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Lung Cancer and Interstitial Lung Diseases: A Systematic Review  [PDF]
Kostas Archontogeorgis,Paschalis Steiropoulos,Argyris Tzouvelekis,Evangelia Nena,Demosthenes Bouros
Pulmonary Medicine , 2012, DOI: 10.1155/2012/315918
Abstract: Interstitial lung diseases (ILDs) represent a heterogeneous group of more than two hundred diseases of either known or unknown etiology with different pathogenesis and prognosis. Lung cancer, which is the major cause of cancer death in the developed countries, is mainly attributed to cigarette smoking and exposure to inhaled carcinogens. Different studies suggest a link between ILDs and lung cancer, through different pathogenetic mechanisms, such as inflammation, coagulation, dysregulated apoptosis, focal hypoxia, activation, and accumulation of myofibroblasts as well as extracellular matrix accumulation. This paper reviews current evidence on the association between lung cancer and interstitial lung diseases such as idiopathic pulmonary fibrosis, sarcoidosis, systemic sclerosis, dermatomyositis/polymyositis, rheumatoid arthritis, systemic lupus erythematosus, and pneumoconiosis. 1. Introduction Interstitial lung diseases (ILDs) represent a heterogeneous group of more than two hundred diseases of either known or unknown etiology with different pathogenesis and prognosis. It is estimated that one-third is attributed to endogenous and exogenous causes including environmental/occupational factors, infections, medications, radiation, and collagen diseases. The remaining two-thirds are characterized as idiopathic since no specific cause is recognized [1]. Lung cancer is the leading cause of cancer death in the developed countries with an incidence that is augmenting steadily worldwide, particularly among women [2]. Even though cigarette smoking and exposure to inhaled carcinogens are the major causes of lung cancer, a link between ILDs and lung cancer has been suggested. The first report was published in 1939 [3], and since then pulmonary fibrosis has been investigated for its role in tumor formation and development. Although different hypotheses have suggested various interpretations for this association, specific mechanisms have never been established. This paper will review the relationship between ILDs and lung cancer. 2. ILDs as a Cause of Lung Cancer Several common features in the pathogenesis of ILDs and lung cancer have been determined during the last years. The continuous accumulation and the rapid proliferation of differentiated fibroblasts in the regions of repeated epithelial injury, in combination with an increased resistance in apoptosis, features of pulmonary fibrosis, represent pathogenic mechanisms similar to those followed by cancer cells [4], including unlimited cell multiplication, cellular immortality, and rapid immigration, which
The Frequency of Epidermal Growth Factor Receptor Mutation of Nonsmall Cell Lung Cancer according to the Underlying Pulmonary Diseases  [PDF]
Kazuhiro Usui,Tomonori Ushijima,Yoshiaki Tanaka,Chiharu Tanai,Hiromichi Noda,Norifumi Abe,Hajime Horiuchi,Teruo Ishihara
Pulmonary Medicine , 2011, DOI: 10.1155/2011/290132
Abstract: Background. Although epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are effective in patients with nonsmall cell lung cancer with epidermal growth factor receptor (EGFR) mutation, EGFR-TKIs have a risk of inducing fatal interstitial lung disease (ILD). The selection of chemotherapy based on the EGFR mutation status is recommended, however, the frequency of EGFR mutation in patients with ILD and the efficacy and safety of EGFR-TKI in patients with ILD and EGFR mutation are unknown. Methods. We retrospectively reviewed the association of the EGFR mutation status of nonsmall cell lung cancer and pulmonary diseases. Based on high-resolution computed tomography (HRCT) performed at diagnosis of lung cancer, patients were categorized into three groups: normal, emphysema, and fibrosis. Results. Of 198 patients with nonsmall cell lung cancer, we identified 52 (26.3%) patients with an EGFR mutation. EGFR mutations were identified in 43 (35.2%) of 122 patients with normal lungs, 8 (13.6%) of 59 with emphysema, and 1 (5.9%) of 17 with pulmonary fibrosis. Of the 52 patients with EGFR mutation, 43 patients received gefitinib. One patient with an EGFR mutation and fibrosis developed fatal ILD. There was not a significant difference in median overall survival from gefitinib treatment between never-smokers and smokers (797 days versus not reached; ). Conclusions. Patients with sensitive EGFR mutation and normal lungs may benefit from an EGFR-TKI treatment even if they have smoking history. 1. Introduction Gefitinib is a reversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) used for the treatment of nonsmall cell lung cancer patients [1]. Although demographic and clinical factors such as East-Asian race, female gender, nonsmoking status, and adenocarcinoma were shown to be predictive of the efficacy of gefitinib, two pivotal studies showed that the presence of somatic mutations in the kinase domain of epidermal growth factor receptor (EGFR) strongly correlates with increased responsiveness to EGFR-TKIs in patients with nonsmall cell lung cancer [2, 3]. It was later found that the subgroups of patients with nonsmall cell lung cancer who had sensitivity to gefitinib had a high incidence of EGFR mutations [4, 5]. Selecting patients on the basis of EGFR mutations, rather than clinical factors, would likely result in a population with a greater sensitivity to gefitinib. First-line gefitinib for patients with advanced nonsmall cell lung cancer who are selected on the basis of EGFR mutations improves progression-free survival,
Effects of summer acupoint application therapy in reducing exacerbation frequency of chronic lung diseases: protocol of a retrospective and prospective study
Jin Peng,Bao-yan Liu
Zhong Xi Yi Jie He Xue Bao , 2012,
Abstract: BACKGROUND: Chronic lung diseases, including bronchial asthma, chronic obstructive pulmonary disease (COPD), chronic bronchitis, allergic rhinitis and repeated respiratory tract infection (RRTL) in infants, exacerbate frequently in winter because of respiratory viral infections and low temperature. Summer acupoint application therapy (SAAT) is thought to be effective in reducing exacerbation frequency of chronic lung diseases in winter. It is a kind of therapy using a herbal mixture for external application on special acupoints during summer. The herbal mixture basically contains Semen Sinapis Albae, Herba Asari, Radix Euphorbiae Kansui and Rhizoma Corydalis. The acupoints include Feishu (BL13), Dazhui (GV14) and Danzhong (CV17). Through a large-scale multicenter trial based on three years of clinical observation, and retrospective and prospective analyses, this study aims to explore the efficacy of SAAT.METHODS AND DESIGN: In this clinical observation trial, patients who have been diagnosed with bronchial asthma, COPD, chronic bronchitis, allergic rhinitis or RRTL will be enrolled from 13 centers. All patients enrolled will be treated with SAAT over a two-year period by medical practitioners. After this, an initial case report form (CRF) will be completed and forwarded to the central study site (China Academy of Chinese Medical Sciences, Beijing, China). The CRF is designed to investigate patients’ history of medical treatment (including SAAT) and chronic lung disease exacerbation, also self-reported health condition. For retrospective analyses, the authors will focus on those who have accepted SAAT before enrollment and will collect their SAAT history and chronic lung disease exacerbation history, to evaluate the effects of SAAT. For prospective analyses, medical students will follow up with patients by phone interviews in winter once a year. The primary outcome is frequency of chronic lung disease exacerbation in winter. The secondary outcomes include conditions of lung disease recovery, non-SAAT therapy, and a self health report.DISCUSSION: The authors aim to collect 7 400 patients from July 2008 to August 2009. The final follow-up has been completed in December 2010. To reduce the selection bias, a total of 13 clinical centers from different areas of China have participated in this study. The results from this study will provide a high-quality evidence base for evaluating the efficacy of SAAT in reducing exacerbation frequency of chronic lung diseases in winter.TRIAL REGISTRATION NUMBER: This trial has been registered in Chinese Clinical Trial Regi
Antineutrophil cytoplasmic antibody (ANCA)-associated autoimmune diseases induced by antithyroid drugs: comparison with idiopathic ANCA vasculitides
Branka Bonaci-Nikolic, Milos M Nikolic, Sladjana Andrejevic, Svetlana Zoric, Mirjana Bukilica
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1789
Abstract: Antineutrophil cytoplasmic antibodies (ANCA) specific for proteinase 3 (PR3) and myeloperoxidase (MPO) are associated with necrotizing vasculitides, especially Wegener's granulomatosis (WG), microscopic polyangiitis (MPA) and idiopathic crescentic glomerulonephritis [1]. Pathogenesis of ANCA-associated idiopathic systemic vasculitides (ISV) is not well understood, but it has been shown that ANCA-activated neutrophils contribute to oxidative and proteolytic damage of blood vessels [2]. Cytoplasmic PR3-ANCA has high specificity (99%) for the newly diagnosed WG [3]. Perinuclear MPO-ANCA is a good serological marker for MPA, but it can also be found in patients with systemic lupus erythematosus (SLE), rheumatoid arthritis, drug-induced vasculitides (DIV), etc [4].ANCA-associated ISV are rare and their annual incidence is approximately 9.5 per million (in Germany) [3]. Although WG and MPA belong to the ISV group, they can be triggered by some chemicals, viral and bacterial infections and certain drugs, among which antithyroid drugs (ATDs) are very common [5]. Propylthiouracil (PTU) and methimazole (MM) may induce ANCA-positive vasculitides [6].The clinical and serological profiles of idiopathic and drug-induced autoimmune diseases (DIDs) can be very similar. Contrary to idiopathic vasculitides, DIDs have a milder course and often do not necessitate cytotoxic drug therapy [5]. Pathogenesis and clinical/serological characteristics of ANCA-associated diseases triggered by ATD have not been sufficiently investigated. In a retrospective study, we compared data from idiopathic and ATD-induced ANCA-positive patients.From 1993 to 2003, 2474 patients were tested for ANCA in the Laboratory for Allergy and Clinical Immunology in Belgrade, and 72/2474 (2.9%) were PR3-ANCA or MPO-ANCA positive. The maximal follow-up period was 11 years and the minimal was 6 months, while the median follow-up time was 4.5 years.PR3-ANCA- and MPO-ANCA-positive patients were divided into two groups. The
Role of Interleukin 17 in Lung Carcinogenesis and Lung Cancer Progression  [PDF]
Jiandong MEI, Lunxu LIU
- , 2016, DOI: : 10.3779/j.issn.1009-3419.2016.01.06
Abstract: Interleukin 17 (IL-17) is an important pro-inflammatory cytokine. It plays a critical role in mediating pathogen defense reactions, and the pathological inflammation of autoimmune diseases. IL-17 is also involved in various inflammation-related carcinogenesis. Cigarette smoking is one of the most important risk factors of lung cancer. Chronic inflammation caused by smoking and other factors is accompanied with overexpression of IL-17 within the airway, which reveals a potential relationship between IL-17 and lung carcinogenesis. Furthermore, IL-17 also plays a role in lung cancer progression via different mechanisms. In this paper, we summarized the results of current studies on IL-17 and lung carcinogenesis, as well as lung cancer progression.
Previous Lung Diseases and Lung Cancer Risk: A Systematic Review and Meta-Analysis  [PDF]
Darren R. Brenner,John R. McLaughlin,Rayjean J. Hung
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0017479
Abstract: In order to review the epidemiologic evidence concerning previous lung diseases as risk factors for lung cancer, a meta-analysis and systematic review was conducted.
Misdiagnosis of Other Lung Diseases as Asthma:69 Cases Analysis

- , 2015, DOI: 10.7507/1671-6205.2015007
Abstract: 目的分析误诊为支气管哮喘(简称哮喘)的其他疾病, 以减少临床误诊。 方法对广州呼吸疾病研究所2012年2月至2014年2月误诊为哮喘的69例患者的临床资料进行回顾性分析, 并总结疾病的特点。 结果多达13种疾病误诊为哮喘, 占前5位的分别为嗜酸粒细胞性支气管炎(21.74%)、上气道咳嗽综合征(20.29%)、慢性阻塞性肺疾病(13.04%)、变态反应性支气管肺曲霉病(7.25%)和过度换气综合征(7.25%), 少见疾病有嗜酸性肉芽肿性血管炎及声带功能障碍等。 结论许多疾病与哮喘有相似表现, 加强对哮喘及与其有相似症状的其他疾病的认识是避免和减少误诊的关键。
ObjectiveTo analyze misdiagnosis of other lung diseases as asthma to avoid medical error. MethodsSixty-nine cases who were misdiagnosed as asthma between February 2012 and February 2014 were recruited. Clinical data was collected and analyzed including characteristics of symptoms, induced sputum, pulmonary function and blood tests. ResultsThere were 13 diseases misdiagnosed as asthma, and eosinophilic bronchitis(21.74%), upper airway cough syndrome(20.29%), chronic obstructive pulmonary disease(13.04%), allergic bronchopulmonary aspergillosis(7.25%) and hyperventilation syndrome (7.25%) were the top five diseases in these cases. Some rare diseases were also found such as idiopathic hypereosinophilic syndrome and vocal cord dysfunction. ConclusionsA variety of diseases have the similar clinical symptoms with asthma. The key to avoid and reduce misdiagnosis is to strengthen the understanding of asthma and similar diseases.
Proteinase-3 as the major autoantigen of c-ANCA is strongly expressed in lung tissue of patients with Wegener's granulomatosis
Holger Brockmann, Andreas Schwarting, J?rg Kriegsmann, Peter Petrow, Andreas Gaumann, Klaus-Michael Müller, Peter Robert Galle, Werner Mayet
Arthritis Research & Therapy , 2002, DOI: 10.1186/ar410
Abstract: Proteinase-3 (PR-3) is a 29,000 Da neutral serine proteinase stored in the azurophil granules of polymorphonuclear leukocytes [1]. An increasing number of physiological and pathological properties of PR-3 have been reported. PR-3 has broad proteolytic activity and degrades a variety of extracellular matrix proteins, including fibronectin, type IV collagen and laminin [2,3]. PR-3 is identical to myeloblastin, which is a growth-promoting protein from myeloid cells [4]. Via a nonproteolytic mechanism, PR-3 has potent antimicrobial activity both against bacteria and fungi [5,6]. PR-3 was recently shown to induce apoptosis in cultured human endothelial cells [7]. PR-3 is also identical to the target antigen (antineutrophil cytoplasmic antibodies with a cytoplasmic staining pattern [c-ANCA]) associated with some systemic vasculitides such as WG and microscopic polyarteritis [8]. It is not yet known whether antineutrophil cytoplasmic antibodies (ANCA) are directly involved in the pathogenesis of WG or are merely an epiphenomenon [9-11].It has previously been thought that PR-3 expression was confined to the promyelocytic/myelocytic stage of hematopoiesis [12]. However, other cells are also capable of de novo synthesis of PR-3 mRNA. In vitro studies revealed that PR-3 expression can be induced by cytokines in human endothelial cells [13,14].The lung is the organ most frequently involved in WG, and in some cases it is the only organ affected [15]. Given the potential importance of PR-3 in the pathogenesis of WG, we sought to define the expression pattern of PR-3 in lung tissue.Normal tissues were obtained from five patients undergoing total pneumonectomy because of lung cancer. Tissue samples were snap-frozen in OCT Tissue Tek embedding medium (Leica Instruments, Hamburg, Germany).We also obtained samples from five patients with WG and a proven lung involvement from the Institute of Pathology, University of Bochum/Clinic Bergmannsheil. All of these patients had a c-ANCA titer
Advances in Classification and Research Methods of Lung Epithelial Stem ?and Progenitor Cells  [PDF]
Minhua DENG, Jinhua LI, Ye GAN, Ping CHEN
- , 2017, DOI: : 10.3779/j.issn.1009-3419.2017.02.08
Abstract: Isolation and characterization of lung epithelial stem and progenitor cells and understanding of their specific role in lung physiopathology are critical for preventing and controlling lung diseases including lung cancer. In this review, we summarized recent advances in classification and research methods of lung epithelial stem and progenitor cells. Lung epithelial stem and progenitor cells were region-specific, which primarily included basal cells and duct cells in proximal airway, Clara cells, variant Clara cells, bronchioalveolar stem cells and induced krt5+ cells in bronchioles, type II alveolar cells and type II alveolar progenitor cells in alveoli. The research methods of lung epithelial stem and progenitor cells were mainly focused on lung injury models, lineage-tracing experiments, three dimensional culture, transplantation, chronic labeled cells and single-cell transcriptome analysis. Lastly, the potential relationship between lung epithelial stem and progenitor cells and lung cancer as well as lung cancer stem cell-targeted drug development were briefly reviewed.
Serum and Lung Tissue Selenium Measurements in Subjects with Lung Cancer from Xuanwei, China  [PDF]
Lan ZHOU,Yunchao HUANG,Zhu WANG,Lianhua YE
Chinese Journal of Lung Cancer , 2011,
Abstract: Background and objective Xuanwei is an area of the highest incidence and mortality with lung cancer in China. The aim of this study is to determine serum selenium concentrations in lung cancer patients from Xuanwei as well as selenium levels of cancerous tissues, cancer-adjacent pulmonary tissues, and normal pulmonary lung tissues from lung cancer patients, and the relationship between selenium and the high incidence of lung cancer in Xuanwei. Methods One hundred and twenty female adults from Xuanwei were enrolled in the study (60 lung cancer patients and 60 with non-tumor and non-respiratory diseases, respectively) and blood samples were collected. Sixty fresh cancerous tissues and their adjacent as well as normal tissues were collected (31 samples from lung cancer patients living in Xuanwei for more than 2 years and 29 from patients in other regions of Yunnan Province outside of Xuanwei, respectively). Serum and tissue selenium concentrations were assayed using a fluorometric method. Results Women with lung cancer had a mean serum selenium value (55.22 μg/L±13.34 μg/L) of averagely 8.47%, significantly lower than that in subjects with non-tumor and non-respiratory disease controls (60.33 μg/L±13.82 μg/L)(P < 0.05). Selenium concentrations in the tumor tissues (0.105 μg/g±0.034 μg/g) were statistically lower than that of normal ones (0.140 μg/g±0.048 μg/g)(P < 0.05) from lung cancer patients in Xuanwei. Statistical differences had not been found between the cases from Xuanwei and non-Xuanwei district, adenocarcinoma and squamous cell carcinoma, among Stage I, Stage II, stage III groups. Conclusion Lower serum selenium state was negatively related to the incidence of lung cancer in Xuanwei. It was likely that lower selenium level of lung tissues was potential risk factor to lead to lung cancer.
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