亚叶酸钙片（CF）／5—FU治疗消化道肿瘤的人体耐受性临床研究

目的：探讨在持续静脉滴注5－FU时,口服CF片增效方案中人体对5－FU的耐受性及毒性反应。方法：对确诊为消化道肿瘤的20例患者,在静滴和口服恒定剂量CF,同时采用逐级增加持续灌注5－FU剂量,逐级增加至患者出现较明显的毒性。结果：主要的不良反应为静脉炎、口腔炎、恶性呕吐、腹痛、腹泻、便秘、骨髓抑制。口腔炎、腹泻为剂量限制性毒性。少见的不良反应为头痛、失眠、肝肾损害。结论：5－FU持续静脉滴注并分次口服CF的增效方案中,消化道肿瘤患者的人体最大耐受剂量（MTD）持续灌注5－FU为4．0g/m^2的剂量。剂量限制性毒性为口腔炎、腹泻,推荐临床使用本方案中持续滴注5－FU的剂量为3．75g/m^2.     

血液病粒细胞缺乏症并发肺结核的研究

血液病粒细胞缺乏症并发肺结核的研究张怀国，王慧，管剑龙，王冠利，管霞，刘洪瑞（临沂地区人民医院内科）（临沂市第一人民医院付庄分院）关键词白血病；粒细胞缺乏症；结核病某些血液病常需接受大剂量化疗、放疗等，因而易引起粒细胞缺乏症，此时病人易患各种感染，但...     

老年人粒细胞缺乏症3例报告并文献复习

报告3例老年人药物所致的粒细胞缺乏症患者应用重组人粒细胞—巨噬细胞集落刺激因子(rhGM-CSF)治疗情况、并就其疗效、剂量、副作用及注意事项等问题结合文献进行了讨论。     

他巴唑致粒细胞缺乏症14例的临床观察及护理

他巴唑是治疗甲状腺功能亢进症的主要药物之一。然而,该药可引起粒细胞缺乏症的严重不良反应。据统计,在甲状腺功能亢进症服用他巴唑的过程中,粒细胞缺乏症的突发率为0.1%~0.8%[1]。其发生机制可能与药物对骨髓造血系统的直接损害、破坏定向干细胞和初级干细胞而致粒细胞缺乏,并与血液或骨髓储存的成熟粒细胞破坏有关[2],也可能与自身免疫有关[3]。如不及时处理,会增加病人的感染机会,甚至因败血症而引起死亡[4]。粒细胞缺乏症的首发症状中有发热、咽痛[5]。现将我科2001~2006年收治的14例他巴唑致白细胞下降及粒细胞缺乏症进行分析,旨在为…     

抗甲状腺药物致粒细胞缺乏症相关因素探讨

目的 探讨抗甲状腺药物（ＡＴＤ）引起粒细胞缺乏症的影响因素、治疗措施及周围血白细胞计数监测的重要性。方法 对２６例因抗甲状腺药物引起的粒细胞缺乏症住院患者进行因顾性分析。结果 ＡＴＤ引起的粒细胞缺乏症不论服药剂量大小、患者年龄、服药时间长短、以及是否为初治或复治,均可发生。碳酸锂,Ｇ－ＣＳＦ、糖皮质激素对ＡＴＤ引起的粒细胞缺乏症治疗效果明显。常规监测周围血白细胞发现的无感染症状粒细胞缺乏症恢复时间     

抗甲状腺药物致粒细胞缺乏症临床观察

目的观察甲状腺功能亢进症（甲亢）初发及复发患者应用抗甲状腺药物致粒细胞缺乏症的临床特征和治疗措施。方法收集2000～2010年收治的甲亢应用抗甲状腺药物致粒细胞缺乏症患者的临床资料,对甲亢复发（5例）与初发（13例）患者应用抗甲状腺药物导致粒细胞缺乏症的临床特征和治疗措施进行总结。结果两组临床特征和治疗措施相似,均极易发生在较大剂量的抗甲状腺药物（甲巯咪唑30mg/d、丙硫氧嘧啶300mg/d）开始治疗的2～8周。结论甲亢复发患者应用抗甲状腺药物治疗与初发患者相似,均可以导致粒细胞缺乏症,易引起上呼吸道感染,甚至诱发甲状腺危象,临床上要高度重视,避免本症的出现。     

氯氮平治疗精神分裂症副反应200例临床分析

用氯氮平治疗精神分裂症２００例，出现副反应２１种，副反应最多的流涎、口干、心电图、脑电图异常４项均达５０％以上。亦有心、肝损害，癫痫，粒细胞缺乏症等重要副反应。副反应同氯氮平日剂量有关，但不一定都呈平行关系。     

抗甲状腺药物治疗导致粒细胞缺乏症36例患者临床资料分析

目的 分析抗甲状腺药物（ATDs）导致的粒细胞缺乏症的临床特征。方法 对北京协和医院14年间36例患者的临床资料进行回顾性分析和总结。结果 发生粒细胞缺乏患者的年龄16~62岁。88.9％的粒细胞缺乏发生在大剂量ATD治疗时。91.7%是在治疗3个月内出现。最长1例患者为持续治疗8个月时发生粒细胞缺乏。99.4%的患者继发感染。结论 ATDs诱导的粒细胞缺乏症,与年龄、性别无关。与药物种类无关,但存在剂量依赖性。     

急性药物性粒细胞缺乏症66例临床分析

急性药物性粒细胞缺乏症６６例临床分析许忠仁（△江阴市人民医院内科，江阴２１４４００）⒇关键词急性粒细胞缺乏症，药源性；药物急性粒细胞缺乏症为临床急症之一，如不及时识别和处理可引起严重感染，甚至威胁生命。本文收集我院１９８６—１９９６年１０年来资料较完...     

小儿药物性粒细胞减少及缺乏症(附19例分析)

本文对小儿药物性粒细胞减少及缺乏症分析,其中粒少5例,粒缺14例.解热镇痛药引起者占31.6%,氯霉素引起者占26.3%.2例左旋咪唑引起者由于粒细胞缺乏,发生致命性的败血症,同时伴有流感样症状、皮疹和血小板减少.青霉胺、甲基苄肼以及6—疏基嘌呤引起者发生骨髓抑制与药物剂量有关,5例粒少经治疗10～14天恢复,14例粒缺发生不同程度的感染,其中3例死亡.     

Hematological Complications of Phenylbutazone Therapy: Review of the Literature and Report of Two Cases

Two examples of hematological toxicity following phenylbutazone therapy are described, one of agranulocytosis and one of aplastic anemia. In the first case, prednisolone in a dosage of 20 mg. daily restored neutrophil percentage and the total leukocyte count to normal, but the patient with aplastic anemia, having shown no response to corticosteroid therapy, became dependent on repeated blood transfusion.

The English literature on the hematological toxicity of phenylbutazone is reviewed. Ten fatal cases of agranulocytosis have been recorded, as have eight cases of aplastic anemia, of which five proved fatal. Other toxic effects noted have included leukopenia, depression of erythropoiesis, megaloblastic anemia, thrombocytopenia and leukemia.

     

5-氟尿嘧啶对Jurkat和EL-4细胞周期解偶联的影响

目的：研究5-氟尿嘧啶（5-FU）不同剂量和给药后不同时间Jurkat和EL-4细胞周期解偶联的变化规律。方法：采用不同剂量（0、0.001、0.010、0.100和1.000 mg•L^-1）5-FU处理Jurkat和EL-4细胞,给药0、4、8、16、24和48 h后分别收集细胞,应用碘化丙啶（PI）荧光标记及流式细胞术（FCM）检测分析细胞倍体变化的剂量-效应和时间-效应规 律。结果：不同剂量5-FU给药后16 h,Jurkat细胞八倍体细胞百分率在0.001、0.010、0.100和 1.000 mg•L^-1各个剂量组均显著低于0 mg•L^-1组（P<0.01） ,无剂量依赖性;EL-4细胞八倍体细胞百分率在0.010 和 0.100 mg•L^-1组显著高于0 mg•L^-1组（P<0.05）。0.100 mg•L^-15-FU 给药后,Jurkat细胞八倍体细胞百分率在8、16和24 h显著低于相应对照组（P<0.01）,48 h显著高于相应对照组（P<0.01）;EL-4细胞八倍体细胞百分率在4、8和16 h显著高于相应对照组（P<0.05）,48 h显著低于相应对照组（P<0.01）。结论：5-FU可以诱导EL-4细胞发生细胞周期解偶联,而不能诱导Jurkat细胞发生细胞周期解偶联。     

Induction of micronucleated erythrocytes in mouse peripheral blood after cutaneous application of 5-fluorouracil

BACKGROUND: For topically applied drugs such as 5-fluorouracil (5-FU), dosage is not as precise as for other drug administration pathways. Consequently, quantity of drug delivered may differ among individuals and applications. 5-FU is used in treatment of different diseases and has been reported as a clastogenic compound by micronucleus assay. METHODS: To determine whether 5-FU cream (5% 5-FU) absorbed through skin can produce genotoxic or cytotoxic effect in mouse bone marrow, induction of micronucleated erythrocytes (MNE) in mouse peripheral blood was examined after cutaneous application of 5-FU daily for 5 days. RESULTS: 5-FU cream induced significant micronuclei at doses of 37.5 mg (total weight of cream)/2 cm(2) and 75.0 mg/2 cm(2), as well as cytotoxic effects at doses of 150.0 and 300.0 mg/2 cm(2). CONCLUSIONS: Cutaneous application of 5-FU increased number of MNE in mouse peripheral blood. These data emphasize the importance of using correct dose when applying drugs topically.     

抗甲状腺药致粒细胞缺乏症18例回顾性分析

目的 分析常规白细胞计数对预测抗甲状腺药物致粒细胞缺乏症的意义及抗甲状腺药物致粒细胞缺乏症的危险因子。方法 回顾性分析１８例抗甲状腺药致粒细胞缺乏临床资料。结果和结论 粒缺乏我数发生在服药后２－１２周,且与抗甲状腺药物剂量有关。有些患者的粒缺发生是突然的。每１－２周白细胞和粒细胞计数有预测某些粒的发生,抗关腺药物治疗维持剂量时,不需作常规白细胞检查。粒、巨噬集落刺激因子治疗对粒细胞恢复是有效的,糖     

Advanced gastric cancer with liver metastasis effectively treated by intra-hepatic arterial infusion of 5-FU, MMC and peroral administration of 5-FU: a case report

We have experienced a case of advanced gastric cancer with liver metastasis effectively treated by intra-hepatic arterial infusion of 5-fluorouracil (5-FU), mitomycin C (MMC) and peroral administration of 5-FU. The patient was a 48-year-old male diagnosed as having advanced gastric cancer with multiple liver metastasis in the bilateral lobes of the liver. This patient was treated by intra-hepatic arterial infusion of 5-FU (250 mg/2 days x 8 doses), MMC (20 mg x 1 dose, 6 mg/2 weeks x 6 doses) and peroral administration of 5-FU (200 mg/day). At 14 weeks later, a CT revealed that the metastatic liver tumors had disappeared. However, at 7 months after the therapy, the patient eventually died of liver and brain metastasis. These results suggested that intra-hepatic arterial infusion of 5-FU and MMC was an effective therapy for metastatic tumors in the liver, but we need to perform intra-hepatic arterial infusion using a new prolonged regimen to treat the liver metastasis.     

四君子汤与5-FU联用对结肠癌HT-29细胞生长的抑制效应

目的探索传统中药复方四君子汤与临床常用化疗药物氟尿嘧啶(5-FU)联用对体外培养的结肠癌HT-29细胞的生长抑制作用,为临床上应用四君子汤作为5-FU的增效剂联合治疗结肠癌提供实验依据。方法将体外培养的结肠癌HT-29细胞分成不含药血清对照组、5-FU组、高剂量四君子汤血清加5-FU组、中剂量四君子汤血清加5-FU组和低剂量四君子汤血清加5-FU组5组。将制备好的四君子汤含药血清和5-FU按所需的剂量分别加入到各组培养瓶中作用于细胞24h,应用基于酶标仪的MTT方法检测各组细胞的OD值,计算不同浓度药物处理对细胞生长的抑制率。结果四君子汤血清与5-FU联用能显著抑制结肠癌HT-29细胞的生长(均P0.01),且高剂量四君子汤血清与5-FU合用组细胞生长抑制率显著高于5-FU单用组(P0.01)。四君子汤血清与5-FU联用对结肠癌HT-29细胞周期的运行产生显著的影响。结论四君子汤可以增强5-FU对结肠癌HT-29细胞的生长作用和细胞周期的干扰作用。     

噻唑蓝还原法测脂肪乳剂对人结肠癌细胞增殖的影响

目的:测定脂肪乳剂和5-FU单独或共同培养情况下对人结肠癌细胞增殖的影响,为肿瘤患者应用脂肪乳剂作为营养支持手段提供必要的理论基础。方法:应用噻唑蓝还原法(MTT法)观察LoVo结肠癌细胞株与不同浓度脂肪乳剂和5-FU单独或共同培养情况下,脂肪乳剂和5-FU对LoVo细胞增殖的影响。结果:5-FU对LoVo细胞增殖的抑制随其浓度的增加而增加;较高浓度脂肪乳剂对LoVo细胞的增殖有促进作用;不同浓度的脂肪乳剂与5-FU联合应用并不影响5-FU对LoVo细胞的抑制作用。结论:体外实验表明,脂肪乳剂并不影响化疗药物抑制肿瘤细胞增殖的作用,化疗期间可应用脂肪乳剂提供必要的营养支持。     

Aplastic anemia and agranulocytosis in patients using methazolamide for glaucoma.

Carbonic anhydrase inhibitors used in the treatment of glaucoma, seizure disorders, and hypertension are rarely associated with blood dyscrasias. Several case reports of aplastic anemia with use of acetazolamide, and two cases with use of methazolamide, have appeared in the literature. This article describes two cases of aplastic anemia, at least one of which was almost certainly induced by the use of methazolamide, and one case of agranulocytosis related to the use of methazolamide.     

大剂量宁红欣冲击治疗恶性肿瘤贫血的疗效观察

目的观察大剂量宁红欣冲击治疗恶性肿瘤贫血的疗效及不良反应。方法将94例恶性肿瘤贫血患者随机分入试验组或对照组,前者接受大剂量宁红欣冲击治疗,用法为第1天、第3天给予宁红欣4万U皮下注射,在第5,7,9,11,13,15,17天给予宁红欣2万U皮下注射;后者接受常规剂量宁红欣治疗6周。对患者的有效率、血红蛋白值、输血需求率、卡氏评分及药物不良反应进行观察。结果试验组患者治疗2周后血红蛋白值明显升高,对照组患者治疗4周后血红蛋白值明显升高;试验组4周、6周血红蛋白值均高于对照组(P<0.05);试验组2周、4周、6周有效率为43.5%、63.0%、83.3%,高于对照组的17.8%、31.1%、53.3%(P<0.01);两组患者卡氏评分、输血需求率及不良反应差异无统计学意义(P>0.05)。结论大剂量宁红欣冲击治疗恶性肿瘤贫血疗效确切,优于常规剂量法,不良反应相似。     

Amodiaquine induced agranulocytosis and liver damage

Seven cases of agranulocytosis and two of liver damage that were probably due to amodiaquine treatment were studied. In five cases agranulocytosis was combined with liver damage, and in one case of primary liver damage moderate neutropenia was present. Three patients died. High total doses or prolonged duration of treatment, or both, appear to favour the occurrence of these reactions. The clustering of five of the seven cases of agranulocytosis within six months in one medical centre indicates that the risk to benefit ratio of amodiaquine for malaria prophylaxis should be re-evaluated.