D-Dimer to rule out pulmonary embolism in renal insufficiency.
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D-Dimer levels are often elevated in renal insufficiency. The diagnostic accuracy of D-Dimer to rule out pulmonary embolism in patients with renal insufficiency is unclear.
METHODS: We evaluated the data of patients presenting to our emergency department and receiving computed tomography angiography (CTA) to rule out pulmonary embolism with measurement of D-Dimer and creatinine. Glomerular filtration rate was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula.
RESULTS: 1,305 patients were included. 1,067 (82%) had an eGFR exceeding 60 ml/min, 209 (16%) 30-60 ml/min and 29 (2%) <30 ml/min. 152 patients (12%) had D-Dimer below 500 μg/L. eGFR (R= -0.1122) correlated significantly with D-Dimer (p<0.0001). 169 patients (13%) were found to have pulmonary embolism. Sensitivity of D-Dimer for patients with an eGFR>60 ml/min was 96% (0.93 to 0.99) and 100% (100 to 100) for those with 30-60 ml/min, while specificity declined significantly with impaired renal function. AUC of the ROC for D-Dimer was 0.734 in patients with an eGFR of > 60 ml/min and 0.673 for 30-60 ml/min.
CONCLUSIONS: D-Dimer levels were elevated in patients with an eGFR<60 ml/min, but proved to be highly sensitive for the exclusion of pulmonary embolism. However, since almost all patients with impaired renal function had elevated D-Dimer irrespective of the presence of pulmonary embolism studies should be performed to determine renal function adjusted D-Dimer cut-offs.
Re-emergence of chronic obstructive pulmonary disease: it is time to think COPDifferently.
Knowledge of chronic obstructive pulmonary disease (COPD) as a common, preventable and treatable condition has advanced in the last two decades, as evidenced by the increase in scientific literature. Tobacco smoking still remains a predominant risk factor for COPD. Thus smoking cessation management should be obligatory in every case. Although spirometry is integral to the diagnosis of COPD, one should also be aware of its limitations. COPD is a chronic disease associated with comorbidities that define its extrapulmonary manifestations. Systemic inflammation provides the biological link, while exacerbations play a prominent role in the current approach to disease evaluation. This paper reviews the latest Global Initiative for Chronic Obstructive Pulmonary Disease revision, focusing on the paradigm shift in assessment that would directly influence therapeutic decisions. Also discussed are the newer drugs and combinations of existing inhaler therapies that now present clinicians with more options, as well as bronchoscopic interventions that may perhaps offer a lower-morbidity alternative than surgical lung volume reduction. Finally, this review highlights how integrated care models can bridge the gap between components and complete a comprehensive sphere of COPD care.
Passive smoking exposure is associated with increased risk of COPD in never-smokers.
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Passive smoking, or environmental tobacco smoke (ETS), is a risk factor for lung cancer, cardiovascular disease and childhood asthma, but a relationship with COPD has not been fully established. AIM To study ETS as a risk factor for COPD in never-smokers. METHODS Data from three cross-sectional studies within the Obstructive Lung Disesease in Northern Sweden (OLIN) database were pooled. Of the 2182 lifelong never-smokers 2118 completed structured interviews and spirometry of acceptable quality. COPD was defined according to the GOLD criteria using post-bronchodilator spirometry. The association of COPD with ETS in single and multiple settings was calculated by multivariate logistic regression adjusting for known risk factors for COPD. RESULTS COPD prevalence was associated with increased ETS exposure: 4.2% (no ETS), 8.0% (ETS ever at home), 8.3% (ETS at previous work) and 14.7% (ETS ever at home and at both previous and current work), test for trend p=0.003. Exclusion of subjects aged ≥65 years and subjects reporting asthma yielded similar results. ETS in multiple settings, such as ever at home and at both previous and current work was strongly associated to COPD, OR 3.80 (95% CI 1.29-11.2). CONCLUSIONS In this population-based sample of never-smokers, ETS was independently associated with COPD. The association was stronger for ETS in multiple settings. ETS in multiple settings was, after age, the strongest risk factor for COPD and comparable to personal smoking of up to 14 cigarettes/day in comparable materials. The findings strongly advocate measures against smoking in public places.
Screening of biomarkers for lung cancer with gene expression profiling data.
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Screening of biomarkers for lung cancer with gene expression profiling data.
Eur Rev Med Pharmacol Sci. 2013 Dec;17(23):3221-8
Authors: Wu QP, Min JX, Jiang L, Li JM, Yao K
Abstract
OBJECTIVES: Lung cancer is one of the most common malignant tumors, but the etiology is not yet clear. Our study aims to deepen the understandings about the mechanisms of lung cancer via screening relevant key genes and functional pathways.
MATERIALS AND METHODS: Microarray data set was collected and differentially expressed genes (DEGs) were selected out. KEGG pathway analysis and Gene Ontology (GO) enrichment analysis were performed for the DEGs. Interaction networks were constructed for the lung cancer-related DEGs with information from Human Protein Reference Database (HRPD) to screen out potential biomarkers.
RESULTS: Functional annotation revealed that cell cycle, DNA replication, immune system, and signal molecules and interactions were significantly over-represented in all the DEGs, suggesting their close involvement in the development of lung cancer. 40 genes with high degree, betweenness and clustering coefficient were identified from the interaction network. 26 out of them are known cancer genes according to the database F-census. Besides, 4 biomarkers were revealed through analyzing their interactions with oncogenes.
CONCLUSIONS: Our study not only advances the understandings about the molecular mechanisms of lung cancer, but also provides several potential biomarkers for clinical use.
PMID: 24338465 [PubMed - in process]
The role of molecular analyses in the diagnosis and treatment of non-small-cell lung carcinomas.
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The role of molecular analyses in the diagnosis and treatment of non-small-cell lung carcinomas.
Semin Diagn Pathol. 2013 Nov;30(4):298-312
Authors: Rossi G, Graziano P, Leone A, Migaldi M, Califano R
Abstract
Non-small-cell lung cancer (NSCLC) subtyping has recently been a key factor in determining patient management with novel drugs. In addition, the identification of distinct oncogenic driver mutations frequently associated with NSCLC histotype and coupled to the clinical responses to targeted therapies have revolutionized the impact of histologic type and molecular biomarkers in lung cancer. Several molecular alterations involving different genes (EGFR, KRAS, ALK, BRAF, and HER2) seem to have a remarkable predilection for adenocarcinoma and specific inhibitors of EGFR and ALK are now available for patients with adenocarcinoma harboring the relevant gene alterations. The efficacy of histology-based and molecular-targeted therapies had a deep impact in (1) re-defining classification of lung cancer (particularly adenocarcinomas) and (2) routine clinical practice of pathologists involved in optimization of handling of tissue samples in order to guarantee NSCLC subtyping with the help of immunohistochemistry and adequately preserve tumor cells for molecular analysis. In agreement with the modern multidisciplinary approach to lung cancer, we reviewed here the diagnostic and predictive value of molecular biomarkers according to the clinical, pathologic, and molecular biologist viewpoints.
PMID: 24342286 [PubMed - in process]