Database : MEDLINE
Search on : pulmonary and emphysema [Words]
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[PMID]: 29522352
[Au] Autor:Petersen H; Vazquez Guillamet R; Meek P; Sood A; Tesfaigzi Y
[Ad] Address:Lovelace Respiratory Research Institute, Health and Environmental Epidemiology Program, Albuquerque, New Mexico, United States.
[Ti] Title:Early Endotyping - A Chance for Intervention in COPD.
[So] Source:Am J Respir Cell Mol Biol;, 2018 Mar 09.
[Is] ISSN:1535-4989
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Chronic obstructive pulmonary disease (COPD) is a syndrome that comprises several lung pathologies, but subphenotyping the various disease subtypes has been difficult. One reason may be that current efforts which are focused on studying COPD once it has occurred do not allow to trace back the different origins of disease. This prespective proposes that emphysema originates when susceptible airway, endothelial, and/or hematopoietic cells are exposed to environmental toxins, such as cigarette smoke, biomass fuel, or traffic emissions. These susceptible cell types may initiate different distinct pathobiological mechanisms ("COPD endotypes") that ultimately manifest the emphysematous destruction of the lung. Based on evidence from the "Airway" endotype, we suggest that grading these endotypes by severity may allow to better diagnose disease at early stages when intervention can be designed based on the mechanisms involved. Therefore, genomic, proteomic, and metabolomic studies on at risk patients will be important to identify biomarkers that help designate each endotype. Together with understanding of the involved molecular pathways that lead to disease manifestation, these efforts may provide intervention strategies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1165/rcmb.2018-0002PS

  2 / 18955 MEDLINE  
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[PMID]: 29381718
[Au] Autor:Sasaki M; Chubachi S; Kameyama N; Sato M; Haraguchi M; Miyazaki M; Takahashi S; Nakano T; Kuroda Y; Betsuyaku T; Matsuo K
[Ad] Address:Division of Pulmonary Medicine, Keio University School of Medicine, Tokyo, Japan.
[Ti] Title:Effects of long-term cigarette smoke exposure on bone metabolism, structure, and quality in a mouse model of emphysema.
[So] Source:PLoS One;13(1):e0191611, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Smoking is a common risk factor for both chronic obstructive pulmonary disease (COPD) and osteoporosis. In patients with COPD, severe emphysema is a risk factor for vertebral fracture; however, the effects of smoking or emphysema on bone health remain largely unknown. We report bone deterioration in a mouse model of emphysema induced by nose-only cigarette smoke (CS) exposure. Unexpectedly, short-term exposure for 4-weeks decreased bone turnover and increased bone volume in mice. However, prolonged exposure for 20- and 40-weeks reversed the effects from suppression to promotion of bone resorption. This long-term CS exposure increased osteoclast number and impaired bone growth, while it increased bone volume. Strikingly, long-term CS exposure deteriorated bone quality of the lumbar vertebrae as illustrated by disorientation of collagen fibers and the biological apatite c-axis. This animal model may provide a better understanding of the mechanisms underlying the deterioration of bone quality in pulmonary emphysema caused by smoking.
[Mh] MeSH terms primary: Bone and Bones/metabolism
Disease Models, Animal
Emphysema/metabolism
Smoke
Tobacco Products
[Mh] MeSH terms secundary: Animals
Bone Remodeling
Mice
Mice, Inbred C57BL
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Smoke)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191611

  3 / 18955 MEDLINE  
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[PMID]: 29415880
[Au] Autor:Houssaini A; Breau M; Kebe K; Abid S; Marcos E; Lipskaia L; Rideau D; Parpaleix A; Huang J; Amsellem V; Vienney N; Validire P; Maitre B; Attwe A; Lukas C; Vindrieux D; Boczkowski J; Derumeaux G; Pende M; Bernard D; Meiners S; Adnot S
[Ad] Address:INSERM U955, Département de Physiologie-Explorations Fonctionnelles, and DHU A-TVB Hôpital Henri Mondor, AP-HP, Créteil, France.
[Ti] Title:mTOR pathway activation drives lung cell senescence and emphysema.
[So] Source:JCI Insight;3(3), 2018 Feb 08.
[Is] ISSN:2379-3708
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Chronic obstructive pulmonary disease (COPD) is a highly prevalent and devastating condition for which no curative treatment is available. Exaggerated lung cell senescence may be a major pathogenic factor. Here, we investigated the potential role for mTOR signaling in lung cell senescence and alterations in COPD using lung tissue and derived cultured cells from patients with COPD and from age- and sex-matched control smokers. Cell senescence in COPD was linked to mTOR activation, and mTOR inhibition by low-dose rapamycin prevented cell senescence and inhibited the proinflammatory senescence-associated secretory phenotype. To explore whether mTOR activation was a causal pathogenic factor, we developed transgenic mice exhibiting mTOR overactivity in lung vascular cells or alveolar epithelial cells. In this model, mTOR activation was sufficient to induce lung cell senescence and to mimic COPD lung alterations, with the rapid development of lung emphysema, pulmonary hypertension, and inflammation. These findings support a causal relationship between mTOR activation, lung cell senescence, and lung alterations in COPD, thereby identifying the mTOR pathway as a potentially new therapeutic target in COPD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  4 / 18955 MEDLINE  
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[PMID]: 29411159
[Au] Autor:Maeda R; Funasaki A; Motono N; Sekimura A; Usuda K; Uramoto H
[Ad] Address:Department of Thoracic and Breast Surgery, Faculty of Medicine, University of Miyazaki, Kihara 5200, Kiyotake, Miyazaki, 889-1692, Japan. ryo_maeda@med.miyazaki-u.ac.jp.
[Ti] Title:Combined pulmonary fibrosis and emphysema predicts recurrence following surgery in patients with stage I non-small cell lung cancer.
[So] Source:Med Oncol;35(3):31, 2018 Feb 06.
[Is] ISSN:1559-131X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The purpose of this study was to clarify the clinicopathologic characteristics of non-small cell lung cancer (NSCLC) patients with combined pulmonary fibrosis and emphysema (CPFE). We investigated the association between CPFE, the cancer survival, and the pathological features of clinical stage I NSCLC patients. Between 2005 and 2014, 218 consecutive patients with clinical stage I NSCLC underwent complete resection with systematic lymph node dissection. A univariate analysis by log-rank tests was performed to determine the risk factors for recurrence, and the Cox proportional hazards regression model was used to identify potential independent predictors. The 5-year recurrence-free proportion of patients with CPFE was 36%, which was significantly lower than in those without CPFE (82%; p < 0.001). On multivariate analysis, the presence of CPFE was one of the statistically significant independent predictors for tumor recurrence (p = 0.005). Postoperative pathological prognostic factors, including moderate or poor histological differentiation, lymphatic permeation, intratumoral vascular invasion, and lymph node metastasis, were detected more often in patients with CPFE. NSCLC patients with CPFE have histologically more invasive tumors than those without CPFE. In patients with clinical stage I NSCLC, the presence of CPFE was a statistically significant predictor of recurrence.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1007/s12032-018-1091-x

  5 / 18955 MEDLINE  
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[PMID]: 29294041
[Au] Autor:Moya CM; Zaballos MA; Garzón L; Luna C; Simón R; Yaffe MB; Gallego E; Santisteban P; Moreno JC
[Ad] Address:Thyroid Molecular Laboratory, Institute for Medical and Molecular Genetics, La Paz University Hospital, Madrid, Spain.
[Ti] Title:TAZ/WWTR1 Mediates the Pulmonary Effects of NKX2-1 Mutations in Brain-Lung-Thyroid Syndrome.
[So] Source:J Clin Endocrinol Metab;103(3):839-852, 2018 Mar 01.
[Is] ISSN:1945-7197
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Context: Identification of a frameshift heterozygous mutation in the transcription factor NKX2-1 in a patient with brain-lung-thyroid syndrome (BLTS) and life-threatening lung emphysema. Objective: To study the genetic defect that causes this complex phenotype and dissect the molecular mechanism underlying this syndrome through functional analysis. Methods: Mutational study by DNA sequencing, generation of expression vectors, site-directed mutagenesis, protein-DNA-binding assays, luciferase reporter gene assays, confocal microscopy, coimmunoprecipitation, and bioinformatics analysis. Results: We identified a mutation [p.(Val75Glyfs*334)] in the amino-terminal domain of the NKX2-1 gene, which was functionally compared with a previously identified mutation [p.(Ala276Argfs*75)] in the carboxy-terminal domain in other patients with BLTS but without signs of respiratory distress. Both mutations showed similar protein expression profiles, subcellular localization, and deleterious effects on thyroid-, brain-, and lung-specific promoter activity. Coexpression of the coactivator TAZ/WWTR1 (transcriptional coactivator with PDZ-binding motif/WW domain-containing transcription regulator protein 1) restored the transactivation properties of p.(Ala276Argfs*75) but not p.(Val75Glyfs*334) NKX2-1 on a lung-specific promoter, although both NKX2-1 mutants could interact equally with TAZ/WWTR1. The retention of residual transcriptional activity in the carboxy-terminal mutant, which was absent in the amino-terminal mutant, allowed the functional rescue by TAZ/WWTR1. Conclusions: Our results support a mechanistic model involving TAZ/WWTR1 in the development of human congenital emphysema, suggesting that this protein could be a transcriptional modifier of the lung phenotype in BLTS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1210/jc.2017-01241

  6 / 18955 MEDLINE  
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[PMID]: 29514663
[Au] Autor:Yang M; Kohler M; Heyder T; Forsslund H; Garberg HK; Karimi R; Grunewald J; Berven FS; Nyrén S; Magnus Sköld C; Wheelock ÅM
[Ad] Address:Respiratory Medicine Unit, Department of Medicine Solna & Center for Molecular Medicine, Karolinska Institutet, Lung Research Lab L4:01, SE-171 76, Stockholm, Sweden. 2002ymx02@gmail.com.
[Ti] Title:Proteomic profiling of lung immune cells reveals dysregulation of phagocytotic pathways in female-dominated molecular COPD phenotype.
[So] Source:Respir Res;19(1):39, 2018 Mar 08.
[Is] ISSN:1465-993X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Smoking is the main risk factor for chronic obstructive pulmonary disease (COPD). Women with COPD who smoke experienced a higher risk of hospitalization and worse decline of lung function. Yet the mechanisms of these gender-related differences in clinical presentations in COPD remain unknown. The aim of our study is to identify proteins and molecular pathways associated with COPD pathogenesis, with emphasis on elucidating molecular gender difference. METHOD: We employed shotgun isobaric tags for relative and absolute quantitation (iTRAQ) proteome analyses of bronchoalveolar lavage (BAL) cells from smokers with normal lung function (n = 25) and early stage COPD patients (n = 18). Multivariate modeling, pathway enrichment analysis, and correlation with clinical characteristics were performed to identify specific proteins and pathways of interest. RESULTS: More pronounced alterations both at the protein- and pathway- levels were observed in female COPD patients, involving dysregulation of the FcγR-mediated phagocytosis-lysosomal axis and increase in oxidative stress. Alterations in pathways of the phagocytosis-lysosomal axis associated with a female-dominated COPD phenotype correlated well with specific clinical features: FcγR-mediated phagocytosis correlated with FEV /FVC, the lysosomal pathway correlated with CT < -950 Hounsfield Units (HU), and regulation of actin cytoskeleton correlated with FEV and FEV1/FVC in female COPD patients. Alterations observed in the corresponding male cohort were minor. CONCLUSION: The identified molecular pathways suggest dysregulation of several phagocytosis-related pathways in BAL cells in female COPD patients, with correlation to both the level of obstruction (FEV /FVC) and disease severity (FEV ) as well as emphysema (CT < -950 HU) in women. TRIAL REGISTRATION: No.: NCT02627872 , retrospectively registered on December 9, 2015.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Data-Review
[do] DOI:10.1186/s12931-017-0699-2

  7 / 18955 MEDLINE  
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[PMID]: 29514383
[Au] Autor:Meier-Schroers M; Sprinkart AM; Becker M; Homsi R; Thomas D
[Ad] Address:Radiology, University of Bonn, Germany.
[Ti] Title:Quantitative and qualitative Bewertung von Lungenemphysemen mit T2-gewichteter PROPELLER-MRT in einer Hochrisiko-Population verglichen mit Niedrigdosis-CT. Quantitative and Qualitative Assessment of Pulmonary Emphysema with T2-Weighted PROPELLER MRI in a High-Risk Population Compared to Low-Dose CT.
[So] Source:Rofo;, 2018 Mar 07.
[Is] ISSN:1438-9010
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:PURPOSE: To determine the suitability of T2-weighted PROPELLER MRI for the assessment of pulmonary emphysema. MATERIALS AND METHODS: 60 participants in a lung cancer screening program (30 subjects with pulmonary emphysema, and 30 control subjects without emphysema) were included for this retrospective study. All subjects were examined with low-dose CT (LDCT) and MRI within the screening program. The use of a T2-weighted PROPELLER sequence for the assessment of emphysema was analyzed and correlated with the results of LDCT. The presence and the extent of pulmonary emphysema were first assessed qualitatively using a three-point score, and then quantitatively with a semi-automated software program to obtain emphysema indices. RESULTS: All 30 cases with pulmonary emphysema were accurately detected by MRI. There were 3 cases with emphysema according to MRI without emphysematous changes on LDCT (false-positive results). The qualitative scores as well as the emphysema indices were significantly higher in the emphysema group compared to the control group for MRI and LDCT (p < 0.001). Both the scores and the indices correlated significantly between MRI and LDCT (qualitative score of severity: r = 0.912/p < 0.001 in the emphysema group and r = 0.668/p < 0.001 in the control group; emphysema index: r = 0.960/p < 0.001 in the emphysema group and r = 0.746/p < 0.001 in the control group). CONCLUSION: The presence and the extent of pulmonary emphysema may be assessed qualitatively and quantitatively by T2-weighted PROPELLER MRI with very good correlation to LDCT. KEY POINTS: · T2-weighted PROPELLER MRI may be suitable for the assessment of pulmonary emphysema.. · There was significant correlation between MRI and LDCT regarding qualitative scores and quantitative emphysema indices in our study with correlation coefficients for different subgroups ranging from r = 0.668 to r = 0.960.. · T2-weighted PROPELLER MRI may have the potential to be used for follow-up examinations in patients with severe emphysema to avoid radiation exposure of repeated CTs.. CITATION FORMAT: · Meier-Schroers M, Sprinkart AM, Becker M et al. Quantitative and Qualitative Assessment of Pulmonary Emphysema with T2-Weighted PROPELLER MRI in a High-Risk Population Compared to Low-Dose CT. Fortschr Röntgenstr 2018; DOI: 10.1055/a-0577-5619.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1055/a-0577-5619

  8 / 18955 MEDLINE  
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[PMID]: 29394349
[Au] Autor:Tao H; Onoda H; Okabe K; Matsumoto T
[Ad] Address:Division of Thoracic Surgery, Department of Surgery, National Hospital Organization Yamaguchi-Ube Medical Center, Ube, Japan.
[Ti] Title:The impact of coexisting lung diseases on outcomes in patients with pathological Stage I non-small-cell lung cancer.
[So] Source:Interact Cardiovasc Thorac Surg;, 2018 Jan 31.
[Is] ISSN:1569-9285
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Cigarette smoking is a well-known cause of interstitial lung disease (ILD), pulmonary emphysema and lung cancer. Coexisting pulmonary disease can affect prognosis in patients with lung cancer. The aim of this study was to determine the influence of pulmonary disease on outcomes in patients with a smoking history who had undergone surgery for pathological Stage I non-small-cell lung cancer. METHODS: Medical records of 257 patients with a smoking history who underwent surgery for pathological Stage I non-small-cell lung cancer between June 2009 and December 2014 were reviewed. Coexisting ILDs were evaluated using high-resolution computed tomography. The degree of pulmonary emphysema was determined using image analysis software according to the Goddard classification. The impact of clinicopathological factors on outcome was evaluated. RESULTS: Among the 257 patients, ILDs were detected via high-resolution computed tomography in 60 (23.3%) patients; of these, usual interstitial pneumonia (UIP) patterns and non-UIP patterns were seen in 25 (9.7%) and 35 (13.6%) patients, respectively. The degree of pulmonary emphysema was classified as none, mild and moderate and included 50 (19.5%), 162 (63.0%) and 45 (17.5%) patients, respectively. The 5-year overall survival, cancer-specific survival and relapse-free survival were 80.7%, 88.0% and 74.9%, respectively, during a median follow-up period of 50.5 months. In multivariate analysis, the presence of a UIP pattern was shown to be an independent risk factor for poor outcome. CONCLUSIONS: The presence of a UIP-pattern ILD on high-resolution computed tomography images was shown to be a risk factor for poor outcome in patients with a smoking history who had undergone surgery for pathological Stage I non-small-cell lung cancer.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/icvts/ivx441

  9 / 18955 MEDLINE  
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[PMID]: 28460004
[Au] Autor:Schäfer M; Humphries S; Stenmark KR; Kheyfets VO; Buckner JK; Hunter KS; Fenster BE
[Ad] Address:Department of Cardiology, National Jewish Health, 1400 Jackson St, Denver, CO 80206, USA.
[Ti] Title:4D-flow cardiac magnetic resonance-derived vorticity is sensitive marker of left ventricular diastolic dysfunction in patients with mild-to-moderate chronic obstructive pulmonary disease.
[So] Source:Eur Heart J Cardiovasc Imaging;, 2017 Apr 27.
[Is] ISSN:2047-2412
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Aims: To investigate the possibility that vorticity assessed by four-dimensional flow cardiac magnetic resonance (4D-Flow CMR) in the left ventricle of patients with mild-to-moderate chronic obstructive pulmonary disease (COPD) is a potential marker of early LV diastolic dysfunction (LVDD) and more sensitive than standard echocardiography, and whether changes in vorticity are associated with quantitative computed tomography (CT) and clinical markers of COPD, and right ventricular (RV) echocardiographic markers indicative of ventricular interdependency. Methods and results: Sixteen COPD patients with presumptive LVDD and 10 controls underwent same-day 4D-Flow CMR and Doppler echocardiography to quantify early and late diastolic vorticity as well as standard evaluation for LVDD. Furthermore, all patients underwent detailed CT analysis for COPD markers including percent emphysema and air trapping. The 4D-Flow CMR derived diastolic vorticity measures were correlated with CT measures, standard clinical and CMR markers, and echocardiographic diastolic RV metrics. Early diastolic vorticity was significantly reduced in COPD patients (P < 0.0001) with normal left ventricular (LV) mass, geometry, systolic function, and no or mild signs of Doppler LVDD when compared with controls. Vorticity significantly differentiated COPD patients without echocardiographic signs of LVDD (n = 11) from controls (P < 0.0001), and from COPD patients with stage I LVDD (n = 5) (P < 0.0180). Vorticity markers significantly correlated with CT computed measures, CMR-derived RV ejection fraction, echocardiographic RV diastolic metrics, and 6-minute walk test. Conclusion: 4D-Flow CMR derived diastolic vorticity is reduced in patients with mild-to-moderate COPD and no or mild signs of LVDD, implying early perturbations in the LV flow domain preceding more obvious mechanical changes (i.e. stiffening and dilation). Furthermore, reduced LV vorticity appears to be driven by COPD induced changes in lung tissue and parallel RV dysfunction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1705
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/ehjci/jex069

  10 / 18955 MEDLINE  
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[PMID]: 29510429
[Au] Autor:Zoeller C; Ure BM; Dingemann J
[Ad] Address:Department of Pediatric Surgery, Hannover Medical School, Hannover, Germany.
[Ti] Title:Perioperative Complications of Video-Assisted Thoracoscopic Pulmonary Procedures in Neonates and Infants.
[So] Source:Eur J Pediatr Surg;, 2018 Mar 06.
[Is] ISSN:1439-359X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Video-assisted thoracoscopic surgery (VATS) has gained broad acceptance among pediatric surgeons. Today, VATS can be regarded as a routine approach for various conditions in neonates and infants. However, there is a lack of information concerning the complications of thoracoscopic pulmonary surgery in neonates and infants. We aimed to review the available data. PATIENTS AND METHODS: A systematic review of the literature was performed using PubMed. All publications reporting on VATS for pulmonary procedures in neonates and infants up to the age of 1 year were included. Articles were reviewed in detail for occurrence of perioperative complications and their treatment. RESULTS: Nine case series were eligible for analysis. Entities treated included lung sequestration, congenital pulmonary airway malformation, congenital lobar emphysema, and bronchogenic cyst. Case series reported on a total number of 135 patients. Complications occurred in 14 patients (10.4%). The major complication was an accidental transection of the middle lobar bronchus that concluded in a later resection of a prior unaffected lung lobe. Other relevant complications reported were bleeding in four patients (3.0%) and persistent air leak in four cases (3.0%). Infectious complications were reported in four patients (3.0%). Additionally, iatrogenic phrenic nerve paralysis occurred in one patient. There were no deaths related to the VATS technique. In 11 cases (8.1%), conversion to thoracotomy had been necessary. General recommendations on the treatment of complications could not be derived due to small patient numbers and lack of details of the complications reported. CONCLUSION: Reports on major complications of pulmonary VATS in neonates and infants below 1 year of age are scarce. As severe complications such as accidental bronchus transection have been described, feasibility of neonatal/infant VATS cannot be unequivocally confirmed. No literature-based recommendation can be given on the treatment of complications.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher
[do] DOI:10.1055/s-0038-1636917


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