Genetic susceptibility, residential radon, and lung cancer in a radon prone area.

INTRODUCTION: Radon exposure has been classified as the second cause of lung cancer, after tobacco, and the first in never smokers. GSTM1 and GSTT1 genes deletion increase the risk of lung cancer. We aim to know whether the risk of lung cancer because of residential radon is modulated by these genetic polymorphisms. METHODS: Hospital-based, case-control study where cases had confirmed lung cancer. Cases and controls did not have previous neoplasm and were older than 30. Controls attended hospital for noncomplex surgery. We analyzed the results for the whole sample and separately for never/light smokers and moderate/heavy smokers. RESULTS: Seven-hundred and ninety-two participants were analyzed. GSTM1 and GSTT1 deletion conferred an odds ratio (OR) of 1.38 (95% confidence interval [CI] 0.93-2.04) and 1.13 (95% CI 0.70-1.82), respectively. Individuals with GSTM1 present and residential radon concentrations higher than 148 Bq/m had an OR of 1.48 (95% CI 0.73-3.00), whereas those with GSTM1 deleted had an OR of 2.64 (95% CI 1.18-5.91) when compared with participants with GSTM1 present and radon concentrations below 50 Bq/m3. Similar results were observed for GSTT1 deletion. These results were basically the same for the moderate/heavy smokers' subgroup. CONCLUSIONS: The absence of GSTM1 and GSTT1 genes increases the risk of lung cancer because of radon exposure. These genes might modulate the carcinogenic pathway of alpha radiation. Further studies are warranted analyzing this association in never smokers.

Interleukin 27 could be useful in the diagnosis of tuberculous pleural effusions.

BACKGROUND: The diagnosis of tuberculous pleural effusion (TBPE) has some limitations. We studied the efficacy of interleukin-27 (IL-27) in the diagnosis of TBPE. METHODS: We measured IL-27, adenosine deaminase (ADA), ADA-2, interferon-gamma (IFNγ), and the ADA·IL-27 and ADA-2·IL-27 products in all the pleural effusion fluids. The diagnostic yield of IL-27 was evaluated with receiver operating characteristic curves. RESULTS: Of 431 pleural effusions, 70 were tuberculous, 146 were neoplastic, 58 were parapneumonic, 28 were empyemas, 88 were transudates, and 41 were other types. With a cutoff point of 0.55 ng/mL, IL-27 had a sensitivity of 91.4% and a specificity of 85.1%, which were significantly less than ADA, ADA-2, IFNγ, ADA·IL-27, or ADA-2·IL-27. The area under the receiver operating characteristic curve for IL-27 (0.963) was also significantly lower than that for the other markers, except for IFNγ. However, IL-27 improved the sensitivity of ADA and ADA-2 through ADA·IL-27 and ADA-2·IL-27 products (100% for both). CONCLUSIONS: IL-27 is less efficient than ADA and ADA-2 in the diagnosis of TBPE. However, ADA·IL-27 and ADA-2·IL-27 improve the diagnostic sensitivity of ADA and ADA-2, and thus could be useful in situations of high clinical suspicion and low ADA level. A value above the cutoff point of the latter is practically diagnostic of TBPE.

Role of blind closed pleural biopsy in the managment of pleural exudates.

INTRODUCTION: The performance of blind closed pleural biopsy (BCPB) in the study of pleural exudates is controversial. OBJECTIVE: To assess the diagnostic yield of BCPB in clinical practice and its role in the study of pleural exudates. METHODS: Data were retrospectively collected on all patients who underwent BCPB performed between January 1999 and December 2011. RESULTS: A total of 658 BCPBs were performed on 575 patients. Pleural tissue was obtained in 590 (89.7%) of the biopsies. A malignant pleural effusion was found in 35% of patients. The cytology and the BCPB were positive in 69.2% and 59.2% of the patients, respectively. Of the patients with negative cytology, 21 had a positive BCPB (diagnostic improvement, 15%), which would have avoided one pleuroscopy for every seven BCPBs that were performed. Of the 113 patients with a tuberculous effusion, granulomas were observed in 87 and the Lowenstein culture was positive in an additional 17 (sensitivity 92%). The overall sensitivity was 33.9%, with a specificity and positive predictive value of 100%, and a negative predictive value of 71%. Complications were recorded in 14.4% of patients (pneumothorax 9.4%; chest pain 5.6%; vasovagal reaction, 4.1%; biopsy of another organ 0.5%). CONCLUSIONS: BCPB still has a significant role in the study of a pleural exudate. If an image-guided technique is unavailable, it seems reasonable to perform BCPB before resorting to a pleuroscopy. These results support BCPB as a relatively safe technique.

Pulmón no expansible / Unexpandable Lung

Un pulmón no expansible (PNE) es una complicación mecánica por la cual el pulmón no se expande hasta contactar con la pared torácica, lo que impide una normal aposición entre ambas hojas pleurales. El principal mecanismo implicado es la restricción de la pleura visceral al formarse una capa fibrosa a lo largo de toda esta hoja pleural. Ocurre por la presencia de una enfermedad pleural activa (pulmón en proceso de atrapamiento [PPA]), que se puede resolver si se toman las medidas terapéuticas oportunas, o remota (pulmón atrapado [PA]), en el que ya se ha formado la capa fibrosa pleural irreversible. La sospecha clínica viene dada por la presencia de un hidroneumotórax post-toracocentesis o un derrame pleural que no se puede drenar por la aparición de dolor torácico. Su diagnóstico se basa en el análisis del líquido pleural, en la determinación de las presiones pleurales a medida que drenamos el derrame, y en la TC de tórax con contraste de aire. Dado que ambos representan la continuidad de un mismo proceso, los resultados dependerán del momento en que llevemos a cabo estos procedimientos. Si en el PPA no se toman con prontitud medidas terapéuticas apropiadas, el resultado final será un PA. En este, la mayoría de pacientes se encuentran asintomáticos o tienen una pequeña disnea de esfuerzo, por lo que no suelen requerir tratamiento pero, en casos de disnea incapacitante, puede ser necesario realizar una decorticación pleural para conseguir la resolución de los síntomas(AU)

Unexpandable lung is a mechanical complication by which the lung does not expand to the chest wall, impeding a normal apposition between the two pleural layers. The main mechanism involved is the restriction of the visceral pleura due to the formation of a fibrous layer along this pleural membrane. This happens because of the presence of an active pleural disease (lung entrapment), which can be resolved if proper therapeutic measures are taken, or a remote disease (trapped lung), in which an irreversible fibrous pleural layer has been formed. The clinical suspicion arises with the presence of post-thoracocentesis hydropneumothorax or a pleural effusion that cannot be drained due to the appearance of thoracic pain. The diagnosis is based on the analysis of the pleural liquid, the determination of pleural pressures as we drain the effusion and on air-contrast chest CT. As both represent the continuity of one same process, the results will depend on the time at which these procedures are done. If, when given a lung that is becoming entrapped, the necessary therapeutic measures are not taken, the final result will be a trapped lung. In this instance, most patients are asymptomatic or have mild exertional dyspnea and therefore they do not require treatment. Nevertheless, in cases of incapacitating dyspnea, it may be necessary to use pleural decortication in order to resolve the symptoms(AU)

Unexpandable lung.

Unexpandable lung is a mechanical complication by which the lung does not expand to the chest wall, impeding a normal apposition between the two pleural layers. The main mechanism involved is the restriction of the visceral pleura due to the formation of a fibrous layer along this pleural membrane. This happens because of the presence of an active pleural disease (lung entrapment), which can be resolved if proper therapeutic measures are taken, or a remote disease (trapped lung), in which an irreversible fibrous pleural layer has been formed. The clinical suspicion arises with the presence of post-thoracocentesis hydropneumothorax or a pleural effusion that cannot be drained due to the appearance of thoracic pain. The diagnosis is based on the analysis of the pleural liquid, the determination of pleural pressures as we drain the effusion and on air-contrast chest CT. As both represent the continuity of one same process, the results will depend on the time at which these procedures are done. If, when given a lung that is becoming entrapped, the necessary therapeutic measures are not taken, the final result will be a trapped lung. In this instance, most patients are asymptomatic or have mild exertional dyspnea and therefore they do not require treatment. Nevertheless, in cases of incapacitating dyspnea, it may be necessary to use pleural decortication in order to resolve the symptoms.

Derrames pleurales eosinofílicos: incidencia, etiología y significado pronóstico / Eosinophilic Pleural Effusion: Incidence, Etiology and Prognostic Significance

Introducción: Los derrames pleurales eosinofílicos (DPE) se asociaban a un menor riesgo de malignidad con una potencial relación causal con la presencia de aire y/o sangre en el espacio pleural. Sin embargo, ambas teorías han quedado en entredicho tras las últimas publicaciones. Objetivos: Conocer la incidencia y etiología de los DPE y comprobar si en toracocentesis sucesivas aumentan los eosinófilos en el líquido pleural (LP). Material y métodos: Analizamos 730 muestras de LP correspondientes a 605 pacientes ingresados entre enero-2004 y diciembre-2010. Resultados: Identificamos 55 muestras con un DPE correspondientes a 50 pacientes (8,3%). Las etiologías más frecuentes de DPE fueron: desconocida (36%) y neoplasia (30%). No hubo diferencias significativas en la incidencia de neoplasias entre los derrames pleurales no eosinofílicos (DPNE) (25,9%) y los DPE (30%) (p=0,533). A 100 pacientes (16,5%) se les repitió la toracocentesis. De los 9 con un DPE en la primera, 6 lo mantenían en la segunda. De los 91 con un DPNE en la primera toracocentesis, 8 (8,8%) tuvieron un DPE en las sucesivas. El porcentaje de eosinófilos no aumentó en las toracocentesis sucesivas (p=0,427). En los DPE se encontró correlación significativa entre los números de hematíes y de eosinófilos en LP (r=0,563; p=0,000). Conclusiones: Un DPE no puede considerarse un indicador de benignidad por lo que debe ser estudiado como cualquier derrame pleural. La repetición de toracocentesis no parece que aumente el número de eosinófilos y, por último, la presencia de sangre en el LP podría justificar la existencia de un DPE(AU)

Introduction: Eosinophilic pleural effusion (EPE) has been associated with less risk for malignancy with a potential causal relationship with the presence of air and/or blood in the pleural space. However, these theories have fallen by the wayside in the light of recent publications. Objectives: To determine the incidence and etiology of EPE and to observe whether the eosinophils in the pleural liquid (PL) increase in successive thoracocenteses. Patients and Methods: We analyzed 730 PL samples from 605 patients hospitalized between January 2004 and December 2010. Results: We identified 55 samples with EPE from 50 patients (8.3%). The most frequent etiologies of EPE were: unknown (36%) and neoplasm (30%). There were no significant differences in the incidence of neoplasms between the non-eosinophilic pleural effusions (non-EPE) (25.9%) and the EPE (30%) (p=0.533). One hundred patients (16.5%) underwent a second thoracocentesis. Out of the 9 who had EPE in the first, 6 maintained EPE in the second. Out of the 91 with non-EPE in the first thoracocentesis, 8 (8.8%) had EPE in the repeat thoracocentesis. The percentage of eosinophils did not increase in the successive thoracocenteses (p=0.427). In the EPE, a significant correlation was found between the number of hematites and eosinophils in the PL (r=0.563; p=0.000) .Conclusions: An EPE cannot be considered an indicator of benignancy, therefore it should be studied as any other pleural effusion. The number of eosinophils does not seem to increase with the of repetition of thoracocentesis and, lastly, the presence of blood in the PL could explain the existence of EPE(AU)

Eosinophilic pleural effusion: incidence, etiology and prognostic significance.

INTRODUCTION: Eosinophilic pleural effusion (EPE) has been associated with less risk for malignancy with a potential causal relationship with the presence of air and/or blood in the pleural space. However, these theories have fallen by the wayside in the light of recent publications. OBJECTIVES: To determine the incidence and etiology of EPE and to observe whether the eosinophils in the pleural liquid (PL) increase in successive thoracocenteses. PATIENTS AND METHODS: We analyzed 730 PL samples from 605 patients hospitalized between January 2004 and December 2010. RESULTS: We identified 55 samples with EPE from 50 patients (8.3%). The most frequent etiologies of EPE were: unknown (36%) and neoplasm (30%). There were no significant differences in the incidence of neoplasms between the non-eosinophilic pleural effusions (non-EPE) (25.9%) and the EPE (30%) (p=0.533). One hundred patients (16.5%) underwent a second thoracocentesis. Out of the 9 who had EPE in the first, 6 maintained EPE in the second. Out of the 91 with non-EPE in the first thoracocentesis, 8 (8.8%) had EPE in the repeat thoracocentesis. The percentage of eosinophils did not increase in the successive thoracocenteses (p=0.427). In the EPE, a significant correlation was found between the number of hematites and eosinophils in the PL (r=0.563; p=0.000). CONCLUSIONS: An EPE cannot be considered an indicator of benignancy, therefore it should be studied as any other pleural effusion. The number of eosinophils does not seem to increase with the of repetition of thoracocentesis and, lastly, the presence of blood in the PL could explain the existence of EPE.

Valor diagnóstico de los niveles del N-terminal pro-póptido natriurótico cerebral en los derrames pleurales de origen cardiaco / Diagnostic Value of N-Terminal Pro-Brain Natriuretic Peptide in Pleural Effusions of Cardiac Origin

Introducción: El diagnóstico del derrame pleural (DP) cardiogénico plantea dificultades con frecuencia.El objetivo de nuestro estudio fue evaluar la utilidad diagnóstica en el DP en pacientes con insuficienciacardíaca, de los niveles del fragmento N terminal del pro-póptido natriurítico cerebral (NT-proBNP),tanto en líquido pleural (LP) como en sangre (S), y compararlo con los criterios de Light, el colesterol en líquido pleural (COL LP) y en suero (COL S).Pacientes y método: Todos los biomarcadores fueron evaluados en 398 DP (26,9% trasudados). El ¨¢rea bajola curva (ABC) cuantificó la precisión diagnóstica global; y mediante curvas ROC se evaluó la precisión diagnóstica de los diversos parámetros. Resultados: El ABC ROC para el NT-proBNP pleural fue 0,894, sin diferencias significativas con el COL LP(0,914) ni con los criterios de Light (0,896). La sensibilidad, especificidad, razón de probabilidad positiva(RPP) y razón de probabilidad negativa (RPN) fueron 85,1% (94,1% para COL LP), 79,9% (90,2% para loscriterios de Light), 4,24 (7,27 para los criterios de Light) y 0,19 (0,07 para COL LP), respectivamente. La combinación del NT-proBNP en LP ¡Ý 276 pg/ml y COL LP ¡Ü 57 mg/dL consiguieron clasificar el mayorn¨²mero de DP correctamente (sensibilidad 97,8%, especificidad 85,4%). Conclusiones: El rendimiento diagnóstico del NT-proBNP en DP cardiogónicos no es superior al COL LP nia los criterios de Light, aunque pudiera ser diagnóstico en trasudados de otro origen (AU)

Introduction: The diagnosis of cardiogenic pleural effusion (PE) is often difficult to make. The objectiveof our study was to evaluate the diagnostic usefulness of N-terminal pro-brain natriuretic peptide (NTproBNP)levels in PE patients with heart failure, in pleural fluid (PF) and blood (B), and to compare thecholesterol in pleural fluid (CHOL PF) and in serum (CHOL S) with the Light criteria.Patients and methods: All the biomarkers were evaluated in 398 PF (26.9% transudates). The area underthe curve (AUC) quantified the overall diagnostic precision. The diagnostic precision of the different parameters was also assessed using the ROC curves.Results: The AUC of the ROC for pleural fluid NT-proBNP was 0.894, with no significant differences withCHOL LP (0.914) or with the Light criteria (0.896). The sensitivity, specificity, the positive probabilityratio (PPR) and negative probability ratio (NPR) were 85.1% (94.1% for CHOL LP), 79.9% (90.2% for the Lightcriteria), 4.24 (7.27 for the Light criteria) and 0.19 (0.07 for CHOL LP), respectively. The combination of NTproBNPin PF ¡Ý 276 pg/ml and CHOL LP ¡Ü 57 mg/dL managed to classify the highest number PE correctly(sensitivity 97.8%, specificity 85.4%). Conclusions. The diagnostic yield of NT-proBNP in cardiogenic PE isnot superior to the CHOL LP or the Light criteria, although it could be diagnostic in transudates of anotherorigin(AU)

Diagnostic value of N-terminal pro-brain natriuretic peptide in pleural effusions of cardiac origin.

INTRODUCTION: The diagnosis of cardiogenic pleural effusion (PE) is often difficult to make. The objective of our study was to evaluate the diagnostic usefulness of N-terminal pro-brain natriuretic peptide (NT-proBNP) levels in PE patients with heart failure, in pleural fluid (PF) and blood (B), and to compare the cholesterol in pleural fluid (CHOL PF) and in serum (CHOL S) with the Light criteria. PATIENTS AND METHODS: All the biomarkers were evaluated in 398 PF (26.9% transudates). The area under the curve (AUC) quantified the overall diagnostic precision. The diagnostic precision of the different parameters was also assessed using the ROC curves. RESULTS: The AUC of the ROC for pleural fluid NT-proBNP was 0.894, with no significant differences with CHOL PF (0.914) or with the Light criteria (0.896). The sensitivity, specificity, the positive probability ratio (PPR) and negative probability ratio (NPR) were 85.1% (94.1% for CHOL PF), 79.9% (90.2% for the Light criteria), 4.24 (7.27 for the Light criteria) and 0.19 (0.07 for CHOL PF), respectively. The combination of NT-proBNP in PF ≥ 276 pg/ml and CHOL PF ≤ 57 mg/dL managed to classify the highest number PE correctly (sensitivity 97.8%, specificity 85.4%). CONCLUSIONS: The diagnostic yield of NT-proBNP in cardiogenic PE is not superior to the CHOL LP or the Light criteria, although it could be diagnostic in transudates of another origin.