Chemokine Involvement in Lung Injury Secondary to Ischaemia/Reperfusion.

INTRODUCTION: During transplant surgeries, the lung experiences an ischaemia-reperfusion (I/R)-induced damage identified as a significant cause of morbidity and mortality. However, the mechanisms by which I/R induces leucocyte accumulation and subsequent tissue damage in lung surgeries remain unknown. Therefore, the present study aims to assess the role of monocyte chemotactic protein 1 (MCP-1) and macrophage inflammatory protein 2 (MIP-2) in leucocyte chemotaxis related to lung injury secondary to I/R. METHODS: Six pigs were subjected to an orthotopic left caudal lobe lung transplantation with a subsequent 60-min graft reperfusion (Transplant group). In addition, six animals underwent to sham surgery (Sham Group). Plasma samples and lung biopsies were collected before the beginning of pneumonectomy, before starting the reperfusion, and 30 min and 60 min after the beginning of the reperfusion. Plasma levels of intercellular adhesion molecule 1 (ICAM-1) and lung expressions of MCP-1, MIP-2, myeloperoxidase (MPO), and lung oedema were measured. RESULTS: Lung I/R caused substantial damage observed as pulmonary oedema. The oedema was evident after the ischemic insult and increased after reperfusion. After reperfusion, increased levels of MPO were observed which suggests an activation and infiltration of neutrophils into the lung tissue. After 30 min of reperfusion, MCP-1, MIP-2, and ICAM-1 levels were significantly increased compared to prepneumonectomy levels (p < 0.05) and a further increase was observed after 60 min of reperfusion (p < 0.05). CONCLUSION: The present study demonstrates that activated neutrophils, as well as MCP-1, MIP-2, and ICAM-1, are involved in inflammatory response induced by ischaemia-reperfusion-induced lung injury.

Metaloptisis: ¿un nuevo caso con otra causa? / Metalloptysis: A new case with another cause?

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Programa de rehabilitación multimodal en cirugía torácica / Multimodal rehabilitation program in thoracic surgery

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Ischaemic preconditioning prevents the liver inflammatory response to lung ischaemia/reperfusion in a swine lung autotransplant model.

OBJECTIVES: Lung ischaemia/reperfusion (IR) induces a systemic inflammatory response that causes damage to remote organs. The liver is particularly sensitive to circulating inflammatory mediators that occur after IR of remote organs. Recently, remote ischaemic preconditioning has been proposed as a surgical tool to protect several organs from IR. The present study was designed to investigate a possible protective effect of lung ischaemic preconditioning (IP) against the liver inflammatory response to lung IR. METHODS: Two groups [IP and control (CON)] of 10 Large White pigs underwent lung autotransplants (left pneumonectomy, ex situ cranial lobectomy and caudal lobe reimplantation). Before pneumonectomy was performed in the study group, IP was induced with two 5-min cycles of left pulmonary arterial occlusion and a 5-min interval of reperfusion between the two occlusions. Five animals underwent sham surgery. Liver biopsies were obtained during surgery at (i) prepneumonectomy, (ii) prereperfusion, (iii) 10 min after reperfusion of the implanted lobe and (iv) 30 min after reperfusion. The expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-1, IL-10 and inducible form of nitric oxide synthase (iNOS) was analysed by western blotting. The expression of mRNA for TNF-α, IL1, IL-10, monocyte chemoattractant protein-1 (MCP-1), nuclear factor kappa beta and iNOS was analysed by reverse transcription-polymerase chain reaction. Caspase-3 activity was determined by enzyme-linked immunosorbent assay. Non-parametric tests were used to compare differences between and within groups. RESULTS: Lung IR markedly increased expression of TNF-α (P = 0.0051) and IL-1 (P = 0.0051) and caspase-3 activity (P = 0.0043) in the CON group compared with the prepneumonectomy levels. A decrease of IL-10 mRNA expression was observed in the CON group after lung reperfusion. In the IP group, TNF-α (P = 0.0011) and IL-1 (P = 0.0001) expression and caspase-3 activity (P < 0.0009) were lower after reperfusion than in the CON group. IP caused reversion of the observed decrease of IL-10 mRNA expression (P = 0.016) induced in liver tissue by lung IR. Lung IR markedly increased the expression of mRNA MCP-1 after 10 min (P = 0.0051) and 30 min (P = 0.0051) of reperfusion. These increases were not observed in the IP or sham groups. CONCLUSIONS: IP prevented liver injury induced by lung IR through the reduction of proinflammatory cytokines and hepatocyte apoptosis.

Site of mitochondrial reactive oxygen species production in skeletal muscle of chronic obstructive pulmonary disease and its relationship with exercise oxidative stress.

Exercise triggers skeletal muscle oxidative stress in patients with chronic obstructive pulmonary disease (COPD). The objective of this research was to study the specific sites of reactive oxygen species (ROS) production in mitochondria isolated from skeletal muscle of patients with COPD and its relationship with local oxidative stress induced by exercise. Vastus lateralis biopsies were obtained in 16 patients with COPD (66 ± 10 yr; FEV(1), 54 ± 12% ref) and in 14 control subjects with normal lung function who required surgery because of lung cancer (65 ± 7 yr; FEV(1), 91 ± 14% ref) at rest and after exercise. In these biopsies we isolated mitochondria and mitochondrial membrane fragments and determined in vitro mitochondrial oxygen consumption (Mit$$\stackrel{.}{\hbox{ V }}$$o(2)) and ROS production before and after inhibition of complex I (rotenone), complex II (stigmatellin), and complex III (antimycin-A). We related the in vitro ROS production during state 3 respiration), which mostly corresponds to the mitochondria respiratory state during exercise, with skeletal muscle oxidative stress after exercise, as measured by thiobarbituric acid reactive substances.State 3 Mit$$\stackrel{.}{\hbox{ V }}$$o(2) was similar in patients with COPD and control subjects (191 ± 27 versus 229 ± 46 nmol/min/mg; P = 0.058), whereas H(2)O(2) production was higher in the former (147 ± 39 versus 51 ± 8 pmol/mg/h; P < 0.001). The addition of complexI, II, and III inhibitors identify complex III as the main site of H(2)O(2) release by mitochondria in patients with COPD and in control subjects. The mitochondrial production of H(2)O(2) in state 3 respiration was related (r = 0.69; P < 0.001) to postexercise muscle thiobarbituric acid reactive substance levels. Our results show that complex III is the main site of the enhanced mitochondrial H(2)O(2) production that occurs in skeletal muscle of patients with COPD, and the latter appears to contribute to muscle oxidative damage.

Modulation of monocyte chemoattractant protein-1 expression by ischaemic preconditioning in a lung autotransplant model.

OBJECTIVES: Monocyte chemoattractant protein-1 (MCP-1) is believed to play a crucial role in lung ischaemia-reperfusion injury (LIRI). Ischaemic preconditioning (IP) has been shown to protect several organs from ischaemia-reperfusion (IR) injury, although less is known about IP's effect on MCP-1 modulation. The objective of this study was to investigate IP's effect on MCP-1 expression in lung tissue and its relationship with oxidative stress and proinflammatory cytokine production in an experimental LIRI model. METHODS: Two groups (IP and control groups) of seven large white pigs underwent a lung autotransplant (left pneumonectomy, ex situ superior lobectomy and lower lobe reimplantation). Before pneumonectomy was performed in the study group, IP was induced with two cycles of 5 min of left pulmonary artery occlusion with a 5 min interval of reperfusion between the two occlusions. Blood samples and lung biopsies were obtained at prepneumonectomy (PPn), at prereperfusion (PRp) and up to 30 min after reperfusion of the implanted lobe (Rp-10' and Rp-30'). Haemodynamic and blood-gas measurements, evaluation of oxidative stress in lung tissue and MCP-1, tumour necrosis factor-α (TNF-α) and IL-1 protein and mRNA measurements in lung tissue were performed. Nonparametric tests were used to compare differences between groups. Data are expressed as mean ± SEM. RESULTS: In control lungs, MCP-1 protein levels were found to be higher at PRp, Rp-10' and Rp-30' than at PPn (0.59 ± 0.1 vs. 0.21 ± 0.05, 0.47 ± 0.01 vs. 0.21 ± 0.05 and 0.56 ± 0.01 vs. 0.21 ± 0.05, respectively; P < 0.05). These differences were not evident in the IP group. MCP-1 levels at PRp, Rp-10' and Rp-30' were significantly higher in the control group than in the IP group (0.59 ± 0.1 vs. 0.15 ± 0.02, 0.47 ± 0.01 vs. 0.13 ± 0.01 and 0.56 ± 0.01 vs. 0.27 ± 0.01, respectively; P < 0.05). MCP-1, TNF-α and IL-1 mRNA expressions were lower at PRp, Rp-10' and Rp-30' (control vs. IP group, P < 0.05) when IP was carried out. Lipid peroxidation metabolites and myeloperoxidase activity increase in lung tissue were prevented by IP. CONCLUSIONS: In this model, LIRI induced the expression of MCP-1 and the proinflammatory proteins TNF-α and IL-1 in control lungs. IP significantly reduced the expression of these chemokines and cytokines. These features may explain the reduction of oxidative stress observed with IP.

Influencia pronóstica de la pérdida de la expresión del antígeno del grupo sanguíneo A en el carcinoma no microcítico de pulmón en estadio I patológico / Prognostic Influence of Loss of Blood Group A Antigen Expression in Pathologic Stage I Non-Small-Cell Lung Cancer

Introducción: En la literatura científica se han publicado resultados contradictorios sobre el valor pronóstico de la pérdida de la expresión del antígeno de grupo sanguíneo A (GSA) en el cáncer de pulmón, por lo que analizamos retrospectivamente este hecho en nuestra serie quirúrgica. Pacientes y métodos. En un estudio multicéntrico de 402 pacientes con carcinoma no microcítico de pulmón (CNMP) en estadio I patológico según la nueva clasificación TNM-2009 se analizó la influencia pronóstica de la pérdida de la expresión del antígeno del GSA en los 209 pacientes con grupos sanguíneos A o AB. Resultados: La supervivencia a los 5 años de los pacientes en estadio I patológico que mantenían la expresión del antígeno del GSA fue del 73%, frente a una supervivencia del 53% en los pacientes que habían perdido la expresión del mismo (p=0,03). Cuando se analizó la supervivencia subdividiendo la muestra en estadios IA y IB, solo se alcanzó la significación estadística en el estadio IA (p=0,038). Al analizar la supervivencia según el tipo histológico, los pacientes con adenocarcinoma que perdían la expresión del antígeno del GSA tenían una menor supervivencia, con una p estadísticamente muy significativa (p=0,003). El análisis multivariable mostró que la edad, el género y la expresión del antígeno del GSA eran factores pronósticos independientes. Conclusiones: La pérdida de la expresión del antígeno del grupo sanguíneo A tiene una influencia pronóstica negativa en el CNMP estadio I patológico, sobre todo en el tipo histológico adenocarcinoma(AU)

Introduction: In the scientific literature, contradictory results has been published on the prognostic value of the loss of expression of blood group antigen A (BAA) in lung cancer. The objective of our study was to analyze this fact in our surgical series. Patients and methods: In a multicenter study, 402 non-small-cell lung cancer (NSCLC) patients were included. All were classified as stage-I according to the last 2009-TNM classification. We analyzed the prognostic influence of the loss of expression of BAA in the 209 patients expressing blood group A or AB. Results: The 5-year cumulative survival was 73% for patients expressing BAA vs 53% for patients with loss of expression (P=.03). When patients were grouped into stages IA and IB, statistical significance was only observed in stage I-A (P=.038). When we analyzed the survival according to histologic type, those patients with adenocarcinoma and loss of expression of BAA had a lower survival rate that was statistically very significant (P=.003). The multivariate analysis showed that age, gender and expression of BAA were independent prognostic factors. Conclusions: The loss of expression of blood group antigen A has a negative prognostic impact in stage I NSCLC, especially in patients with adenocarcinoma(AU)

Prognostic influence of loss of blood group A antigen expression in pathologic stage I non-small-cell lung cancer.

INTRODUCTION: In the scientific literature, contradictory results has been published on the prognostic value of the loss of expression of blood group antigen A (BAA) in lung cancer. The objective of our study was to analyze this fact in our surgical series. PATIENTS AND METHODS: In a multicenter study, 402 non-small-cell lung cancer (NSCLC) patients were included. All were classified as stage-I according to the last 2009-TNM classification. We analyzed the prognostic influence of the loss of expression of BAA in the 209 patients expressing blood group A or AB. RESULTS: The 5-year cumulative survival was 73% for patients expressing BAA vs 53% for patients with loss of expression (P=.03). When patients were grouped into stages IA and IB, statistical significance was only observed in stage I-A (P=.038). When we analyzed the survival according to histologic type, those patients with adenocarcinoma and loss of expression of BAA had a lower survival rate that was statistically very significant (P=.003). The multivariate analysis showed that age, gender and expression of BAA were independent prognostic factors. CONCLUSIONS: The loss of expression of blood group antigen A has a negative prognostic impact in stage I NSCLC, especially in patients with adenocarcinoma.

Análisis multicéntrico de supervivencia y factores pronósticos en el carcinoma no microcítico de pulmón en estadio I patológico según la nueva clasificación TNM de 2009 / Multicenter Analysis of Survival and Prognostic Factors in Pathologic Stage I Non-Small-Cell Lung Cancer According to the New 2009 TNM Classification

Introducción: La nueva clasificación TNM de 2009 ha introducido importantes modificaciones en la estadificacióndel cáncer de pulmón. El objetivo de este trabajo es validar nuestra serie de pacientes concarcinoma no microcítico de pulmón en estadio I patológico según la séptima edición de la clasificaciónTNM de los tumores malignos y analizar los factores relacionados con el pronóstico.Pacientes y métodos: Se realizó un estudio retrospectivo y multicéntrico. Para el análisis de supervivenciase utilizó el método de Kaplan-Meier y para el análisis multivariable, la regresión de Cox. Se analizaronlas siguientes variables: edad, sexo, estadio patológico, categoría T, tipo histológico, tipo de resección ytamaño tumoral.Resultados: Se incluyó a 402 pacientes con un seguimiento medio de 70,18 meses. La supervivencia globala los 5 años fue del 68%. Los varones y los pacientes mayores de 70 años tenían una menor supervivencia.El pronóstico empeoraba a medida que aumentaba el estadio patológico, la categoría T y el tamañotumoral. No encontramos diferencias pronósticas estadísticamente significativas en relación con el tipohistológico y el tipo de resección practicada. El análisis multivariable mostró que la edad, el sexo y elestadio patológico son factores pronósticos independientes.Conclusiones: Los resultados de supervivencia y el análisis de factores pronósticos de nuestra serie seajustan a los publicados en la nueva clasificación TNM de 2009. El factor pronóstico más importante esel estadio patológico. Otros factores pronósticos desfavorables son el sexo masculino y la edad mayor de70 años (AU)

Introduction: The new 2009 TNM classification introduced important modifications in lung cancer staging. The aim of this study is to validate our series of patients with pathologic stage I non-small-cell lung canceraccording to the 7th edition of the TNM classification of malignant tumors and to the factors related withprognosis.Patients and methods: A multicenter retrospective study was performed. Survival rates were calculated by the Kaplan-Meier method, and for multivariate analyses, Cox proportional hazards regression model was used. The following variables were analyzed: age, sex, pathologic stage, T category, histology, type of resection and tumor size. Results: A total of 402 patients were included. Mean follow-up was 70.18 months. Overall 5-year survivalwas 68%. Males and patients over 70 had lower survival. Prognosis worsened with increasing pathologicstage, T category and tumor size. We found no statistically significant differences in prognosis for histologyor type of resection. Multivariate analysis showed age, sex and pathologic stage to be independentprognostic factors.Conclusions: Survival results and the analysis of prognostic factors in our series are similar to those publishedin the new 2009 TNM classification. The most important prognostic factor is pathologic stage. Otheradverse prognostic factors include male sex and age over 70 (AU)

Multicenter analysis of survival and prognostic factors in pathologic stage I non-small-cell lung cancer according to the new 2009 TNM classification.

INTRODUCTION: The new 2009 TNM classification introduced important modifications in lung cancer staging. The aim of this study is to validate our series of patients with pathologic stage I non-small-cell lung cancer according to the 7th edition of the TNM classification of malignant tumors and to the factors related with prognosis. PATIENTS AND METHODS: A multicenter retrospective study was performed. Survival rates were calculated by the Kaplan-Meier method, and for multivariate analyses, Cox proportional hazards regression model was used. The following variables were analyzed: age, sex, pathologic stage, T category, histology, type of resection and tumor size. RESULTS: A total of 402 patients were included. Mean follow-up was 70.18 months. Overall 5-year survival was 68%. Males and patients over 70 had lower survival. Prognosis worsened with increasing pathologic stage, T category and tumor size. We found no statistically significant differences in prognosis for histology or type of resection. Multivariate analysis showed age, sex and pathologic stage to be independent prognostic factors. CONCLUSIONS: Survival results and the analysis of prognostic factors in our series are similar to those published in the new 2009 TNM classification. The most important prognostic factor is pathologic stage. Other adverse prognostic factors include male sex and age over 70.

Procedimiento de autotrasplante pulmonar en el cerdo como modelo experimental para el estudio del síndrome de isquemia-reperfusión / Experimental Swine Lung Autotransplant Model to Study Lung Ischemia-Reperfusion Injury

Introducción: El daño pulmonar agudo por isquemia reperfusión (IR) ha sido estudiado fundamentalmenteen modelos experimentales y clínicos con IR fría. Son limitados los estudios que profundizan en lasalteraciones bioquímicas durante la IR normotérmica (caliente). El objetivo del este trabajo es presentarun modelo de autotrasplante pulmonar en cerdo para el estudio de las fases más precoces del síndromede IR normotérmica pulmonar.Animales y métodos: Seis cerdos de la raza Large-White fueron sometidos a neumonectomía izquierda,lobectomía craneal ex situ, reimplantación del lóbulo caudal y reperfusión del mismo durante 30 min.Durante el procedimiento se analizaron diferentes parámetros para identificar cambios hemodinámicos,gasométricos y bioquímicos en el modelo. El estudio estadístico se realizó con pruebas no paramétricas.Resultados: Tras la isquemia, se observó en tejido pulmonar un aumento significativo (p < 0,05) de metabolitosde peroxidación lipídica, de citoquinas y quemoquinas proinflamatorias (TNF- , IL-1 y MCP-1),de actividad leucocitaria (mieloperoxidasa o MPO), de actividad óxido nítrico sintasa inducible y de laproteína quinasaMAPKp38, mientras que se observóundescenso de actividad tisular de las formas constitutivasde NOS y de monóxido de carbono sérico. Estas alteraciones se mantuvieron o acentuaron durantela reperfusión, donde se observó también una mayor actividad tisular hemo-oxigenasa constitutiva.Conclusiones: Se presenta un procedimiento experimental de IR normotérmica pulmonar describiendo enprofundidad cambios hemodinámicos, gasométricos y bioquímicos. Tanto el modelocomolos parámetrosanalizados podrían ser útiles en el estudio de nuevas terapias moduladoras del da˜no pulmonar agudo ensituaciones clínicas de IR normotérmica(AU)

Introduction: Ischemia-reperfusion (IR) lung injury has been investigated extensively on clinical andexperimental models of cold ischemia. However, relatively few studies examine the detailed biochemicalchanges occurring during normothermic (warm) IR.The objective of this work was to establish an experimental lung autotransplant model to be carried outon pigs in order to study the early stages of normothermic lung IR.Animals y methods: Six Large-White pigs underwent a lung autotransplant which entailed left pneumonectomy,ex situ cranial lobectomy, caudal lobe reimplantation and its reperfusion for 30 min. Throughoutthe procedure, several parameters were measured in order to identify hemodynamic, gasometric andbiochemical changes. Non-parametric statistical analyses were used to compare differences between periods. Results: After ischemia, a significant increase (P < 0.05) in lipid peroxidation metabolites, proinflammatorycytokines and chemokines (TNF- , IL-1 y MCP-1), neutrophil activation, inducible nitric oxide synthaseactivity and protein-kinase MAPK p38 levels were observed in lung tissue. However, constitutive nitricoxide synthase activity in lung tissue and carbon monoxide plasma levels were decrease. The same heldtrue throughout the reperfusion period, when an increase in the constitutive heme-oxygenase activitywas also shown.Conclusions: An experimental model of normothermic lung IR injury is presented and detailed changes inhemodynamic, gasometric and biochemical parameters are shown. Both the model and the studied parametersmay be clinically useful in future investigations testing new therapies to prevent normothermicIR induced lung injury(AU)

Experimental Swine lung autotransplant model to study lung ischemia-reperfusion injury.

INTRODUCTION: Ischemia-reperfusion (IR) lung injury has been investigated extensively on clinical and experimental models of cold ischemia. However, relatively few studies examine the detailed biochemical changes occurring during normothermic (warm) IR. The objective of this work was to establish an experimental lung autotransplant model to be carried out on pigs in order to study the early stages of normothermic lung IR. ANIMALS Y METHODS: Six Large-White pigs underwent a lung autotransplant which entailed left pneumonectomy, ex situ cranial lobectomy, caudal lobe reimplantation and its reperfusion for 30 min. Throughout the procedure, several parameters were measured in order to identify hemodynamic, gasometric and biochemical changes. Non-parametric statistical analyses were used to compare differences between periods. RESULTS: After ischemia, a significant increase (P < 0.05) in lipid peroxidation metabolites, proinflammatory cytokines and chemokines (TNF-α, IL-1ß y MCP-1), neutrophil activation, inducible nitric oxide synthase activity and protein-kinase MAPK p38 levels were observed in lung tissue. However, constitutive nitric oxide synthase activity in lung tissue and carbon monoxide plasma levels were decrease. The same held true throughout the reperfusion period, when an increase in the constitutive heme-oxygenase activity was also shown. CONCLUSIONS: An experimental model of normothermic lung IR injury is presented and detailed changes in hemodynamic, gasometric and biochemical parameters are shown. Both the model and the studied parameters may be clinically useful in future investigations testing new therapies to prevent normothermic IR induced lung injury.

Surgery of female genital tract tumour lung metastases.

INTRODUCTION: Lung metastases originating from tumours of the female genital tract are rare. Due to this rarity and their variable histology, it has been difficult to compare different patient series. MATERIAL AND METHODS: A retrospective study of patients undergoing resection of lung metastases of female genital tract tumours (uterine and cervical cancer) during the period 01/01/1989 to 12/31/2006. Epidemiological, diagnostic and treatment data were collected. Non-parametric tests and survival analysis were performed using the Kaplan-Meier and log-rank test. RESULTS: A resection was performed on 27 patients during the study period. Disease-free interval (DFI) from initial diagnosis of lung metastases was 58 months (1-195 months). The median survival from diagnosis of metastases was 94 months. The overall survival at 5 years after diagnosis of metastasis was 84.1%. A second surgery of metastases was performed on 5 patients (18.5%). Survival after second surgery of metastases: 80.5 months. Survival from diagnosis of metastasis at five years: endometrial carcinoma 100%, cervical cancer 62.5%, uterine sarcoma 60%. Adjuvant hormonal therapy was prescribed in 15 out of 16 patients with endometrial carcinoma. There was a statistically significant difference in the survival depending on the histological type and disease free interval. CONCLUSION: Surgical treatment of lung metastases originating from female genital tract tumours (mainly endometrial carcinoma) is associated with a high long-term survival.

Cirugía de las metástasis pulmonares de tumores del tracto genital femenino / Surgery of female genital tract tumour lung metastases

IntroducciónLos tumores del tracto genital femenino constituyen una etiología poco frecuente de metástasis pulmonares. Debido a esto y a su variada histología, la comparación de resultados ha resultado complicada hasta la fecha.Material y métodosEstudio retrospectivo de pacientes intervenidos de metástasis pulmonares de tumores del tracto genital femenino (cuerpo, trompa y cuello de útero) en el periodo 01/01/1989–31/12/2006. Se recogen datos referentes a aspectos epidemiológicos, de diagnóstico y tratamiento. Se han utilizado tests no paramétricos, y el análisis de supervivencia se ha realizado con curvas de Kaplan-Meier y el log-rank test.ResultadosDurante el periodo descrito se ha intervenido a 27 pacientes. Intervalo libre de enfermedad (ILE) desde el diagnóstico inicial al de metástasis pulmonares 58 meses (1-195 meses). Mediana de supervivencia desde el diagnóstico de metástasis 94 meses. Supervivencia global tras diagnóstico de metástasis a 5 años: 84,1%. Segunda cirugía de metástasis: 5 pacientes (18,5%). Supervivencia tras segunda cirugía de metástasis: 80,5 meses. Supervivencia desde el diagnóstico de metástasis a 5 años: carcinoma de endometrio 100%; cáncer de cérvix 62,5%; sarcoma uterino 60%. Recibieron hormonoterapia adyuvante 15 de 16 pacientes con carcinoma de endometrio. Hallamos diferencias estadísticamente significativas en la supervivencia en función de: tipo histológico, e intervalo libre de enfermedad.ConclusiónEl tratamiento quirúrgico de las metástasis del tracto genital femenino (principalmente de las de carcinoma de endometrio) se asocia a una elevada supervivencia a largo plazo(AU)

IntroductionLung metastases originating from tumours of the female genital tract are rare. Due to this rarity and their variable histology, it has been difficult to compare different patient series.Material and MethodsA retrospective study of patients undergoing resection of lung metastases of female genital tract tumours (uterine and cervical cancer) during the period 01/01/1989 to 12/31/2006. Epidemiological, diagnostic and treatment data were collected. Non-parametric tests and survival analysis were performed using the Kaplan-Meier and log-rank test.ResultsA resection was performed on 27 patients during the study period. Disease-free interval (DFI) from initial diagnosis of lung metastases was 58 months (1-195 months). The median survival from diagnosis of metastases was 94 months. The overall survival at 5 years after diagnosis of metastasis was 84.1%. A second surgery of metastases was performed on 5 patients (18.5%). Survival after second surgery of metastases: 80.5 months. Survival from diagnosis of metastasis at five years: endometrial carcinoma 100%, cervical cancer 62.5%, uterine sarcoma 60%. Adjuvant hormonal therapy was prescribed in15 out of 16 patients with endometrial carcinoma. There was a statistically significant difference in the survival depending on the histological type and disease free interval.ConclusionSurgical treatment of lung metastases originating from female genital tract tumours (mainly endometrial carcinoma) is associated with a high long-term survival(AU)

Early and long-term validation of an algorithm assessing fitness for surgery in patients with postoperative FEV1 and diffusing capacity of the lung for carbon monoxide < 40%.

BACKGROUND: There is evidence in the literature that the incidence of pulmonary complications and mortality is fair enough in patients with lower pulmonary function than conventionally accepted. In this article, we validate in patients with low baseline lung function (ie, FEV(1) or diffusing capacity of the lung for carbon monoxide [DLCO] < 80%) an algorithm to evaluate anatomic lung surgery in patients with low predicted postoperative lung function (ie, either FEV(1)-postoperative estimated [ppo] or DLCO-ppo < 40% or both between 30% and 40% predicted) if peak oxygen uptake (VO(2)peak)-ppo > 10 mL/kg/min. METHODS: We prospectively studied 126 consecutive patients evaluated for anatomic resection of lung tumors by thoracotomy. RESULTS: Ninety-two patients were operated on: age 67 (8 SD) years; FEV(1) 63 (14)% pp; DLCO 71 (19)% pp; VO(2)peak 71 (19)% predicted; and 2-year Kaplan-Meier conditional probability of survival (CPS) 0.62 (0.06). Thirty-day perioperative mortality was 6.4%. Thirty-four patients were not functionally fit, or rejected the procedure: age 69 (8) years; FEV(1) 58 (16)% predicted; DLCO 67 (26)% predicted; VO(2)peak 66 (16)% predicted. In this group, 2-year CPS was 0.18 (0.08), P < .01. Subgroups A (FEV(1)-ppo and DLCO-ppo > 40% predicted) and B (either FEV(1)-ppo or DLCO-ppo < 40% predicted or both between 30% and 40% predicted) were comparable in terms of perioperative morbidity; however, they were different in terms of 30-day mortality (A, 1/53 [1.9%]; B, 5/37 [13.5%]; P = .047; relative risk, 7.2; 95% CI 1.1-27.7). The survival functions of both subgroups were significantly different (P < .01) from nonsurgical subjects. CONCLUSIONS: Adherence to the proposed algorithm results in a reasonable preoperative mortality in patients with low preoperative lung function. Although perioperative mortality is significantly higher when predicted postoperative lung function is low, 2-year survival of patients is better than if such patients had not undergone surgery.

[Detection of lymph node involvement and surgical treatment of pulmonary neoplastic processes. Current state of diagnostic and therapeutic procedures]. / Detección de la afectación ganglionar y tratamiento quirúrgico de los procesos neoplásicos pulmonares. Estado actual de distintos procederes diagnósticos y terapéuticos.

An analysis is made of different publications associated with the surgical staging and treatment of primary and metastasic pulmonary neoplastic processes. A suitable treatment program is essential to determine lymph node involvement in patients with bronchogenic carcinoma. The indication and sequence of the procedure to use (CT-PET, transbronchial puncture, videomediastinoscopic ultrasound guided transbronchial needle aspiration) is evaluated in accordance to the sensitivity, specificity and positive and negative predictive value of the different methods. Another interesting challenge is to define the criteria for indicating a sublobar resection in certain tumours and patients. Different factors, age, lung function, tumour location and type of sublobar resection, are analysed. Levels of evidence and recommendations of the procedure are also considered. Surgical resection is an accepted therapeutic option in the treatment of colorectal cancer lung metastases. Its indication is based on acceptable survival rates and knowledge of the impact of various factors (interval free of disease, number of metastases, presence of liver metastasis, presence of lymph node involvement, or increased pre-operative levels of carcinoembryonic antigen), is analysed in detail.