COPD与肺癌发病的相关性

目的：研究COPD与肺癌发病的相关性。方法收集2010年11月至2013年11月我院收治的门诊或住院患者210例肺癌患者作为实验组,同时选取在玉林市红十字会医院体检中心体检的非癌健康人226例作为对照组,观察2组研究对象个人呼吸系统疾病史、家族呼吸系统疾病史与肺癌之间的关系,同时观察2组中吸烟患者和不吸烟患者的 COPD 发生率。结果呼吸系统疾病中肺炎、哮喘与肺癌的发生无显著关系(P 值均>0.05)；伴有 COPD、支气管炎、肺气肿、肺结核的患者,发生肺癌的风险显著增高(P 值均<0.05),其中 COPD 与肺癌发生的关联性最强(OR =2.73)。具有COPD及肺癌家族史的人群,发生肺癌的风险显著增加(P<0.05)。吸烟患者中实验组COPD的发生率显著高于对照组(χ2=5.482,P<0.05)；实验组未吸烟患者中实验组 COPD的发生率显著高于对照组(χ2=5.901,P<0.05)。结论患有COPD病史及有 COPD家族史的患者,发生肺癌的风险增加,且COPD患者无论是否吸烟,COPD仍然会导致肺癌发生的风险性增加。     

浅谈慢性阻塞性肺疾病与肺癌的关系

有研究表明在原有慢性阻塞性肺疾病基础上肺癌发病率比一般人群高3倍以上[1],它与慢性支气管炎和肺气肿密切相关。肺癌是起源于支气管肺组织的一类异质性疾病。COPD与肺癌的发病因素和基础包括以下几个方面。一、吸烟COPD患者巨噬细胞的活化和聚集,并且释放大量的弹性蛋白酶,这是COPD炎症过程的一个重要环节。吸烟使巨噬细胞在肺泡腔聚集活化,     

老年慢性阻塞性肺疾病合并肺癌筛查评分模型建立及相关血清学标志物研究

目的探讨老年慢性阻塞性肺疾病(COPD)中肺癌筛查评分模型建立及相关血清学标志物水平。方法本研究为病例对照研究。采用非随机抽样的方法纳入2018年9月至2020年9月山西医科大学第一医院收治的年龄≥60岁, 且第一次诊断为COPD或COPD合并肺癌患者109例, 其中COPD合并肺癌患者55例(COPD合并肺癌组), 单纯COPD患者54例(单纯COPD组)。收集2组患者临床资料, 包括年龄、体质量指数、吸烟史、吸烟指数、肺气肿、病程时间及相关血清学标志物等。采用SPSS 26.0统计软件对上述结果进行统计分析。选取危险因素赋值后建立筛查评分模型并验证。结果 COPD合并肺癌组与单纯COPD组的淋巴细胞计数、中性粒细胞/淋巴细胞比值、血小板/淋巴细胞比值差异均有统计学意义(Z值分别为2.53、2.42、2.95, P值均<0.05)。病程时间≥23年、吸烟指数≥55包年、年龄≥73岁、肺气肿是老年COPD合并肺癌的危险因素。建立7分筛查评分模型并进行验证, 发现2组间差异有统计学意义(χ²=35.52, P<0.001)。结论可用7分筛查评分筛选老年COPD人群中患肺癌高危人群, 血清学标志物中淋巴细胞计数、中性粒细胞/淋巴细胞比值、血小板/淋巴细胞比值可用于进一步探究COPD患肺癌风险指标。     

COPD影像学表型与肺癌关系的研究进展

COPD是一种可预防和治疗的呼吸系统疾病,以气流受限不完全可逆、进行性发展为特征,高分辨率CT能够定量显示早期的肺气肿并进行分级,且能先于肺功能检查发现肺部解剖结构异常。肺癌是最常见的恶性肿瘤之一,研究发现COPD影像学表型可能会增加肺癌的发病风险。该文就COPD影像学表型与肺癌的关系研究进展予以综述,为肺癌的早期预防、诊断提供帮助。     

慢性阻塞性肺疾病合并肺癌的研究进展

<正>慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者中肺癌的发病率和病死率逐年升高,对患者的劳动能力、生活质量及家庭经济带来严重影响,且相比单纯COPD或者肺癌更复杂、更易产生不良后果[1-2]。目前,全球COPD 40岁以上发病率已高达9%～10%。根据WHO最新数据显示,肺癌发病率占全球新发癌症的11.6%,病死率达18.4%,是中国乃至全球发病率和病死率最高的癌症。且COPD合并肺癌的发病率也在不断上升,年发病率约为16.7%[3]。因此,COPD合并肺癌的早期诊断至关重要,针对病因、发病机制及高危人群早期预防,对于该合并症的早期诊断和个体化治疗尤为重要。本文对COPD合并肺癌的     

慢性阻塞性肺疾病合并肺癌的危险因素研究现状

摘要 肺癌是慢性阻塞性肺疾病（COPD）患者最常见的合并症之一，合并肺癌的COPD患者往往预后更差，故在预防及治疗COPD时应对肺癌发病的危险因素进行控制。既往研究中发现，COPD患者合并肺癌的危险因素可能包括：吸烟、过低或过高的BMI、空气污染、炎症反应与易感基因。应用吸入性糖皮质激素治疗COPD可能降低合并肺癌的发病率。本文旨在回顾COPD患者并发肺癌的危险因素研究进展，并为后续研究提供新思路。     

慢性阻塞性肺疾病合并肺癌的临床特征分析

目的探讨慢性阻塞性肺疾病(COPD)合并肺癌与单纯COPD患者之间临床特征的差异,提高COPD合并肺癌在临床工作中的早期识别及诊断。方法回顾性分析COPD合并肺癌及单纯COPD各48例患者的临床资料,包括年龄、性别、体重指数(BMI)、吸烟史、吸烟指数、临床症状及体征、肺功能、发病部位及病理类型等。采用SPSS 22.0统计软件对上述结果进行统计分析。结果 COPD合并肺癌患者吸烟指数高于单纯COPD患者(P0.05);COPD合并肺癌患者出现咯血、消瘦、胸痛等高于单纯COPD患者(P0.05);COPD合并肺癌以肺上叶多见(64.6%),肺功能分级多为Ⅰ-Ⅱ级(83.3%),且DLCO较单纯COPD显著降低(P0.01);COPD合并肺癌患者病理类型以鳞癌常见(54.2%)。结论 COPD合并肺癌多发生于男性吸烟者,以鳞癌常见,肺上叶发生率高,COPD患者出现咯血、消瘦、胸痛等临床症状及DLCO较前明显下降时应高度警惕肺癌的发生。     

慢性阻塞性肺疾病与肺癌的相关性

以人群为基础的研究、肺癌筛查、流行病学调查、病例对照研究、以及生物学机制研究等都发现慢性阻塞性肺疾病（chronicobstructivepulmonarydisease,COPD）与肺癌之间存在特殊的相关性。在吸烟人群中,肺功能异常以及CT检测到肺气肿是肺癌及其最终预后的重要危险因素。     

慢性阻塞性肺疾病合并肺癌108例临床分析

<正>慢性阻塞性肺疾病(COPD)的发病率已高达10%〔1〕,在全球人口死亡原因中排第4位〔2〕;肺癌发病率占所有肿瘤发病的12%,是最常见的恶性肿瘤,全球每年约135万人罹患肺癌,死于肺癌者高达100万人〔3〕。临床上COPD合并肺癌并不少见,这两种疾病与吸烟密切相关,有资料显示COPD是肺癌发病的主要危险因素〔4〕,二者是同源性疾病〔5〕。但单纯的COPD患者     

合并慢性阻塞性肺疾病对老年肺癌患者术后并发症及预后的影响

目的探讨合并慢性阻塞性肺疾病(COPD)对老年肺癌患者术后并发症及预后的影响。方法选择行手术治疗的老年肺癌患者156例,依据患者是否合并COPD分为对照组(未并发疾病)89例和观察组(有并发疾病)67例。统计并分析两组患者术后并发症发生情况,Spearman方法分析COPD与患者术后并发症的相关性,Kaplan-Meier方法分析肺癌患者术后12个月生存率。结果与对照组患者比较,观察组患者术后出现肺部感染、呼吸衰竭、心律失常和胸腔出血并发症发生率较高(P0.05)。合并COPD肺功能为Ⅲ级肺癌患者肺部感染和呼吸衰竭发生率显著高于肺功能为Ⅰ级和Ⅱ级的患者(P0.05),Spearman分析发现合并COPD与行手术治疗肺癌患者术后并发症发生率高呈正相关性(r=0.542,P0.01)。术后12个月肺癌患者总生存率为75.00%,合并COPD肺癌患者生存率低于对照组患者,且患者肺功能分级越高其术后12个生存率越低。结论合并COPD是行手术治疗老年肺癌患者术后并发症发生率高的独立危险因素,而且影响肺癌患者术后12个月生存率。     

慢性阻塞性肺疾病合并肺癌临床特征分析

目的分析慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)合并肺癌患者的临床特征,以及COPD患者发生肺癌的危险因素,为COPD中的肺癌高危人群筛查提供思路,以提高肺癌的早期诊断率。 方法回顾性分析西安交通大学第二附属医院2017年3月至2019年12月收治的195例COPD合并肺癌患者(COPD合并肺癌组)和同期住院的189例单纯COPD患者(COPD组)。 结果COPD合并肺癌组≥60岁患者比例、吸烟患者比例、吸烟指数≥400年支患者比例、男性患者比例均高于COPD组(均为P<0.05);与COPD组相比,COPD合并肺癌组咯血、胸痛、胸腔积液、乏力、体重减轻发生率均显著增加;COPD合并肺癌组动脉血pH、FEV₁、GOLD分级≤Ⅱ级患者比例高于COPD组(P<0.05);COPD合并肺癌组外周静脉血白细胞计数(WBC)、血小板计数(PLT)、中性粒细胞计数(NEUT)、嗜酸性粒细胞计数(EO)、嗜酸性粒细胞百分比(EO%)、凝血酶原时间(PT)、国际正常化比值(INR)、纤维蛋白原(FIB)、纤维蛋白降解产物(PFDP)、C反应蛋白(CRP)均高于COPD组(均为P<0.05);COPD合并肺癌确诊方式以气管镜活检为主,病变部位以右肺为主,肿瘤解剖学位置以中央型肺癌为主,病理类型男性以鳞癌为主,女性以腺癌为主,TNM分期以Ⅲ/Ⅳ期为主,初次确诊时大部分患者已发生转移;COPD组患者接受吸入糖皮质激素(ICS)治疗的比例显著高于COPD合并肺癌组(P<0.05);吸烟、EO升高和FIB含量增高是COPD患者发生肺癌的危险因素;吸入ICS治疗是其保护性因素。 结论COPD患者应该坚持规律吸入ICS治疗;当COPD患者在疾病进程中出现咯血、胸痛、胸腔积液、乏力、体重减轻等情况和/或无其他原因PLT、EO、凝血指标、CRP升高时,需要警惕合并肺癌的发生。     

COPD合并肺癌的发病机制与治疗进展

COPD是老年人呼吸系统多发疾病,与吸烟有着密切关系。近年来,COPD 的发病率仍在不断地上升,现已位居全球人口死亡原因的第4位,据 WHO 预测,到2030年将升至第3位。肺癌是危害人类健康的常见恶性肿瘤之一,是癌症死亡的首位原因,其发病率与病死率也逐年上升,目前已占全球癌症的12%以上。多年来,人们将COPD和肺癌作为2个独立的疾病进行研究。已有研究显示,在原有COPD基础上肺癌发病率比一般人群高2.76倍,COPD被视为独立于吸烟之外可以导致肺癌的另一项危险因素。本文将对两者的发病机制和治疗进展作一简要综述。     

Screening for lung cancer in high-risk groups: current status of low-dose spiral CT scanning and sputum markers

Lung cancer is the number one cause of death from cancer in the United States. Currently, there is no official recommendation to screen for lung cancer even in high-risk populations. Accordingly, we wait for patients to present with symptoms. Only 15-20% of patients are stage I lung cancer at diagnosis. Past screening trials with chest roentgenogram and sputum cytology did not show a reduction of lung cancer mortality in the screened population. Since the completion of those trials in the early 1980s we have learned that the chest X ray is not sensitive at detecting lesions <2 cm in size, and patients with chronic obstructive pulmonary disease (COPD) have a 4- to 6-fold increased risk of lung cancer independent of their smoking history. Recent trials with spiral computed tomography (CT) scan screening have detected 80-85% of lung cancers while they are stage I. The problems related to spiral CT screening are the cost and the frequent detection of benign lesions. Algorithms are being developed to try and prevent unnecessary biopsies and/or surgery. Sputum cytology is currently the only clinically approved sputum test for detecting lung cancer. However, in patients with moderate dysplasia of cytology, the LIFE autofluorescence bronchoscopy system may yield an increased sensitivity of detecting precancerous or cancerous lesions. More studies are needed before the LIFE system can be adopted as a standard clinical tool. Currently, investigators are evaluating the sputum for early lung cancer detection markers. The marker that is the most developed is the monoclonal antibody to the heterogeneous nuclear ribonucleoprotein A2/B1 on the sputum epithelial cell surface. Encouraging preliminary results have been reported and trials are ongoing. The future looks bright for the field of lung cancer screening.     

Exposing a deadly alliance: Novel insights into the biological links between COPD and lung cancer

Chronic obstructive pulmonary disease (COPD) affects more than 200 million people worldwide and is expected to become the third leading cause of death in 2020. COPD is characterized by progressive airflow limitation, due to a combination of chronic inflammation and remodeling of the small airways (bronchiolitis) and loss of elastic recoil caused by destruction of the alveolar walls (emphysema). Lung cancer is the most important cause of cancer-related death in the world. (Cigarette) smoking is the principal culprit causing both COPD and lung cancer; in addition, exposure to environmental tobacco smoke, biomass fuel smoke, coal smoke and outdoor air pollution have also been associated with an increased incidence of both diseases. Importantly, smokers with COPD – defined as either not fully reversible airflow limitation or emphysema – have a two- to four-fold increased risk to develop lung cancer. In this review, we highlight several of the genetic, epigenetic and inflammatory mechanisms, which link COPD and carcinogenesis in the lungs. Elucidating the biological pathways and networks, which underlie the increased susceptibility of lung cancer in patients with COPD, has important implications for screening, prevention, diagnosis and treatment of these two devastating pulmonary diseases.     

Genetic epidemiology of cigarette smoke-induced lung disease

Chronic obstructive pulmonary disease (COPD) and lung cancer represent two diseases that share a strong risk factor in smoking, and COPD increases risk of lung cancer even after adjusting for the effects of smoking. These diseases not only occur jointly within an individual but also there is evidence of shared occurrence within families. Understanding the genetic contributions to these diseases, both individually and jointly, is needed to identify the highest risk group for screening and targeted prevention, as well as aiding in the development of targeted treatments. The chromosomal regions that have been identified as being associated either jointly or independently with lung cancer, COPD, nicotine addiction, and lung function are presented. Studies jointly measuring genetic variation in lung cancer and COPD have been limited by the lack of detailed COPD diagnosis and severity data in lung cancer populations, the lack of lung cancer-specific phenotypes (histology and tumor markers) in COPD populations, and the lack of inclusion of minorities. African Americans, who smoke fewer cigarettes per day and have different linkage disequilibrium and disease patterns than whites, and Asians, also with different patterns of exposure to lung carcinogens and linkage patterns, will provide invaluable information to better understand shared and independent genetic contributions to lung cancer and COPD to more fully define the highest risk group of individuals who will most benefit from screening and to develop molecular signatures to aid in targeted treatment and prevention efforts.     

Chronic obstructive pulmonary disease and interstitial lung disease in patients with lung cancer

Background and objective:   Although lung cancer is frequently accompanied by COPD and interstitial lung disease (ILD), the precise coincidence of these diseases with lung cancer is not well understood. The objectives of this study were to determine the prevalence of abnormal CT and spirometric findings suggestive of COPD or ILD in a population of patients with untreated lung cancer, and to estimate the lung cancer risk in this population.
Methods:   The study population consisted of 256 patients with untreated lung cancer and 947 subjects participating in a CT screening programme for lung cancer. Semi-quantitative analysis of low attenuation area (LAA), fibrosis and ground glass attenuation (GGA) on CT was performed by scoring. Gender- and age-matched subpopulations, with stratification by smoking status, were compared using the Mantel–Haenszel projection method.
Results:   Inter-observer consistency was excellent for LAA, but not as good for fibrosis or GGA scores. Pooled odds ratios for lung cancer risk using LAA, fibrosis, GGA scores and reduced FEV₁/FVC and %VC were 3.63, 5.10, 2.71, 7.17 and 4.73, respectively ( P  < 0.0001 for all parameters). Multivariate regression analyses confirmed these results.
Conclusion:   Abnormal CT and spirometric parameters suggestive of COPD and ILD were strong risk factors for lung cancer, even after adjusting for gender, age and smoking status.     

Do inhaled corticosteroids protect against lung cancer in patients with COPD? A systematic review

Inhaled corticosteroids (ICS) are commonly prescribed to COPD patients, particularly those with more advanced stages of the disease. These patients are also at increased risk of lung cancer. A systematic review was undertaken to identify studies that examined the association between lung cancer risk and ICS therapy in COPD patients. The search strategy was created in MEDLINE and extended to EMBASE as well as other relevant databases. Both randomized controlled trials (RCTs) and observational studies were considered for inclusion. Studies were required to have incident lung cancer or deaths from lung cancer as an outcome in order to be included in the review. Six studies met the inclusion criteria. Two observational studies directly addressed the specific research. Four RCTs presented sufficient data to calculate the relative risk of lung cancer in COPD patients. None of the identified RCTs showed a statistically significant association of ICS use with lung cancer risk. Observational studies showed a protective effect from ICS use, particularly at high doses. Given the observational evidence and the low numbers of lung cancer events in the RCTs, these results may be prone to type II error. The observational studies dealt with very specific patient populations and exposure definitions, which might not have adequately captured the complex relationship between ICS exposure and lung cancer risk. Results from RCTs suggest no effect of ICS on the risk of lung cancer. However, results from observational studies suggest the potential that ICS may confer a protective effect, particularly at high doses.     

Familial lung cancer: genetic susceptibility and relationship to chronic obstructive pulmonary disease

Lung cancer continues to be the leading cause of cancer death, and although most lung cancer is attributable to cigarette smoking, underlying genetic susceptibility is suggested by studies demonstrating familial aggregation. The first family linkage study of lung cancer has identified linkage of lung, laryngeal, and pharyngeal cancer in families to a region on chromosome 6q23-25. Because lung cancer and chronic obstructive pulmonary disease (COPD) are known to aggregate in families beyond shared risk associated with smoking, the linkage results are compared and contrasted with results from genomewide linkage and association studies and candidate gene studies searching for genes for lung cancer, lung function, and COPD. Linkage on chromosome 6q to both lung cancer and lung function, and on 12 to lung cancer, COPD, and lung function, together with overlap in candidate genes for these outcomes, suggests that future research into underlying genetic mechanisms of lung disease would benefit from broadening the collection of family history data and better defining the "high risk" population. As familial risk of lung disease is better defined, referral into screening programs and prevention trials can be better targeted to reach families with both a history of lung cancer and COPD.     

北京地区慢性阻塞性肺疾病合并肺癌主要危险因素的病例对照研究

目的探讨北京地区慢性阻塞性肺疾病(Chronic obstructive pulmonary diseases,COPD)病人发生肺癌的主要危险因素。方法采用病例对照研究方法,随机选取2013年8月至2018年8月间在北京市普仁医院及北京朝阳医院呼吸科,肿瘤放化疗科收治的门诊及住院70例COPD合并肺癌患者,作为病例组。同时,随机选取同医院、同时期性别、年龄相匹配的单纯COPD患者75例作为对照组。采用统一编制的调查表(包括:一般情况、肺部疾病病史、实验室检查等)由经过专门培训的调查员以面访形式对两组进行问卷调查,发现并分析COPD并发肺癌的相关危险因素。结果居室通风不良(OR=1.892,95%CI 1.194~2.926)、吸烟(OR=1.638,95%CI 1.279~1.756)、COPD分级(OR=1.892,95%CI 1.701~1.982)、具有肿瘤家族史(OR=4.071,95%CI 2.984~16.842)与肺癌发生显著相关,COPD患者发生肺癌的风险增加(OR>1,P<0.05);远离油烟和被动吸烟环境(OR=0.347,95%CI 0.160~0.752),营养良好(OR=0.506,95%CI 0.283~0.906),使用糖皮质激素雾化治疗(OR=0.854,95%CI 0.763~0.993)的COPD患者肺癌发生风险较低(OR<1,P<0.05)。结论居室通风不良,吸烟指数较高,身体消瘦、Ⅱ级COPD、肿瘤家族史是COPD患者发生肺癌的主要危险因素,临床需警惕该类患者发生肺癌的可能性,同时建议COPD患者注意营养支持、戒烟或远离油烟、被动吸烟等环境污染,降低肺癌的发生风险。