本文選題：慢性阻塞性肺疾病 + 肺癌��； 參考：《吉林大學(xué)》2017年碩士論文

【摘要】：背景:在我國(guó)城市人口十大死因中,呼吸系統(tǒng)疾病(主要是慢阻肺)占13.89%,居第四位,在農(nóng)村占22.04%,居第一位,全國(guó)因慢阻肺死亡的人數(shù)約100萬。同時(shí),在我國(guó),肺癌的發(fā)病率、死亡率已躍居所有惡性腫瘤之首,人類的健康已經(jīng)嚴(yán)重受到肺癌的威脅。2005年,我國(guó)大約有536 407例新發(fā)肺癌病例,全年約有475 768人死于肺癌[1]。Young[2]等研究認(rèn)為遺傳、環(huán)境、異常免疫反應(yīng)等是慢阻肺和肺癌發(fā)生、發(fā)展的共同危險(xiǎn)因素。另外Steven Bozinovski等人指出慢阻肺引起的氧化及炎癥反應(yīng)可能通過破壞基因組的穩(wěn)定性、抑制腫瘤免疫監(jiān)視作用以及促進(jìn)腫瘤生長(zhǎng)和遷移引起肺癌的發(fā)生[3]。目前慢阻肺向肺癌轉(zhuǎn)化的機(jī)制尚不明確,但大量流行病學(xué)數(shù)據(jù)表明慢阻肺是肺癌的獨(dú)立危險(xiǎn)因素,肺癌在慢阻肺人群中的患病率是正常人群肺癌患病率的2-5倍。隨著目前空氣污染逐漸加重,長(zhǎng)期暴露于空氣中的PM2.5使得罹患呼吸系統(tǒng)疾病的概率也隨之增加,值得提出的是,煙草煙霧中富含高濃度的PM2.5,是室內(nèi)PM2.5的主要來源,也是慢阻肺及肺癌的共同危險(xiǎn)因素。我們國(guó)家自然科學(xué)基金項(xiàng)目課題組已經(jīng)證實(shí)了暴露于高濃度的香煙煙霧PM2.5下,可直接誘發(fā)支氣管上皮細(xì)胞發(fā)生惡性轉(zhuǎn)變。目前課題組正通過微流控技術(shù)證明表皮生長(zhǎng)因子受體(Epidermal growth factor receptor,EGFR)、信號(hào)轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子3(Signal transducer and activator of transcription 3,STAT3)在慢阻肺誘發(fā)肺癌過程中起到的重要作用[4],為今后深入研究慢阻肺向肺癌的轉(zhuǎn)化提供了良好的理論基礎(chǔ)和技術(shù)支持。目的:通過研究慢性阻塞性肺疾病(慢阻肺)合并肺癌患者的臨床特征,探討肺癌在慢阻肺患者中的發(fā)病率,為早期發(fā)現(xiàn)、診斷肺癌提供幫助。方法:應(yīng)用隨機(jī)數(shù)字表法選取我院2014年01月01日至2016年09月01日收治的符合納入標(biāo)準(zhǔn)的慢阻肺急性加重期患者208例,慢阻肺合并肺癌患者32例進(jìn)行回顧性分析,記錄兩組患者的一般資料、吸煙史、吸煙指數(shù)、臨床癥狀及體征、肺功能檢查結(jié)果、肺癌病理類型、肺癌分期、腫瘤標(biāo)志物等,采用SPSS16.0統(tǒng)計(jì)軟件對(duì)上述結(jié)果進(jìn)行統(tǒng)計(jì)分析。結(jié)果:1、年齡及性別:慢阻肺合并肺癌組患者共32例。其中男性16例,女性16例,年齡(49~80歲),平均年齡(64.44±7.582)歲,慢阻肺急性加重期患者共208例,其中男性110例,女性98例,年齡(42~85歲),平均年齡(62.83±7.628)歲,兩組患者的年齡、性別比較差異無統(tǒng)計(jì)學(xué)意義(P0.05),兩組患病人群均為高齡人群。2、吸煙史及吸煙指數(shù):慢阻肺合并肺癌組吸煙指數(shù)(平均748.209支年)明顯高于慢阻肺組(平均376.015支年)(P0.05),差異具有統(tǒng)計(jì)學(xué)意義。3、肺功能:慢阻肺合并肺癌患者與慢阻肺急性加重期患者肺功能比較,前者FEV1/FVC(%)(平均59.01±9.85)高于后者(平均55.78±11.85),差異具有統(tǒng)計(jì)學(xué)意義(P0.05);前者FVC(L)(平均1.93±0.45)低于后者(平均2.47±0.83),差異具有統(tǒng)計(jì)學(xué)意義(P0.05)。4、臨床癥狀及體征:慢阻肺合并肺癌組痰中帶血、胸痛、肺不張及胸腔積液患者人數(shù)均高于慢阻肺組,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。5、實(shí)驗(yàn)室檢查(腫瘤標(biāo)志物):比較慢阻肺合并肺癌組中不同類型肺癌之間的腫瘤標(biāo)志物,得出CEA、NSE、總前列腺特異抗原、角蛋白19片段在不同類型肺癌之間的差異具有統(tǒng)計(jì)學(xué)意義(P0.05),其他腫瘤標(biāo)志物在各類型肺癌之間無明顯統(tǒng)計(jì)學(xué)差異。6、病理類型、分期:慢阻肺合并肺癌患者中I期患者占6.3%、Ⅱ期患者占21.9%、Ⅲ期患者占40.6%、Ⅳ期患者占31.3%。中央型肺癌占53.1%,周圍型肺癌患者占46.9%。鱗癌患者占25.0%,腺癌患者占46.9%,小細(xì)胞肺癌患者占28.1%。鱗癌患者中男性7例,女性1例;腺癌患者中男性4例,女性11例;小細(xì)胞癌患者中男性5例,女性4例。鱗癌患者中,男性患者占43.8%,明顯高于女性;在腺癌患者中女性占73.3%,明顯高于男性,其差異具有統(tǒng)計(jì)學(xué)意義(P0.05),小細(xì)胞肺癌中男女性別比較,其差異無統(tǒng)計(jì)學(xué)意義(P0.05)。7、肺癌在慢阻肺人群中的患病率:本實(shí)驗(yàn)中符合納入標(biāo)準(zhǔn)的慢阻肺合并肺癌患者與同期入院的慢阻肺急性加重期患者人數(shù)比較,得出慢阻肺患者肺癌的患病率為11.4‰,根據(jù)本組實(shí)驗(yàn)數(shù)據(jù)得出肺癌在慢阻肺人群中的患病率為正常人群的2.85倍。由此可以看出合并有慢阻肺的人群更容易罹患肺癌。結(jié)論：1、肺癌在慢阻肺人群中的患病率為11.4‰,為正常人群肺癌患病率的2.85倍。2、當(dāng)慢阻肺患者出現(xiàn)胸痛、痰中帶血、肺不張及胸腔積液等臨床表現(xiàn)時(shí)應(yīng)高度警惕肺癌的存在。3、腫瘤標(biāo)志物CEA、NSE、角蛋白19片段分別對(duì)腺癌、小細(xì)胞癌及鱗癌的診斷有提示價(jià)值。4、統(tǒng)計(jì)顯示慢阻肺合并肺癌患者多為中央型肺癌,確診時(shí)多為Ⅲ期至Ⅳ期,其病理類型以腺癌為主,其次為小細(xì)胞癌及鱗癌。同時(shí)男性中鱗癌較多見,而在女性中腺癌更多見。
[Abstract]:Background: among the ten major causes of death of urban population in China, respiratory diseases (mainly slow resistance lung) account for 13.89%, occupy fourth, occupy 22.04% in rural areas, occupy the first place, and the number of people who have died of chronic obstructive pulmonary disease is about 1 million. At the same time, in China, the incidence of lung cancer and mortality have been the first of malignant tumors, and human health has been seriously affected by lung cancer. In.2005, there were about 536407 cases of new lung cancer in China, and about 475768 people died of lung cancer [1].Young[2] throughout the year. The genetic, environmental, and abnormal immune responses were the common risk factors for the development of slow resistance lung and lung cancer. In addition, Steven Bozinovski et al. Pointed out that the oxidative and inflammatory reactions caused by slow lung obstruction may pass through. The stability of the genome, the inhibition of the role of the tumor immune surveillance and the promotion of tumor growth and migration, the mechanism of the transformation of lung cancer by [3]. is not clear, but a large number of epidemiological data indicate that the chronic obstructive pulmonary disease is an independent risk factor for lung cancer, and the prevalence rate of lung cancer in the chronic obstructive lung population is normal. The incidence of lung cancer is 2-5 times. As the current air pollution progressively worsens, PM2.5, which is exposed to the air for a long time, increases the probability of respiratory disease. It is worth mentioning that the high concentration of PM2.5 in tobacco smoke is the main source of indoor PM2.5 and a common risk factor for chronic obstructive lung and lung cancer. However, the science foundation project team has confirmed that exposure to high concentration of cigarette smoke PM2.5 can directly induce malignant transformation of bronchial epithelial cells. The research group is currently using microfluidic technology to prove Epidermal growth factor receptor (EGFR), signal transduction and transcription activator 3 (Signal transd). Ucer and activator of transcription 3, STAT3) plays an important role in the process of lung cancer induced by slow resistance lung. It provides a good theoretical basis and technical support for further study of the transformation of chronic obstructive pulmonary disease to lung cancer in the future. Objective: To explore the clinical characteristics of chronic obstructive pulmonary disease (COPD) with lung cancer and to explore the lung cancer in the future. The incidence of chronic obstructive pulmonary disease was helpful for early detection and diagnosis of lung cancer. Methods: a random digital table was used to select 208 cases of acute exacerbation of chronic obstructive pulmonary disease, which were admitted in our hospital from 01 to 2016, 2014 to 2016 09, and 32 cases of chronic obstructive pulmonary disease combined with lung cancer were retrospectively analyzed, and a record of two groups of patients was recorded. Data, smoking history, smoking index, clinical symptoms and signs, lung function examination results, lung cancer pathological types, lung cancer stages, tumor markers, and so on. The results were statistically analyzed by SPSS16.0 software. Results: 1, age and sex: 32 cases of chronic obstructive pulmonary disease combined with lung cancer group, including 16 cases of male, 16 women, age (49~80 years), The average age (64.44 + 7.582) years and the acute exacerbation of the chronic obstructive pulmonary disease were 208 cases, including 110 men, 98 women, age (42~85 years), the average age (62.83 + 7.628) years, the age of the two groups, and the gender difference was not statistically significant (P0.05). The two group of patients were all.2, smoking history and smoking index: slow resistance lung combined lung cancer. The smoking index (average 748.209 years) was significantly higher than that in the slow resistance Lung Group (376.015 years average) (P0.05). The difference was statistically significant.3. The pulmonary function: the pulmonary function of the patients with chronic obstructive pulmonary disease and the acute exacerbation of the chronic obstructive pulmonary disease was FEV1/FVC (59.01%) (average 59.01 + 9.85) higher than that of the latter (mean 55.78 + 11.85), and the difference was statistically significant Meaning (P0.05); the former FVC (L) (average 1.93 + 0.45) was lower than the latter (mean 2.47 + 0.83), the difference was statistically significant (P0.05).4, the clinical symptoms and signs: the number of patients in the sputum with blood, chest pain, atelectasis and pleural effusion in the slow resistance lung combined with lung cancer group were higher than that in the slow obstructive pulmonary group, the difference was statistically significant (P0.05).5, laboratory examination (tumor markers) Compared with the tumor markers of different types of lung cancer in the chronic lung cancer group, the difference of CEA, NSE, total prostatic specific antigen and keratin 19 fragment between different types of lung cancer was statistically significant (P0.05), and there was no significant difference between other tumor markers in different types of lung cancer.6, pathological type, staging: slow resistance lung Of the patients with lung cancer, 6.3% were I, 21.9% in stage II, 40.6% in stage III, 53.1% in central type lung cancer in stage IV, 25% in 46.9%. squamous cell carcinoma, 46.9% in adenocarcinoma, 46.9% in adenocarcinoma, 7 in 28.1%. squamous cell carcinoma and 1 in female, 4 in adenocarcinoma and 11 in women. In cases of small cell carcinoma, there were 5 males and 4 females. Among the squamous carcinoma patients, 43.8% of the male patients were significantly higher than those of women. In adenocarcinoma patients, women accounted for 73.3%, significantly higher than men, and the difference was statistically significant (P0.05). There was no statistical difference between men and women in small cell lung cancer (P0.05).7, and lung cancer in the slow resistance lung population. The prevalence of lung cancer in slow resistance lung patients was 11.4 per thousand, and the prevalence rate of lung cancer in the slow resistance lung was 2.85 times that of the normal population. Conclusion: 1, the prevalence rate of lung cancer in the slow resistance lung population is 11.4 per thousand, which is 2.85 times.2 of the normal population of lung cancer. When the patients with chronic obstructive pulmonary disease have chest pain, phlegm, atelectasis and pleural effusion, we should be highly vigilant for the existence of.3, tumor markers CEA, NSE, horns eggs The 19 fragments of white 19 were valuable for the diagnosis of adenocarcinoma, small cell carcinoma and squamous cell carcinoma. The statistics showed that most of the patients with chronic obstructive pulmonary disease were central type lung cancer, and most of them were stage III to IV. The pathological types were mainly adenocarcinoma, followed by small cell carcinoma and squamous cell carcinoma.

【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R734.2;R563.9

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