase which is the 5-fluorouracil (5-FU) metabolic enzyme, may lead to elevated plasma concentration of 5-FU, thereby increasing myelosuppression and other adverse reactions. If DPYD gene detection results show low enzyme activity, it can cause lethal toxicity through deceleration of 5-FU metabolism and high concentration of blood. DPYD gene dzetection should be performed if allowed, and individualized treatment plan should be formulated after comprehensive evaluation. The overall situation of the patients should be considered before treatment, and then individualized drugs should be administered.