非小细胞肺癌恶性胸腔积液的临床特征及预后影响因素

目的 研究非小细胞肺癌（NSCLC）恶性胸腔积液患者的临床特征及影响疗效、预后的因素。方法 选择安徽省胸科医院2013年1月至2014年12月收治的91例伴恶性胸腔积液NSCLC患者，回顾分析患者临床资料、胸腔积液情况、胸腔积液治疗情况等，分析各因素对疗效及生存期的影响。结果 血性胸水患者RR为48.7%，显著低于非血性胸水患者（P<0.05）；胸腔局部应用IL-2生物治疗RR为70.3%，显著高于不用IL-2进行局部治疗者（P<0.05）。非血性胸水中位生存期位13个月，较血性胸水生存有优势，胸腔局部应用含IL-2生物治疗中位生存期为12个月，较不用IL-2治疗生存有优势，在腺癌患者中EGFR-TKI联合化疗生存优于单纯化疗，而后者生存优于单纯EGFR-TKI治疗（P<0.05）。结论 血性胸水疗效及预后差，胸腔局部应用IL-2生物治疗疗效较好、生存有优势。     

Cyclic AMP enhances resolution of allergic pleurisy by promoting inflammatory cell apoptosis via inhibition of PI3K/Akt and NF-κB

Selective and timely induction of apoptosis is an effective means of resolving inflammation. The effects and putative mechanisms by which cyclic AMP (cAMP) modulates leukocyte apoptosis in vivo are still unclear. The present study aims at identifying intracellular pathways underlying the ability of cAMP elevating agents to resolve eosinophilic inflammation in a model of allergic pleurisy in mice. Ovalbumin (OVA) challenge of immunized mice induced eosinophil recruitment that peaked at 24 h and persisted till 48 h. Treatment with the PDE4 inhibitor rolipram, cAMP mimetic db-cAMP or adenylate cyclase activator forskolin, at 24 h after antigen-challenge resulted in profound resolution of eosinophilic inflammation, without a decrease of mononuclear cell numbers. There was a concomitant increase in number of apoptotic cells in the pleural cavity. The effects of rolipram and db-cAMP were inhibited by the PKA inhibitor H89. Inhibition of PI3K/Akt or NF-κB induced resolution of inflammation that was associated with increased apoptosis. OVA-challenge resulted in a time-dependent activation of Akt and NF-κB, which was blocked by treatment with rolipram or PI3K/Akt pathway inhibitors. Thus, cAMP elevating agents resolve established eosinophilic inflammation by inducing leukocyte apoptosis. Mechanistically, the actions of cAMP are dependent on PKA and target a PI3K/Akt-dependent NF-κB survival pathway.     

康莱特注射液联合胸腔灌注化疗对晚期非小细胞肺癌恶性胸水患者的临床疗效

目的:观察康莱特注射液对晚期非小细胞肺癌恶性胸水患者的临床疗效。方法:将88例晚期非小细胞肺癌恶性胸水患者随机分为三组,实验组(胸腔灌注化疗+康莱特注射液)30例;阳性对照组(胸腔灌注化疗+参芪扶正注射液)29例和对照组(单纯胸腔灌注化疗)29例。对三组患者治疗前后的外周血象(白细胞、血红蛋白、血小板),T细胞亚群分类(CD4、CD8、CD4/CD8),免疫球蛋白(IgA、IgG、IgM),近期临床疗效以及不良反应进行比较。结果:治疗前,三组之间外周血象及T淋巴细胞的免疫活性无统计学差异(P>0.05);治疗后,实验组T淋巴细胞免疫活性高于另外两组(P<0.05),同时阳性对照组T淋巴细胞的免疫活性要高于对照组(P<0.05)。化疗后,对照组免疫球蛋白IgG、IgA及IgM较化疗前均降低(P<0.05);实验组免疫球蛋白IgG和IgM均明显高于阳性对照组和对照组(P<0.05)。实验组近期临床疗效明显高于阳性对照组和对照组（P<0.05);阳性对照组的总有效率也明显高于对照组(P<0.05)。实验组和阳性对照组的粒细胞集落刺激因子使用量明显低于对照组(P<0.05),三组间出现的其他不良反应无显著统计学差异（P>0.05）。结论:康莱特注射液联合胸腔灌注化疗治疗晚期非小细胞肺癌恶性胸水的患者,可以保护机体的细胞免疫和体液免疫功能,提高临床疗效,减轻患者的骨髓抑制不良反应,是配合胸腔灌注化疗的一种较理想的辅助治疗药物。     

水冲式胸腔引流管的研制与应用

目的:探讨水冲式胸腔引流管的临床应用价值。方法:对140例使用水冲式胸腔引流管进行胸腔闭式引流的病人进行临床研究,对其引流不畅发生率进行统计。结果:引流3d以内者111例,引流不畅发生率1.8%;引流3d以上者32例,引流不畅发生率3.1%。结论:水冲式胸腔引流管可降低引流不畅发生率。     

局部热疗联合药物灌注治疗恶性胸腔积液疗效观察

目的探讨局部热疗联合药物治疗恶性胸腔积液的临床疗效及其对患者生活质量的影响。方法恶性胸腔积液患者94例,行胸腔穿刺置入中心静脉导管彻底引流排尽积液后分为A、B2组接受后续治疗。A组（45例）采用药物治疗后予患侧胸腔局部热疗,温度42.5～42.8℃、时间1h,热疗每72小时重复1次。B组（49例）只给予药物治疗及治疗后翻身。结果2组间疗效比较差异有统计学意义（u=3.96,P〈0.01）。2组生存质量间差异有统计学意义（u=2.74,P〈0.01）。结论热疗作为一种杀灭肿瘤细胞的有效方法,与药物联合治疗恶性胸腔积液可明显改善患者的临床症状及生活质量,不良反应可以耐受,值得推广应用。     

尿激酶胸腔内注入治疗结核性胸膜炎的疗效观察

目的通过对比研究的方法,探讨尿激酶胸腔内注射治疗结核性胸膜炎的治疗效果。方法选取60例结核性胸膜炎患者,随机均分为观察组和对照组,观察组给予常规抗结核治疗并行胸腔闭式引流胸腔积液后注入尿激酶治疗,对照组在此基础上采用胸腔内仅注入0.9%氯化钠注射液,治疗结束后进行比较,观察两组的导管留置时间、胸膜厚度、胸水吸收及胸膜黏连情况。结果观察组的疗效明显优于对照组,差异有统计学意义。结论尿激酶胸腔内注射能够促进胸腔积液吸收,使胸膜肥厚减轻、黏连减少,可以缩短静脉导管在胸腔内留置时间,该方法不良反应较少,操作简单,值得临床推广应用。     

不同药物胸腔灌注治疗恶性胸腔积液的临床体会简

目的 比较单独应用顺铂或香菇多糖以及两者联合进行胸腔灌注治疗恶性胸腔积液的疗效及不良反应.方法 采用中心静脉导管留置引流术,对120例恶性胸腔积液患者随机分别采用单纯顺铂、单纯香菇多糖或香菇多糖联合顺铂胸腔灌注治疗,治疗4周后按WHO标准评价近期疗效和毒副反应.结果 联合组有效率优于单纯顺铂或单纯香菇多糖组;联合组患者的不良反应低于单纯顺铂组,但高于单纯香菇多糖组.结论 香菇多糖联合顺铂胸腔灌注是治疗恶性胸腔积液的有效手段.     

Intrapleural cisplatin and OK432 therapy for malignant pleural effusion caused by non-small cell lung cancer

OBJECTIVE: To evaluate the efficacy of combined intrapleural therapy with cisplatin, an antineoplastic agent, and OK432, a sclerosing agent, in controlling malignant pleural effusions, when compared with monotherapy with either agent. METHODS: A total of 49 non-small cell lung cancer patients with malignant pleural effusion were randomly assigned to one of three groups: intrapleural cisplatin therapy (n = 17), intrapleural OK432 therapy (n = 17), or both (n = 15). They were compared in terms of success rate, duration of indwelling chest tube and adverse reactions. RESULTS: Rates of pleural effusion recurrence within 180 days following cisplatin, OK432, or combination therapy were 64.7%, 52.9% and 13.3%, respectively, being significantly lower in the combination therapy group (P = 0.01). The mean duration of chest tube drainage was 8.4 days, 5.5 days and 12.9 days, respectively, being significantly longer in the combination therapy group (P < 0.001). All procedures were well tolerated. CONCLUSIONS: Although chest tube drainage took longer because of the time required for multiple administration of the agents, intrapleural combination therapy with cisplatin and OK432 was more effective in controlling malignant pleural effusions due to non-small cell lung cancer than monotherapy with either agent.     

正压机械通气时腹内压与胸内压的相关性

目的探讨正压机械通气时,患者在麻醉肌松状态下,不同PEEP时腹内压与胸内压的相关性。方法 20例手术后尚处于麻醉肌松状态下,并行机械通气的患者,均留置胸腔闭式引流管和导尿管,在PEEP分别为0 cmH_2O_5 cmH_2O,10 cmH_2O和15 cmH_2O时,进行间接腹内压和直接胸内压测定。结果所有20例患者的初始腹内压为（8.15±3.46）mmHg,初始胸内压为（9.31±5.72） mmHg,增加PEEP后,腹内压,胸内压均升高。当PEEP分别为5 cmH_2O,10 cmH_2O和15 cmH_2O时,腹内压分别增加至（8.31±3.66） mmHg,（9.92±3.75） mmHg和（12.46±5.55） mmHg,胸内压分别增加至（9.15±5.93） mmHg,（12.23±6.29） mmHg和（16.23±5.99） mmHg。不同PEEP时,腹内压各组间两两比较,差异有统计学意义（P〈0.05）。20例患者的腹内压与胸内压之间的相关性进行分析,其Pearson相关系数R~2=0.789,且P〈0.01,两者存在较强的正相关性。结论在机械通气的过程中,提高PEEP值,能增加患者的腹内压。故对机械通气的患者,有必要实行腹内压监测。不同PEEP时,腹内压与胸内压具有较强的正相关性。     

Central nervous system toxicity in a patient receiving continuous intrapleural bupivacaine

A patient developed signs of central nervous system (CNS) toxicity during treatment of postthoracotomy pain with a continuous intrapleural bupivacaine infusion. This incident occurred after the patient's chest tube was clamped, without any decrease in the bupivacaine infusion rate. This is the first reported case of CNS toxicity in a patient receiving a continuous intrapleural bupivacaine infusion. Possible etiologies of this complication are discussed, as are ways to avoid such a complication in the future.