目的 分析CT引导下经皮肺穿刺并发气胸的概率及影响因素.方法 回顾2013年8月至2018年1月呼吸科行CT引导下经皮肺穿刺术的所有患者,按是否并发气胸分为两组,统计分析两组的临床资料.结果 共210例,男性148例、女性62例,年龄63(55,71)岁;病灶直径3.1(2,4.7)cm,CT值35(24,46)Hu;病灶外缘离穿刺点距离1.05(0.2,2.3)cm;术后病理学诊断为肺恶性肿瘤71％、炎性病变29％.并发气胸者47例(22.4％),肺压缩最大面积约80％,1例合并皮下气肿,均治疗后康复,时间1-5天.卡方分析示,肺部病灶密度不均、病灶外缘离穿刺点距离大于、等于3cm或伴有肺气肿、肺大疱的患者,术后气胸发生率较高(P<0.05),气胸与性别等其他因素无明显关联;Logistic回归显示,病灶密度不均、病灶外缘离穿刺点距离大于等于3cm、存在肺气肿、肺大疱,为术后并发气胸的危险因素(P<0.05),相对危险度(OR)分别为6.264、2.971、8.444.结论 气胸是CT引导下经皮肺穿刺的常见并发症;病灶密度不均、病灶外缘离穿刺点距离大于等于3cm或存在肺气肿、肺大疱的患者,术后气胸的发生率显著增高.

1Department of Respiratory Medicine, Ruijin Hospital North, Shanghai Jiaotong University School of Medicine, Shanghai, People’s Republic of China; 2Institute of Respiratory Diseases, Shanghai Jiaotong University School of Medicine, Shanghai, People’s Republic of China; 3Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People’s Republic of China; 4Department of Radiology, Ruijin Hospital North, Shanghai Jiaotong University School of Medicine, Shanghai, People’s Republic of China

The number of H7N9 bird flu cases was high and the situation was grim in guizhou province in 2017. To understand the molecular characteristics of the hemagglutinin gene (HA) and the risk of human infection with avian influenza virus A(H7N9) in Guizhou Province, 2017. Homology, genetic evolution and pivotal sites related to receptor binding regions, pathogenicity and potential glycosylation of 14 avian influenza viruses A(H7N9) were analyzed by a series of bioinformation softwares. It was cleared that there was 95.9%-100% similarity among 14 strains in nucleotide of the HA gene, and there were 96.8%-97.8% and 96.8%-97.9% similarities with vaccine strains A/Shanghai/2/2013 and A/Anhui/1/2013 recommended by WHO, respectively. Phylogenetic analysis showed that 14 HA genes were directly evolved in the Yangtze River Delta evolution branch, but they could be derived from five diffenrent strains. Then 13 of 14 strains cleavage site sequences of HA protein revealed they were low pathogenic avian influenza viruses, while A/Guizhou-Weining/CSY01/2017 was high pathogenic avian influenza virus. Mutation G186V at the receptor binding sites in the HA was found in all 14 strains, and mutation Q226L in 13 strains besides A/Guizhou-Weining/CSY01/2017. All five potential glycosylation motifs in the HA were conservative.

Objective:The diagnostic value of emphysema extent in consistent air flow limitation remains controversial.Therefore, we aimed to assess the value of emphysema extent on computed tomography (CT) on the diagnosis of persistent airflow limitation.Furthermore, we developed a diagnostic criterion for further verification.Materials and methods: We retrospectively enrolled patients who underwent chest CT and lung function test.To be specific, 671 patients were enrolled in the derivation group (Group 1.1), while 479 patients were in the internal validation group (Group 1.2).The percentage of lung volume occupied by low attenuation areas (LAA%) and the percentile of the histogram of attenuation values were calculated.Results: In patients with persistent airflow limitation, the LAA% was higher and the percentile of the histogram of attenuation values was lower, compared with patients without persistent airflow limitation.Using LAA% with a threshold of -950 HU .1.4% as the criterion, the sensitivity was 44.3% and 47.2%, and the specificity was 95.2% and 95.7%, in Group 1.1 and Group 1.2, respectively.The specificity was influenced by the coexistence of interstitial lung disease, pneumothorax, and post-surgery, rather than the coexistence of pneumonia, nodule, or mass.Multivariable models were also developed. Conclusion:The emphysema extent on CT is a highly specific marker in the diagnosis of persistent airflow limitation.

Backgroud and objectives: Although lung attenuation distribution and lung volume on computed tomography (CT) have been widely used in evaluating COPD and interstitial lung disease, there are only a few studies regarding the normal range of these indices, especially in Chinese subjects. We aimed to describe the normal range of lung attenuation distribution and lung volume based on CT. Methods: Subjects with normal lung function and basically normal chest CT findings (derivation group) at Ruijin Hospital, Shanghai (from January 2010 to June 2014) were included according to inclusion and exclusion criteria. The range of the percentage of lung volume occupied by low attenuation areas (LAA%), percentile of the histogram of attenuation values (Perc n), and total lung volume were analyzed. Relationships of these measures with demographic variables were evaluated. Participants who underwent chest CT examination for disease screening and had basically normal CT findings served as an external validation group. Results: The number of subjects in the derivation group and external validation groups were 564 and 1,787, respectively. Mean total lung volumes were 4,468 +/- 1,271 mL and 4,668 +/- 1,192 mL, and median LAA%(-950 HU) was 0.19 (0.03-0.43) and 0.17 (0.01-0.41), in the derivation and external validation groups, respectively. Reference equations for lung volume and attenuation distribution (LAA% using -1,000-210 HU, Perc 1 to Perc 98) were generated: Lung volume (mL) = -1.015 *10(boolean AND)4+605.3*Sex (1= male, 0= female)+92.61*Height (cm) 12.99*Weight (kg) +/- 1766; LAA% (-950 HU)=[0.2027+0.05926*Sex (1= male, 0= female) -4.111*10(boolean AND)-3*Weight (kg) +4.924*10(boolean AND)-3*Height (cm) +8.504*10(boolean AND)-4*Age](boolean AND)7.3410.05; Upper limit of normal range: [0.2027+0.05926*Sex-4.111*10(boolean AND)-3*Weight+4.924*10(boolean AND)-3*Height+8.504*10(boolean AND)-4*Age+0.1993](boolean AND)7.3410.05. Conclusion: This large population-based retrospective study demonstrated the normal range of LAA%, Perc n, and total lung volume measured on CT scans among subjects with normal lung function and CT findings. Reference equations are provided.

Purpose: Asthma affects approximately 30 million patients in China; however, tiotropium data for Chinese patients is limited. This study aimed to assess the efficacy and safety of tiotropium in Chinese patients with moderate symptomatic asthma. Methods: A post hoc subgroup analysis was conducted on 430 Chinese patients pooled from two 24-week, replicate phase 3 trials (NCT01172808 and NCT01172821), in which they received once-daily tiotropium 2.5 mu g (Tio R2.5) or 5 mu g (Tio R5) (n = 106 or 109, respectively), twice-daily salmeterol 50 mu g (Sal 50) (n = 110), or placebo (n = 105), while maintaining inhaled corticosteroids (ICS). The co-primary endpoints assessed in week 24 were forced expiratory volume in 1 second (FEV1) peak(0-3h), response, trough FEV1 response, and responder rate as assessed using the Asthma Control Questionnaire (ACQ). Results: For both FEV1 peak(0-)(3h) responses and trough FEV1 responses, the mean treatment differences were greater for Tio R2.5, no R5, and Sal 50 compared with placebo at 0.249 L, 0.234 L, and 0.284 L, and 0.172 L, 0.180 L, and 0.164 L, respectively (P< 0.001). The ACQ responder rate in placebo, Tio R2.5, Tio R5, and Sal 50 was 58.7%, 62.3%, 59.3%, and 69.1%, respectively. Furthermore, 11 (2.6%) of 430 patients had serious adverse events (Tio R5, n = 4; Tio R2.5, n = 1; Sal 50, n = 1; and placebo, n = 5). Conclusions: Once-daily tiotropium, as add-on to medium-dose ICS, was effective and well tolerated for Chinese patients with moderate symptomatic asthma, consistent with the main analysis.

Chronic obstructive pulmonary disease (COPD) is a persistent airway inflammation influenced by cigarette smoke. Previous studies have reported that Hedgehog (Hh) signaling is aberrantly activated by cigarette smoke and dysregulated in COPD. The present study explored the role of the Hh signaling pathway on the expression levels of certain inflammatory mediators in cigarette‑induced airway inflammation. Herein, a total of three A549 cell populations were generated: The A0 group as control cells, the A1 group cells treated with nicotine at a concentration of 10 µM for 12, 24 and 48 h, and the A2 group cultured simultaneously with nicotine and cyclopamine for the same duration. The total concentrations of the inflammatory mediators interleukin‑6 (IL‑6), IL‑8 and tumor necrosis factor (TNF)‑α, and an anti‑inflammatory cytokine, IL‑10, were assessed in all of the cells by ELISA and western blotting. The protein levels of sonic hedgehog (Shh), glioma‑associated oncoprotein 1 (Gli1) and Smoothened (Smo) in nicotine‑induced Hh signaling were also detected. The results indicated that A549 had increased levels of IL‑6, IL‑8 and TNF‑α when cultured with nicotine when compared with the control cells. By contrast, the expression levels of these inflammatory mediators decreased with varying degrees when treated with cyclopamine that blocked the Hh signaling pathway. The IL‑10 expression levels exhibited the reverse. The expressions of the Shh, Gli1 and Smo proteins were higher in the A1 group when compared with the control and decreased with cyclpoamine treatment. In conclusion, the Hh signaling pathway may partly have an impact on cigarette‑induced airway inflammation via the regulation of inflammatory mediators. Thus, blocking Hh signaling and diminishing the airway inflammation reaction may serve as a potential therapy for COPD.

Background: There are limited population based data on the prevalence of asthma in China. The China Asthma and Risk factors Epidemiologic (CARE) survey was designed to understand the prevalence and risk factors for asthma in mainland China. Objectives: The CARE survey aims to demonstrate the prevalence and risk factors of asthma in mainland China among adolescents (age > 14 years) and adults. Methods: The survey was performed between February 2010 and August 2012 in eight provinces/cities of seven areas in mainland China. The inhabitants (age, > 14 years) recruited in this survey were through multi-stage cluster random sampling. Asthma diagnosis was based on medical history and lung function tests. Multivariable logistic regression was used to analyzed the risk factors for asthma. Results: The study included 164 215 subjects (men, 79 692 [48.53%]; women, 84 523 [51.47%]). 2034 (1.24%) were asthmatic patients. Among all asthmatic patients, 521 (25.61%) were newly diagnosed. Univariable regression analysis showed that risk factors for asthma included smoking, first-degree relatives with asthma, allergic rhinitis, chronic bronchitis, COPD, pollinosis, allergic pneumonia, concomitant allergic diseases, BMI and raising pets. Multivariable logistic regression indicated that asthma risk factors included women, age stratification, smoking, first-degree relatives suffering from asthma or pollinosis, combined with allergic rhinitis, eczema or GERD. Conclusions: We speculated that the prevalence of asthma is increasing in mainland China among individuals aged > 14 years in the past 10 years. A number of risk factors were identified. The risk factors of asthma would be further elucidated in our future work. Clinical implications: Our CARE study highlights that asthma epidemic in mainland China should be paid more attention.

Objective: To understand the molecular characteristics of hemagglutinin (HA) and neuraminidase (NA) as well as the disease risk of influenza virus A H7N9 in Guizhou province. Methods: RNAs were extracted and sequenced from HA and NA genes of H7N9 virus strains obtained from 18 cases of human infection with H7N9 virus and 6 environmental swabs in Guizhou province during 2014-2017. Then the variation and the genetic evolution of the virus were analyzed by using a series of bioinformatics software package. Results: Homology analysis of HA and NA genes revealed that 2 strains detected during 2014-2015 shared 98.8%-99.2% and 99.2% similarities with vaccine strains A/Shanghai/2/2013 and A/Anhui/1/2013 recommended by WHO, respectively. Two strains detected in 2016 and 14 strains detected in 2017 shared 98.2%-99.3% and 97.6%-98.8% similarities with vaccine strain A/Hunan/02650/2016, respectively. Other 6 stains detected in 2017 shared 99.1%-99.4% and 98.9%-99.3% similarities with strain A/Guangdong/17SF003/2016, respectively. Phylogenetic analysis showed that all the strains were directly evolved in the Yangtze River Delta evolution branch, but they were derived from different small branch. PEVPKRKRTAR↓GLF was found in 6 of 24 strains cleavage site sequences of HA protein, indicating the characteristic of highly pathogenic avian influenza virus. Mutations A134V, G186V and Q226L at the receptor binding sites were found in the HA. All the strains had a stalk deletion of 5 amino acid residue "QISNT" in NA protein, and drug resistance mutation R294K occurred in strain A/Guizhou-Danzhai/18980/2017. In addition, potential glycosylation motifs mutations NCS42NCT were found in the NA of 9 of 24 strains. Conclusions: HA and NA genes of avian influenza A (H7N9) virus showed genetic divergence in Guizhou province during 2014-2017. The mutations of key sites might enhance the virulence of the virus, human beings are more susceptible to it. Hence, the risk of infection is increasing.

Background: The meta-analysis aimed to compare the efficacy and safety of erlotinib versus (vs.) chemotherapy (docetaxel/pemetrexed) as second-line therapy in advanced non-small cell lung cancer (NSCLC). Methods: Literature search was completed in databases of PubMed, Embase and Ovid-Medline up to October 20, 2015; and randomized controlled trials (RCTs) met with predefined criteria were selected. Outcomes such as progression-free survival (PFS), overall survival (OS), objective response rate (ORR) and grade 3-4 toxicity between the erlotinib and chemotherapy were evaluated. Risk ratio (RR) and hazard ratio (HR) with their corresponding 95% confidence intervals (Cl) were used to calculate the pooled results. Rev. Man5.2 software was utilized for the meta-analysis. Results: A total of 7 articles (including 900 patients receiving erlotinib and 919 patients receiving pemetrexed/docetaxel) were included in this meta-analysis. There was no significant difference between erlotinib and pemetrexed/docetaxelin on PFS and OS, as well as ORR. Moreover, the total RR of the rash, anemia, neutropenia and alopecia were 15.74 (95% Cl: 4.94-50.19, P<0.001), 0.34 (95% Cl: 0.17-0.66, P = 0.002), 0.02 (95% Cl: 0.01-0.06, P < 0.001) and 0.05 (95% Cl: 0.01-0.40, P = 0.004), respectively. Conclusions: There was no significant difference of the efficacy and safety between erlotinib vs. chemotherapy as the second-line therapy in advanced NSCLC. However, erlotinib might decrease the risk of anemia, neutropenia and alopecia, and increase the risk of rash, compared with the chemotherapy.

Objective Chronic obstructive pulmonary disease (COPD) phenotypes may have individual characteristics and different responses to corticosteroids treatment.Recent advances have provided hope for a therapeutic strategy that restores corticosteroid sensitivity by increasing histone deacetylase-2 activity by low-dose theophylline.We conducted a study to identify phenotypes with good responses to inhaled corticosteroids by high-resolution computed tomography (HRCT) and explored the effect of low-dose theophylline on corticosteroid sensitivity.Methods Sixty-three stable COPD patients were examined by HRCT and classified into three phenotypes:absence of emphysema,with little emphysema with or without bronchial wall thickening (A phenotype),emphysema without bronchial wall thickening (E phenotype),and emphysema with bronchial wall thickening (M phenotype).They were treated with fluticasone propionate/salmeterol with or without theophylline for twenty-four-week follow-up.Results The patients of phenotype A and M responded well to corticosteroid treatment,whereas patients of phenotype E responded poorly.Anti-inflammatory sensitivity of inhaled corticosteroid was increased in the phenotype E treated with low-dose theophylline combination therapy.Conclusions Lowdose theophylline may improve the corticosteroids sensitivities based on HRCT phenotypes of COPD.

The study aimed to ascertain relationships between inhaled corticosteroid (ICS) and the incidence of oral candidiasis (OC) among Chinese patients. Literature retrieve was performed in databases with predefined strategy. Quality assessment was performed by the Cochrane Collaboration's tool. Risk difference (RD) or risk ratio (RR) with corresponding 95% confidence interval (CI) was used as the effect sizes. OC incidence was detected in different study types. Publication bias was detected by funnel plot and Egger's test. In total, 46 studies were included for the meta-analysis, and the overall quality was moderate. Using ICS did not significantly increase the incidence of OC, compared with non-ICS (RD = 1.40%, 95% CI: -0.30% to 3.10%, P = 0.111) in randomized controlled trials (RCTs). However, higher ICS dose significantly increased the incidence of OC than lower ones (RR = 2.48, 95% CI: 1.23 to 4.99, P = 0.011), and ICS with a spacer device showed a significant decreased incidence than that without the device (RR = 0.37, 95% CI: 0.22 to 0.63, P < 0.001). The overall incidence of OC was 5.1%. Thereinto, the OC incidence was 10.0% in RCTs comparing different ICS dosages, 3.2% in observational studies and 1.4% in RCTs comparing ICS vs. non-ICS. In studies focused on preventing OC, the preventive group achieved a decreased incidence than control group (2.4% vs. 16.4%). Higher ICS dose might be significantly associated with OC incidence in Chinese patients. ICS with a spacer device might reduce the incidence and be more preferable for patients. ICS may not increase the OC incidence given the appropriate prevention.

Background Sonic hedgehog (SHH) signaling is important in embryonic development. Previous researches demonstrated that smoke exposure activates abnormally SHH signaling in bronchial epithelial cells which has been implicated in lung cancer. Moreover, the feedback inhibitor of SHH, human hedgehog interacting protein (HHIP), has also been found associated with susceptibility to another cigarette-induced disease, chronic obstructive pulmonary disease (COPD). Aims and objectives Our aim was to explore the role of SHH pathway in cigarette-induced airway inflammation. We hypothesized that SHH activated in alveolar epithelial cells exposed to smoke upregulates expression level of airway inflammatory mediators. Methods: Human alveolar epithelial pulmonary cells (A549) were devided into three groups: control, cells stimulated by nicotine (10mol/L) with or without cyclopamine (10mol/L) (inhibitor of SHH). A549 cells were treated with nicotine respectively for 12h、24h、48h. Expression levels of IL-6、IL-8 and TNF-α in A549 cells were compared among the different groups using RT-PCR and western blot. Results: The study showed that SHH levels increased significantly in A549 incubated with nicotine. We found that IL-6 levels were significantly higher at both mRNA and protein levels in A549 stimulated by nicotine with or without cyclopamine than control group, especially in cells treated for 48h, but lower in cyclopamine group compared with nicotine alone. As to IL-8 and TNF-α levels, compared with the control, their levels also significantly increased in cells exposed to nicotine, but decreased when incubated with cyclopamine. Conclusions: SHH signaling plays an important role in cigarette-induced airway inflammation by upregulating inflammatory mediators.

Invasive pulmonary aspergillosis (IPA) is an infection that often occurs in immunocompromised patients and has a high mortality rate. In recent years, the reported incidence of IPA in the context of chronic obstructive pulmonary disease (COPD) has seemingly increased. The combination of factors such as long-term corticosteroid use, increasing rate of bacterial exacerbations over time, lung immune imbalance, and malnutrition are responsible for the emergence of IPA in COPD patients. A diagnosis of IPA in COPD patients is difficult to make, which explains the delay in antifungal therapy and the high mortality rate. The purpose of this study is to increase the recognition and improve the outcomes associated with this situation through the description of our case. In patients in which IPA is suspected, comprehensive analysis of their clinical manifestations, imaging, microbiology and serological examination results are effective means of increasing the rate of reliable diagnosis. If the patient's condition permits, a pathological specimen should be obtained as soon as possible.

SESSION TITLE: Chest Infections I SESSION TYPE: Case Report Poster PRESENTED ON: Sunday, April 17, 2016 at 11:45 AM - 12:45 PM INTRODUCTION: Percutaneous needle biopsy of the lung is a useful tool in the evaluation of pulmonary abnormalities. However, percutaneous needle biopsy has some complications. We present a case of a pleural empyema secondary to a percutaneous lung biopsy. CASE PRESENTATION: A 30-year-old Chinese male was admitted with a 2-week history of fever and sputum. The peak temperature was about 38.5 ℃ and the sputum had a fishiness smell. He often had toothache. The physical examination was unremarkable. Initial laboratory findings were significant for WBC 11*10^9/L, with 68% neutrophils and CRP 107mg/L. Chest CT scanning showed a patch of infiltration with ground grass density and segmental distribution, two nodular opacities in the infiltration with 1-2 centimeter in diameter and a hole in one of the nodules. Firstly, he was treated with Amoxicillin/clavulanic for 1 week. The symptoms including fever disappeared and blood cell count came to normal. The follow-up CT showed that the infiltration with ground grass density disappeared, the nodule with a hole shrinked with the hole disappeared, but the other nodule seemed a bit larger. A computed tomography guided percutaneous needle biopsy was performed successfully. However, two hours later the operation, he complained of left chest pain and dyspnea. The breath sound of left lung was low. The chest X-ray showed no pneumothorax or obvious pleural effusion. Two days later, he began to have fever, with the peak temperature of 38 ℃ and dyspnea, while the chest pain was alleviated. The WBC was 12*10^9/L, with 79% neutrophils, CRP was 7.3mg/dl and procalcitionin (PCT) was 0.45ng/ml. The chest CT showed moderate pleural effusion in left thorax and bilateral infiltration. A pleurocentesis was performed and the pleural fluid analysis showed: WBC 1.2*10^9/L, neutrophil: 89%, total protein 59g/L, LDH 840U/L, ADA 21U/L. Imipenem/cilastatin and vancomycin were initiated and a pigtail catheter was placed for drainage. His symptom resolved in 3 days. The infiltration of the contralateral lung disappeared 1 week later, and the infiltration and pleural effusion was mostly absorbed in one month. DISCUSSION: Percutaneous needle biopsy of the lung is indispensable in diagnosing malignant tumor, special inflammation and infection. The common complications include pneumothorax and pulmonary hemorrhage. The rare but important complications include air embolism and tumor seeding1. No case has been reported about pleural empyema secondary to a percutaneous lung biopsy to the best of our knowledge. Amoxicillin/clavulanic is indicated in treating lung abscess and pneumonia2. However, the dissemination of the infection suggested that the focus was purulent and bacteria were still alive in it. CONCLUSIONS: As our case demonstrates, pleural empyema can be a complication of percutaneous lung biopsy. Amoxicillin/clavulanic may not very effective in treating lung abscess. Reference #1: Winokur and Pua et al., 2013 Reference #2: Yazbeck and Dahdel et al., 2014 DISCLOSURE: The following authors have nothing to disclose: Ting Cheng, QiJian Cheng, HuanYing Wan No Product/Research Disclosure Information

SESSION TITLE: COPD Phenotypes SESSION TYPE: Original Investigation Poster PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM PURPOSE: Chronic obstructive pulmonary disease (COPD) phenotypes may have individual characteristics and different responses to corticosteroids treatment. Recent advances have provided hope for a therapeutic strategy that restores corticosteroid sensitivity by increasing histone deacetylase-2 activity by low-dose theophylline. We conducted a study to identify phenotypes with good responses to inhaled corticosteroids by high-resolution computed tomography (HRCT) and explored the effect of low-dose theophylline on corticosteroid sensitivity. METHODS: Sixty-three stable COPD patients were examined by HRCT and classified into three phenotypes: absence of emphysema, with little emphysema with or without bronchial wall thickening (A phenotype), emphysema without bronchial wall thickening (E phenotype), and emphysema with bronchial wall thickening (M phenotype). They were treated with fluticasone propionate/salmeterol with or without theophylline for twenty-four week follow-up. RESULTS: The patients of phenotype A and M responded well to corticosteroid treatment, whereas patients of phenotype E responded poorly. Anti-inflammatory sensitivity of inhaled corticosteroid was increased in the phenotype E treated with low-dose theophylline combination therapy. CONCLUSIONS: Low-dose theophylline may improve the corticosteroids sensitivitiy based on HRCT phenotypes of COPD. CLINICAL IMPLICATIONS: COPD phenotypes may have individual characteristics and different responses to corticosteroids treatment. Low-dose theophylline may improve the corticosteroids sensitivitiy based on HRCT phenotypes of COPD. DISCLOSURE: The following authors have nothing to disclose: Xian Wen Sun, Qing Yun Li, Shu Yi Gu, HuanYing Wan, Shao Guang Huang No Product/Research Disclosure Information