胸腔置管引流注入DDP香菇多糖治疗恶性胸腔积液

目的观察胸腔内置管引流并注入DDP香菇多糖治疗恶性胸腔积液疗效。方法34例恶性胸腔积液患者超声引导下置入中心静脉导管,尽量引流尽胸水后腔内注入DDP及香菇多糖。结果完全缓解（CR）12例,部分缓解（PR）16例,缓解不明显（NR）3例,进展（PD）3例,有效（CR＋PR）率82.35%。结论超声引导下微创置管引流并注入DDP,香菇多糖治疗恶性性胸腔积液有显著效果,毒副作用小,可提高患者生存质量。     

经深静脉导管胸腔化疗治疗恶性胸腔积液护理体会

目的：总结经深静脉导管胸腔化疗治疗恶性胸腔积液的护理方法。方法：对56例大量恶性胸腔积液患者进行胸腔留置深静脉导管引流胸腔积液并注射丝裂霉素（MMC）、顺铂（DDP）治疗后,予以术前、术中、术后不同阶段的相应护理。结果：56例病人中,16例完全缓解,35例部分缓解,5例无效。结论：加强术前术中术后护理工作是提高手术成功率减少并发症的重要保证。     

香菇多糖联合顺铂胸腔给药治疗中大量恶性胸腔积液

目的：观察香菇多糖联合顺铂胸腔灌注治疗中大量恶性胸腔积液法的近期疗效及安全性。方法选择我院肿瘤科2008年6月~2013年6月收治的住院患者58例大量胸腔积液患者,随机分为治疗组和对照组。治疗共计组31例,应用香菇多糖联合顺铂胸腔灌注;对照组共计27例,应用顺铂胸腔灌注,2周期后评价疗效及安全性。结果治疗组控制恶性胸腔积液有效率(CR+PR)为76.6%,对照组有效率为48.1%。两组相比差异具有显著性。结论香菇多糖联合顺铂胸腔灌注能有效控制恶性胸水,疗效肯定,安全性好。     

中心静脉导管留置引流并胸腔内灌注药物治疗恶性胸腔积液疗效分析

胸腔积液是晚期恶性肿瘤的常见并发症之一,我们于2007年1月～2008年1月采用中心静脉导管留置引流并胸腔内灌注顺铂(DDP)及天地欣(LNT),治疗恶性胸腔积液68例.     

中心静脉导管引流并胸膜腔内化疗治疗恶性胸腔积液

我院自 1998年 8月～ 2 0 0 1年 8月应用中心静脉导管引流胸腔积液 ,并注入顺铂治疗 2 8例转移性恶性胸腔积液。报告如下 :1　资料与方法1 1　病例资料　 2 8例病人中男 18例 ,女 10例 ,年龄 4 2～ 87岁 ,中位年龄 6 5岁 ,其中肺腺癌 10例、磷癌 4例 ,小细胞肺癌 2例 ,乳腺癌 6     

细胞因子诱导的杀伤细胞联合白细胞介素2治疗恶性胸腔积液

目的 观察应用细胞因子诱导的杀伤（CIK）细胞联合白细胞介素2（IL-2）治疗恶性胸腔积液的疗效.方法 收集2009年7月至2013年7月于本院肿瘤科就诊的恶性胸腔积液患者50例,随机数字表法分为治疗组（n=24）和对照组（n=26）.胸腔积液引流净后,治疗组胸腔灌注CIK细胞联合IL-2,连续3d;对照组灌注IL-2联合顺铂,隔日1次,连续3次.治疗4周后评价疗效和不良反应.结果 治疗组有效率87.50％（21/24）,完全缓解率54.17％（13/24）;对照组有效率57.69％（15/26）,完全缓解率42.31％（11/26）.与对照组比较,治疗组的完全缓解率、有效率均增加（均P＜0.05）.不良反应比较显示,治疗组发热的发生率较高,而对照组胸痛、胃肠道反应、骨髓抑制的发生率较高（均P＜ 0.05）.与治疗前比较,治疗后两组患者的Karnofsky评分均增加（均P＜0.05）.结论 CIK细胞联合IL-2胸腔灌注治疗恶性胸腔积液不良反应小,疗效确切.     

ICU重症胸腔积液患者中心静脉导管的应用效果

目的探讨应用中心静脉导管治疗ICU重症胸腔积液患者的临床疗效。方法选取ICU治疗的重症胸腔积液患者58例,随机平均分为观察组和对照组。观察组应用中心静脉导管穿刺引流胸腔积液,对照组患者则使用传统胸腔穿刺术。比较两种术式的相关指标。结果观察组患者的总有效率较高于对照组,不良反应发生率较低于对照组,且其操作时间、积液吸收时间、ICU停留时间均短于对照组,以上差异均具有统计学意义。结论重症胸腔积液患者使用中心静脉导管引流积液具有良好的临床疗效,且操作时间短,患者恢复快,不良反应发生率低,有利于患者病情恢复。     

滑石粉联合化疗药物治疗恶性胸腔积液的研究

目的探讨胸腔内注入滑石粉混悬液、顺铂（DDP）、氟尿嘧啶（5-FU）治疗恶性胸腔积液的疗效。方法病理确诊的恶性胸腔积液64例，经胸穿于胸腔内留置导管引流尽胸水后，随机分为2组：治疗组32例，在胸腔内注入滑石粉混悬液5～10g、5一Fu（500mg／m^2）、DDP（40mg／m^2）；对照组32例，在胸腔内注入DDP（40mg／m^2），均隔日重复1次，共2次。观察疗效、生活质量、生存率及毒副反应。结果治疗组总有效率84％，病变进展率3％，与对照组50％、22％相比有显著性差异（P〈0．05）。Karnofsky评分大于70分，治疗组较对照组显著提高（P〈0．05）。治疗组半年（0．5a）、1年（1a）、1年半（1．5a）的生存率分别为97％、59％、44％，高于对照组的63％、50％、19％，0．5年、1．5年两组的生存率有显著性差异（P〈0．05）。治疗组的副反应中发热、胸痛高于对照组。结论胸腔内联合注入滑石粉混悬液、5-FU、DDP治疗恶性胸腔积液是一种效果好、副反应轻、患者可耐受的方法。     

中心静脉导管用于恶性胸腔积液引流的护理体会

目的探讨中心静脉导管用于胸腔引流术的利弊及护理体会。方法对恶性胸腔积液的患者在B超定位下进行中心静脉导管穿刺并留置引流管形成密闭引流装置。间断引流胸水及胸腔内给药,时间7~20d。留置期间B超定期复查,护理评价效果,并决定是否拨管。结果中心静脉导管用于恶性胸腔积液的患者,减轻患者反复穿刺的痛苦及创伤,简化传统的胸腔引流术,也减少了气胸、血气胸发生的机率等并发症。结论规范中心静脉导管用于恶性胸腔积液的护理措施,简化了传统的胸腔穿刺引流术,减少术中、术后感染及引流管脱落的几率。     

卡铂联合白介素-2治疗恶性心包积液

目的:观察引流心包积液后,行卡铂联合白介素-2腔内注射治疗恶性心包积液的疗效及安全性。方法:收集53例恶性心包积液患者,先用中心静脉导管行经皮穿刺心包置管引流,待积液基本引尽后,随机抽取12例(卡铂组)经导管注入卡铂300 mg,13例(白介素组)注入白介素-2 200万U,28例(联合治疗组)同时注入卡铂300 mg和白介素-2 200万U,保留48 h后抽净积液,拔管,并作随访。结果:所有患者经治疗后,卡铂组完全缓解(complete response,CR)5例(41.7%),部分缓解(partial response,PR)3例(25.0%),无效(no change,NC)4例(33.3%),总有效率66.7%;白介素组CR 4例(30.8%),PR 4例(30.8%),NC 5例(38.4%),总有效率61.6%;联合治疗组CR 18例(64.3%),PR 9例(32.1%),NC 1例(3.6%),总有效率96.4%。无1例发生穿刺意外;卡铂组1例(8.3%)、联合治疗组2例(7.1%)出现轻度恶心、胃纳轻度减低,胃复安、维生素B6对症治疗后短期好转,白介素组无胃肠反应发生;白介素组2例(15.4%)、联合治疗组5例(17.9%)出现轻度胸痛和低热,用新癀片或吲哚美辛栓剂可控制,卡铂组无胸痛、发热表现;随访2周,无1例发生骨髓抑制;随访3月,无1例发生缩窄性心包炎。结论:卡铂联合白介素-2治疗恶性心包积液安全、有效,值得临床推广应用。     

恩度联合洛铂胸腔热灌注化学治疗恶性胸腔积液的近期临床观察

目的观察恩度联合洛铂胸腔热灌注化学治疗(简称化疗)恶性胸腔积液的近期疗效和不良反应。方法选择2010年1月~2012年8月60例恶性胸腔积液患者,其中男性34例,女性26例;年龄35~65岁,中位年龄50.5岁。按照随机数字法分成观察组和对照组,各30例。所有患者均行胸腔穿刺置管,充分引流胸水,观察组采用恩度30 mg+洛铂30 mg/m2行胸腔热灌注化疗,对照组单纯洛铂30 mg/m2行胸腔热灌注化疗,热疗循环温度控制在41.5℃,每次治疗时间60 min,治疗周期为7~10 d,连续治疗4次。结果观察组患者,16例获得完全缓解,9例部分缓解,总有效率为83.3%;对照组中,12例获得完全缓解,9例部分缓解,总有效率为70.0%;两组间差异有统计学意义(P0.05)。两组患者生活质量(QOL)亦有明显改善(P0.05)。两组患者Ⅲ+Ⅳ度骨髓抑制发生率差异无统计学意义(P0.05)。结论恩度联合洛铂胸腔热灌注化疗恶性胸腔积液疗效显著,QOL改善明显,不良反应轻,值得推广应用。     

深静脉置管引流术在心包积液中的临床应用

目的:探讨经皮心包穿刺置管引流心包积液的疗效及安全性。方法:对28例中到大量心包积液的患者在床边进行心包穿刺置管,置管后引流。结果:28例患者均置管成功,留置时间平均7d(3~15d),均无组织脏器损伤及感染。结论:经皮心包穿刺置管引流治疗心包积液,具有操作方便,疗效可靠,穿刺并发症少等优点。     

Treatment with locally applied mitoxantrone

In 30 patients mitoxantrone was administered via an intracavitary route intraperitoneally, intrapleurally or intrapericardially. From 13 patients with malignant pleural effusion 5 showed a complete and 3 a partial remission. 2 of 2 patients with pericardial effusion showed a complete remission. From 16 patients with peritoneal carcinosis 4 showed a complete and 3 a partial remission.     

Eosinophil colony-stimulating factor induced by administration of interleukin-2 into the pleural cavity of patients with malignant pleurisy

Systemic administration of interleukin (IL)-2 to patients with malignant diseases induces peripheral eosinophilia. In the present study, to clarify the mechanism of eosinophilia induced by IL-2, we examined the changes in the number of eosinophils and eosinophil colony-stimulating factor (Eo-CSF) activity in the pleural fluids of six patients with malignant pleurisy caused by lung cancer or malignant mesothelioma during and after intrapleural administration of IL-2. Results showed that intrapleural administration of IL-2 induced marked eosinophilia in the pleural fluid and moderate eosinophilia in the peripheral blood, and that during IL-2 administration, marked Eo-CSF activity appeared in the pleural fluid before increase in the number of eosinophils, but that this activity did not appear in the peripheral blood. This Eo-CSF activity was inhibited by a combination of anti-IL-5 antibody, anti-IL-3 antibody, and anti-granulocyte/macrophage colony-stimulating factor (anti-GM-CSF) antibody, but not by each antibody alone. Chemotactic activity for eosinophils was also detected in the pleural fluid during IL-2 treatment. These results suggest that eosinophilia in the pleural fluid induced by IL-2 injection into the pleural cavity of patients with malignant pleurisy is due to the Eo-CSF activities of various components, including IL-5, IL-3, and GM-CSF, and chemotactic factors for eosinophils induced locally in the pleural cavity by IL-2.     

The effects of urokinase instillation therapy via percutaneous transthoracic catheter in loculated tuberculous pleural effusion: a randomized prospective study

The purpose of this study was to propose that intrapleural urokinase (UK) instillation could reduce pleural thickening in the treatment of loculated tuberculous pleural effusion. Forty- three patients who were initially diagnosed as having loculated tuberculous pleural effusion were assigned at random to receive either the combined treatment of UK instillation including anti-tuberculosis agents (UK group, 21 patients) or strictly the unaccompanied anti-tuberculous agents (control group, 22 patients). The UK group received 100,000 IU of UK dissolved in 150 ml of normal saline daily, introduced into the pleural cavity via a pig-tail catheter. The control group was treated with anti-tuberculous agents, excepting diagnostic thoracentesis. After the cessation of treatment, residual pleural thickening (RPT) was compared between the two groups. Clinical characteristics and pleural fluid biochemistry were also evaluated. The RPT (4.59 +/- 5.93 mm) of the UK group was significantly lower than that (18.6 +/- 26.37 mm) of the control group (p < 0.05). The interval of symptoms observed prior to treatment of patients with RPT > or = 10 mm (6.0 +/- 3.4 wks) was detected to be significantly longer than in those with RPT < 10 mm (2.1 +/- 1.2 wks) in the control group (p < 0.05). However, there were no discernible differences were seen in the pleural fluid parameter in patients with RPT > or = 10 mm, as compared to patients with RPT < 10 mm in the UK group. These results indicate that the treatment of loculated tuberculous pleural effusion with UK instillation via percutaneous transthoracic catheter can cause a successful reduction in pleural thickening.     

胸水细胞FAK和MMP-9表达在良恶性胸腔积液鉴别中的意义

目的：探讨胸水细胞黏着斑激酶（focaladhesionkinaseFAK）和基质金属蛋白酶-9（MMP-9）检测对良、恶性胸腔积液的鉴别诊断价值。方法：用荧光实时定量RT—PCR和免疫组化方法检测39例恶性、31例良性胸水细胞FAK和MMP-9基因mRNA和蛋白表达,并与胸水细胞学诊断结果进行比较。结果：恶性胸水组FAK和MMP-9mRNA表达水平较良性胸水组和对照明显增加,较良性胸水组分别增加71．9％（P〈0．01）和67．8％（P〈0．01）。免疫组化检测结果显示39例恶性胸水组中FAK基因表达阳性30例（76．9％）,MMP-9基因表达阳性33例（84．6％）,而31良性胸水组FAK基因表达阳性8例（25．8％）,MMP-9基因表达阳性5例（16．1％）（P〈0．01）。结论：胸水细胞MMP-9和FAK基因检测可作为细胞学检查的辅助手段,提高恶性胸腔积液的诊断率。     

Treatment of malignant ascites and pleurisy by a streptococcal preparation OK-432 with fresh frozen plasma--a mechanism of polymorphonuclear leukocyte (PMN) accumulation

A single injection of a streptococcal preparation, OK-432, with fresh frozen plasma (FFP) (or fresh human serum) into the peritoneal or pleural cavity for the treatment of malignant ascites or pleurisy resulted in a complete reduction of ascitic fluid or pleural effusion in 5 out of 11 patients. FFP was used a further source of complement for the effective accumulation of antitumor polymorphonuclear leukocytes (PMNs) by complement-derived chemotactic factors in the cavity. C5a increased in the fluids 3-9 h after the injection and preceded a massive increase in PMNs. C1 inhibitor (C1INH) and C3b inactivator (C3bINA) decreased in several cases 6 h after the treatment. Chemotactic arachidonic acid metabolites, thromboxane B2(TXB2) as a characteristics of TXA2, and leukotriene B4(LTB4) also increased at the same time even in cases where C5a changed only minimally, and may play a role in accumulating antitumor PMNs in the cavity.