肿瘤患者情感障碍及相关因素调查分析

[目的]了解住院肿瘤患者抑郁、焦虑情绪的发生率,并对其相关因素进行分析.[方法]对540例肿瘤住院患者,应用抑郁自评量表(SDS)、焦虑自评量表(SAS)、汉密顿抑郁量表(HAMD)、汉密顿焦虑量表(HAMA)和自行设计的情感障碍影响因素调查表,进行情感状况及其相关因素的调查和分析.[结果]肿瘤患者抑郁和焦虑的发生率分别为51.1%和20.2%;患者的SDS、SAS标准分(50.15±11.62,42.42±9.43)显著高于常模(P＜0.01);化疗组患者情感障碍阳性率均显著高于手术组和放疗组(P＜0.01).与早期及中期相比,晚期肿瘤患者的情感障碍阳性率显著增高(P＜0.01).影响肿瘤患者的情感因素诸多,但以对医疗费用、治疗效果的担心(71.1%,61.9%)最为显著.[结论]接受化疗及晚期的肿瘤患者具有更多的情绪障碍,应及早给予心理干预和必要的社会支持,以提高患者的治疗效果及生存质量.     

盆腔恶性肿瘤患者抑郁、焦虑发生影响因素分析

[目的]探讨盆腔恶性肿瘤患者抑郁、焦虑的发病特点及其相关影响因素.[方法]采用Zung抑郁自评量表(SDS)、焦虑自评量表(SAS)及患者一般临床特征调查表对128例盆腔恶性肿瘤患者进行数据采集及相关因素分析.[结果] 128例盆腔恶性肿瘤患者中有抑郁障碍者87例(67.97％),平均得分62.61±6.97分.有焦虑者38例(29.69％),平均得分58.84±9.49分.Logistic回归多因素分析显示,抑郁、焦虑的发生率均与患者年龄、文化程度、医疗费用来源、临床分期、慢性癌痛呈显著相关性(P＜0.05),而与患者性别、KPS评分、日常锻炼无相关性.[结论]盆腔恶性肿瘤患者中抑郁和焦虑发生率较高.对于老年、肿瘤晚期、伴有慢性癌痛等因素的患者,需要进行心理—生理方面的综合干预.     

妇科恶性肿瘤患者中-重度抑郁影响因素分析

[目的]探讨妇科恶性肿瘤患者中重度抑郁的影响因素．为干预及提高患者的生活质量提供依据。[方法]共有76例患者人组。用Zung氏抑郁自评量表（SDS）和焦虑自评量表（SAS）凋查患者的抑郁和焦虑;用简明疼痛调查表调查疼痛情况：用流式细胞仪测定外周血中的T细胞亚群、NK细胞、CIK细胞、Th1、Th2细胞因子。用Logistic回归分析以上因素与患者中一重度抑郁之间的关系。[结果]影响中一重度抑郁的因素有：肿瘤分期、Hb和焦虑;T细胞亚群、NK细胞、CIK细胞及Th1、Th2因子与中一重度抑郁无关。[结论]影响中一重度抑郁的因素有肿瘤分期、Hb、焦虑：细胞免疫可能与中一重抑郁无关,需要进一步证实。     

胃肠道恶性肿瘤患者焦虑抑郁状态及其影响因素

目的:了解胃肠道恶性肿瘤患者抑郁焦虑情况,并探讨导致胃肠道恶性肿瘤患者抑郁焦虑发生的相关因素。方法:选取2010年-2013年来我院接受治疗的胃肠道恶性肿瘤患者120例,采用问卷方式调查焦虑及抑郁发生情况,与国内常模比较SAS及SDS评分,并找出其中影响胃肠道肿瘤患者放化疗后焦虑抑郁状态的因素。结果:患者整体的焦虑抑郁发生率为44.17%,焦虑抑郁患者的SAS、SDS评分显著高于国内常模（P<0.05）。影响患者焦虑抑郁发生的主要因素为疼痛、担心住院费用、担心医疗费用、担心医护人员的工作情况等11项。结论:影响胃肠道恶性肿瘤患者焦虑、抑郁发生的因素是多方面的,需要采取综合措施才能进行有效干预。     

食管癌患者配偶心理状态的影响因素分析

[目的]调查食管患者配偶的焦虑、抑郁情况,并研究其影响因素。[方法]应用焦虑自评量表(SAS)和抑郁自评量表(SDS)对80例食管癌患者配偶心理状态进行调查,影响心理状态因素的差异程度经t检验、单因素方差分析及多重线性回归处理。[结果]食管癌患者配偶的焦虑(48.53±7.67)、抑郁程度(58.91±8.20)明显高于国内常模(37.23±12.59,41.88±10.57)(P<0.05);食管癌患者配偶的焦虑、抑郁程度在不同年龄、月收入、医疗费用的支付方式、夫妻感情的情况、食管癌的临床分期及配偶是否合并慢性病之间差异有统计学意义(P<0.05);影响食管癌患者配偶焦虑程度的因素为:性别、夫妻感情的情况、年龄及食管癌的临床分期;影响食管癌患者配偶抑郁程度的因素为食管癌的临床分期。[结论]食管癌患者配偶存在不同程度的焦虑、抑郁情况;人口学因素、疾病因素均可影响食管癌患者配偶的焦虑、抑郁程度。该研究结果对医务人员为食管癌患者配偶制定有针对性的干预措施有较重要的指导意义。     

氟西汀干预恶性肿瘤相关性抑郁和焦虑障碍的疗效观察

目的 观察氟西汀对恶性肿瘤相关性抑郁和焦虑障碍的干预效果.方法 选择125例恶性肿瘤伴发抑郁和焦虑障碍的患者,SDS得分和SAS得分均≥50分,之前未应用过抗抑郁和抗焦虑药物.所有患者应用氟西汀10～20 mg/d进行干预.服药4周后分别进行SAS和SDS评测.结果 全组治疗后SAS和SDS平均得分均较治疗前下降,差异...     

晚期恶性肿瘤患者心理状况初步分析

背景与目的：晚期肿瘤患者的生活质量、心理状况等正在受到广泛的关注和重视,本研究初步评估晚期恶性肿瘤患者的心理状况,并分析其影响因素。方法：对2011年9月-2013年3月于复旦大学附属肿瘤医院综合治疗科住院治疗的晚期肿瘤患者,在家属陪同及医师的指导下,分别完成焦虑自评量表(self-ratinganxiety scale,SAS)、抑郁自评量表(self-rating depression scale,SDS)、生活质量调查问卷(EORTCQLQ-C30)、社会支持评定量表、90项症状清单(symptom checklist 90,SCL-90)等调查量表,并对各量表的结果进行统计学分析。结果：共56例患者入组。所有患者中,18例有抑郁倾向,24例有焦虑倾向,16例焦虑合并抑郁。分析显示,有心理障碍组,除认知功能外,躯体、角色、情绪、社会功能评分明显较无心理障碍组低,而SCL-90评分及疲倦、疼痛、呼吸困难、失眠、食欲丧失、经济困难等方面,有心理障碍组评分较无心理障碍组明显升高。患者SAS、SDS评分与整体生活质量呈负相关,而与患者的症状评分呈正相关。结论：晚期恶性肿瘤患者中,存在心理障碍的患者比例较高,且心理障碍会严重影响患者的生活质量。对于主诉症状较多或者自觉生活质量较差的患者,需要更多地关注其心理状况,必要时进行一定的干预,以缓解症状,提高生活质量。     

晚期肺癌患者心理韧性现状调查及影响因素分析

目的 调查晚期肺癌患者心理韧性现状,并探讨其影响因素.方法 采用横断面研究方法,应用心理韧性量表(CD-RISC)、焦虑自评量表(SAS)、抑郁自评量表(SDS)对202例晚期肺癌患者进行问卷调查.调查晚期肺癌患者心理韧性情况,并分析其影响因素.结果 晚期肺癌患者的心理韧性总分为(73.89±19.23)分,力量性维度...     

系统性护理干预对中重度癌痛患者及家属生活质量的影响

目的探讨系统性护理干预对中重度癌痛患者及家属生活质量的影响。方法选取2013年9月至2015年7月间河北工程大学附属医院收治的94例肺癌晚期伴中重度癌痛患者,采用随机数表法分为观察组与对照组,每组47例。观察组患者给予系统性护理干预,对照组患者给予常规护理,干预一个月后,比较两组患者的癌痛缓解程度、依从性和治疗满意程度,采用焦虑自评量表(SAS)和抑郁自评量表(SDS)对患者焦虑和抑郁程度进行评价,并比较两组患者和家属的生活质量与心理状态。结果经过系统性护理干预后,观察组患者的依从性、癌痛缓解有效率及对治疗的总满意率,均显著高于对照组患者,两组组间比较,差异有统计学意义(P<0.05);两组患者疼痛视觉模拟评分表(VAS)、SAS和SDS评分均明显下降,且观察组各指标下降更明显,组间比较,差异有统计学意义(P<0.05);组内治疗前后比较,两组患者的食欲、睡眠、精神状态、日常活动、抑郁、焦虑、恐惧、消极和自信程度均有显著改善,差异有统计学意义(P<0.05);组间治疗后比较,除食欲外的上述指标均表现为观察组好于对照组,组间比较,差异有统计学意义(P<0.05);家属生活质量与心理状态治疗后比较,全部指标均表现为观察组好于对照组,差异有统计学意义(P<0.05)。结论系统性护理干预能改善中重度癌痛患者的依从性,缓解癌痛,提高患者的治疗满意度,并提高患者和家属的生活质量。     

临终关怀护理对晚期肿瘤患者生活质量的影响及护理体会

目的探讨临终关怀护理对晚期肿瘤患者生活质量的影响及护理体会。方法选择2013年2月至2015年2月间收治的96例晚期肿瘤患者,根据随机数字法分为观察组和对照组,每组48例,观察组患者给予临终关怀护理,对照组患者给予常规护理,观察比较两组患者护理前后焦虑自评量表(SAS)、抑郁自评量表(SDS)、生活质量测定量表(EORTC-QLQ-C30)各维度评分及总健康评分,以及患者及其家属对护理服务满意度。结果与对照组比较,观察组患者护理后SAS和SDS评分均明显降低(P<0.05),生活质量各维度评分及总健康评分均明显提高(P<0.05)。观察组患者对护理服务满意度明显改善(P<0.05)。结论临终关怀护理能够提高晚期肿瘤患者的生活质量,改善患者的心理状态,使患者在临终期感受人性化的护理服务。     

Irinotecan and radiation in vitro and in vivo

Loss of chromosome sequences at 13q14 (Rbl) and 17p13 (p53) associated with squamous cell carcinoma of head and neck (SCCHN) was evaluated in 12 recurrent tumors and 51 primary tumors from 63 patients. The incidence of LOH at 17p13 was 19 of 50 (38%) tumors, and at 13q14 was 21 of 57 (37%). LOH affecting Rbl and/or p53 was observed in 30 of 63 (48%) SCCHN. Coincident LOH at Rbl and p53 was detected in 10 of 46 (22%) tumors. There were nine cases in which primary and metastatic tumors were obtained from the same patient. Of these, seven were informative and five of these (71%) manifested LOH at p53 in both primary and metastatic sites. Examination of Rbl in these same tumors showed LOH in six of the nine metastases, and of these six, only three revealed LOH in the primary tumor. LOH at p53 or Rbl alone showed no correlation with clinical outcome. However, tumors that manifested LOH at both loci were associated with poorer patient outcome and poorer histological differentiation.     

TCP and NTCP in preclinical and clinical research in Europe

European research in radiation oncology has a long and successful tradition. The aim of this research is to increase the therapeutic window of radiotherapy by increasing the tumor control probability (TCP) and/or by decreasing the normal tissue complication probability (NTCP). This paper summarizes the basic radiobiological concept underlying treatment optimization by TCP-NTCP data and discusses some of the limitations of currently used models. These are controversial in many aspects and cannot be recommended for clinical routine practice but should rather be considered as a research tool.     

Advances in molecular diagnostics and therapeutics in head and neck cancer

Opinion statement Extensive treatment-related morbidities and stagnant survival rates over the past few decades for patients with squamous cell cancer of the head and neck (SCCHN) emphasize the need for novel diagnostics and therapeutics based on the molecular characteristics of the tumor. The development of an early detection test remains largely preliminary. Much attention has recently been given to saliva-based early detection assays that use accepted tumor markers such as p53 and DNA methylation. Most of these studies have focused on feasibility as opposed to prospective clinical trials. To date, early detection saliva assays have failed to yield a high enough sensitivity and specificity for broad population-based screening. The use of saliva as a noninvasive, inexpensive, and accessible diagnostic substrate remains desirable. Unlike SCCHN diagnostics, molecular-targeted therapies for SCCHN will soon be a reality, with many more compounds in the pipeline. The most promising of these drugs target the epidermal growth factor receptor (EGFR), which is known to be overexpressed in squamous cell carcinomas. Cetuximab, a monoclonal EGFR antibody, has shown efficacy in combination with radiotherapy in advanced SCCHN in a recent phase III trial and is currently being petitioned for US Food and Drug Administration approval. Likewise, erlotinib, an EGFR tyrosine kinase inhibitor, has shown favorable results in phase II trials as monotherapy and in combination with chemotherapy. Gefitinib, another EGFR tyrosine kinase inhibitor, has shown efficacy as monotherapy, in combination with chemotherapy, and with chemoradiotherapy. At least two phase III trials of gefitinib in patients with advanced SCCHN are ongoing. Such low-toxicity, tumor-specific targeting strategies will soon be available for patients with head and neck cancer. The challenge is to establish assays to determine which patients are most likely to benefit from these agents.     

Estrogen and Progesterone in Normal Mammary Gland Development and in Cancer

There is emerging evidence that the mammary epithelium in both mice and humans is arranged as a hierarchy that spans from stem cells to differentiated hormone-sensing, milk-producing and myoepithelial cells. It is well established that estrogen is an important mediator of mammary gland morphogenesis and exposure to this hormone is associated with increased breast cancer risk. Yet surprisingly, the primitive cells of the mammary epithelium do not express the estrogen receptor-α (ERα) or the progesterone receptor. This article will review the mammary epithelial cell hierarchy, possible cells of origin of different types of breast tumors, and the potential mechanisms on how estrogen and progesterone may influence the different subcomponents in normal development and in cancer. Also presented are some hypothetical scenarios on how this underlying biology may be reflected in the behavior of ERα(+) and ERα(-) breast tumors.     

Daunorubicin and daunorubicinol pharmacokinetics in plasma and tissues in the rat

Recent evidence suggests that 13-hydroxy metabolites of anthracyclines may contribute to cardiotoxicity. This study was designed to determine the pharmacokinetics of daunorubicin and the 13-hydroxy metabolite daunorubicinol in plasma and tissues, including the heart. Fisher 344 rats received 5 mg kg^–1 daunorubicin i.v. by bolus injection. Rats were killed at selected intervals for up to 1 week after daunorubicin administration for determination of concentrations of daunorubicin and daunorubicinol in the plasma, heart, liver, kidney, lung, and skeletal muscle. Peak concentrations of daunorubicin were higher than those of daunorubicinol in the plasma (133±7 versus 36±2 ng ml^–1;P<0.05), heart (15.2±1.4 versus 3.4±0.4 g g^–1;P<0.05), and other tissues. However, the apparent elimination half-life of daunorubicinol was longer than that of daunorubicin in most tissues, including the plasma (23.1 versus 14.5 h) and heart (38.5 versus 19.3 h). In addition, areas under the concentration/time curves (AUC) obtained for daunorubicinol exceeded those found for daunorubicin in almost all tissues, with the ratios being 1.9 in plasma and 1.7 in the heart. The ratio of daunorubicinol to daunorubicin concentrations increased dramatically with time from <1 at up to 1 h to 87 at 168 h in cardiac tissue. Thus, following daunorubicin injection, cumulative exposure (AUC) to daunorubicinol was greater than that to daunorubicin in the plasma and heart. If daunorubicinol has equivalent or greater potency than daunorubicin in causing impairment of myocardial function, it may make an important contribution to the pathogenesis of cardiotoxicity.