Endobronchial-ultrasound guided miniforceps biopsy of mediastinal and hilar lesions.
Ann Thorac Surg. 2011 Jul;92(1):284-8
Authors: Chrissian A, Misselhorn D, Chen A
Abstract
BACKGROUND: Linear array endobronchial ultrasound (EBUS) has greatly improved the diagnostic yield of transbronchial needle aspiration (TBNA) for the diagnosis of non-small cell lung carcinoma though its yield in granulomatous disease and lymphoproliferative disorders is less robust. The EBUS-miniforceps biopsy (MFB) uses miniforceps and the convex probe EBUS bronchoscope to obtain forceps biopsies of centrally located lesions under continuous ultrasound guidance. In this prospective study we evaluate the efficacy of this technique for diagnosing mediastinal and hilar abnormalities in patients with a low suspicion for non-small cell lung carcinoma.
METHODS: Patients presenting with mediastinal or hilar lymphadenopathy and a low likelihood of non-small cell lung carcinoma underwent EBUS-TBNA and EBUS-MFB of mediastinal and hilar abnormalities. The diagnostic yield EBUS-TBNA and EBUS-MFB was compared as was the combined yield of both techniques versus either technique alone.
RESULTS: Between June 2008 and July 2010, 50 patients underwent EBUS-TBNA and EBUS-MFB of 74 lymph node stations. The overall diagnostic yield of EBUS-TBNA and EBUS-MFB was 81% (60 of 74) and 91% (67 of 74), respectively (p=0.09). When the 2 techniques were combined, the overall diagnostic yield was 97% (72 of 74) (p<0.001), which was significant when compared with EBUS-TBNA alone. No complications were observed as a result of EBUS-MFB, and EBUS-MFB did not appear to significantly prolong the procedure.
CONCLUSIONS: The EBUS-miniforceps biopsy is an effective, safe, and efficient method of obtaining histopathologic specimens from mediastinal and hilar abnormalities in patients with a low likelihood of non-small cell lung carcinoma, particularly when the technique is combined with EBUS-TBNA.
PMID: 21718857 [PubMed - indexed for MEDLINE]
The IARC Monographs on the carcinogenicity of crystalline silica.
Med Lav. 2011 Jul-Aug;102(4):310-20
Authors: Guha N, Straif K, Benbrahim-Tallaa L
Abstract
BACKGROUND: Through extensive review of the published literature, two independent expert panels convened by the International Agency for Research on Cancer (IARC) Monographs Programme have classified crystalline silica as carcinogenic to humans while amorphous silica was not classifiable as to its carcinogenicity in humans. The panel remarked that crystalline silica in the form of quartz or cristobalite dust causes lung cancer in humans.
OBJECTIVES: We discuss the literature and rationale used to support the IARC evaluations of silica.
METHODS: A critical review, with a focus on lung tumors, was conducted of the pertinent literature on the carcinogenic effects of crystalline silica in humans and experimental animals as well as supportive mechanistic evidence.
RESULTS: The strongest supportive evidence comes from pooled and meta-analyses that employed quantitative exposure assessment, focused on silicotics, accounted for potential confounding and demonstrated exposure-response trends. Consistency of the effect was observed despite some heterogeneity between individual studies. Tumor site concordance was observed with rodents and further supported by mechanistic data.
CONCLUSIONS: Several million workers worldwide are exposed to crystalline silica. Silicosis and lung cancer in these workers are completely preventable diseases. The IARC evaluations are critical to supporting public health interventions to protect persons at high-risk.
PMID: 21834268 [PubMed - indexed for MEDLINE]
Meta-analyses of published epidemiological studies, 1979-2006, point to open causal questions in silica-silicosis-lung cancer research.
Med Lav. 2011 Jul-Aug;102(4):321-35
Authors: Erren TC, Morfeld P, Glende CB, Piekarski C, Cocco P
Abstract
BACKGROUND AND OBJECTIVES: Following up on a previous meta-analysis of lung cancer risk in individuals without silicosis, we provide more detailed results of silica associated lung cancer risk in both silicotics and non-silicotics. The objective was to examine in depth whether current data allows to answer the pressing question "does silica cause lung cancer in the absence of silicosis"?
METHODS: We updated earlier meta-analyses of silicosis and lung cancer and compared the results with our 2009 meta-analysis of risks in individuals without silicosis. We performed fixed (FE) and random (RE) effects meta-analyses, calculated heterogeneity statistics, stratified the study material, performed sensitivity analyses with modified study results and meta-regressions to detect effect modification.
RESULTS: In silicotics, lung cancer risks were found to be doubled in 38 studies (FE: RR = 2.1; 95% CI = 2.0-2.3). In non-silicotics, eight studies without smoking adjustment suggested marginally elevated risks (FE: RR = 1.2; 95% CI = 1.1-1.3; RE: RR = 1.2; 95% CI =1.0-1.4) but three studies which were controlled for smoking showed null results (FE and RE: RR = 1.0; 95% CI = 0.8-1.3). Heterogeneity was substantial but could be linked to study characteristics, like sector of industry, and other second-level data in meta-regression. As no excess was observe dfor other smoking-related effects in studies ofllung cancer among non-silicotics, smoking was not considered to be an important confounder or modifier. CONCLUSIONn: Our meta-analyses further substantiate evidence of a strong association between silicosis and lung cancer. However, questions remain regarding lung cancer caused by silica in non-silicotics. Ideally, future investigations should consider the entire exposure-response range between silica exposure, silicosis development and lung cancer occurrence, and analyze data in terms of processes taking intermediate confounding into account.
PMID: 21834269 [PubMed - indexed for MEDLINE]
Several scoring systems have been derived to identify patients with severe community-acquired pneumonia (CAP). Recently, España et al (Am J Respir Crit Care Med 174:1249-1256, 2006) developed a clinical prediction rule that predicts hospital mortality, the need for mechanical ventilation, and risk for septic shock. We assessed the performance of this rule and compared it with other published scoring systems.
Methods : A prospective study was conducted of patients with CAP who were hospitalized at our hospital from April 2007 till May 2009. Clinical and laboratory features at presentation were recorded and used in order to calculate España rule, the pneumonia severity index (PSI), CURB-65, A-DROP, the 2007 Infectious Diseases Society of America/American Thoracic Society (IDSA/ATS) prediction rule and SMART-COP. The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) were compared for adverse outcomes. We also assessed the association of the España rule criteria and adverse outcomes.
Results : A total of 505 patients were enrolled in the study. The overall in-hospital mortality rate was 6.5%, and 6.3% of patients were admitted to the intensive care unit (ICU). Sixty-two (12.3%) patients were defined as having severe CAP (in-hospital death or need for mechanical ventilation or septic shock). España rule achieved highest sensitivity and NPV in predicting severe CAP. When ICU admission was the outcome measure, the IDSA/ATS rule and SMART-COP were regarded to be good predictors.
Conclusion : España rule performed well in identifying patients with severe CAP. As a result, each of the severity scores has advantages and limitations for predicting adverse outcomes.