Role of Telomere Length in Survival of Patients with Idiopathic Pulmonary Fibrosis and Other Interstitial Lung Diseases.

Interstitial lung diseases (ILDs) constitute a group of more than 200 disorders, with idiopathic pulmonary fibrosis (IPF) being one of the most frequent. Telomere length (TL) shortening causes loss of function of the lung parenchyma. However, little is known about its role as a prognostic factor in ILD patients. With the aim of investigating the role of TL and telomerase activity in the prognosis of patients affected by ILDs, we analysed lung tissue samples from 61 patients. We measured relative TL and telomerase activity by conventional procedures. Both clinical and molecular parameters were associated with overall survival by the Kaplan-Meier method. Patients with IPF had poorer prognosis than patients with other ILDs (p = 0.034). When patients were classified according to TL, those with shortened telomeres reported lower overall survival (p = 0.085); differences reached statistical significance after excluding ILD patients who developed cancer (p = 0.021). In a Cox regression analysis, TL behaved as a risk-modifying variable for death associated with rheumatic disease (RD) co-occurrence (p = 0.029). Also, in patients without cancer, ferritin was significantly increased in cases with RD and IPF co-occurrence (p = 0.032). In relation to telomerase activity, no significant differences were detected. In conclusion, TL in lung tissue emerges as a prognostic factor in ILD patients. Specifically, in cases with RD and IPF co-occurrence, TL can be considered as a risk-modifying variable for death.

Indicadores de calidad asistencial en patología respiratoria en la Comunidad de Madrid / Respiratory Care Quality Indicators in the Community of Madrid

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Factor de necrosis tumoral como marcador de inflamación precoz en fumadores sanos / Tumor necrosis factor as an early marker of inflammation in healthy smokers

Fundamento y objetivo: El tabaco produce una inflamación que conduce a pérdida de función pulmonar. El tumoral necrosis factor α (TNF-α, «factor de necrosis tumoral α») es una citocina implicada en la patogenia de la enfermedad pulmonar obstructiva crónica. Necesitamos desarrollar métodos que permitan detectar precozmente a los fumadores en riesgo de pérdida de función pulmonar. Los objetivos de este trabajo fueron: demostrar que los fumadores tienen valores más elevados de TNF-α en suero y condensado de aire exhalado (CAE); valorar la influencia de sexo, edad y peso en dichos valores; conocer la relación entre consumo de tabaco y función pulmonar con los valores de TNF-α. Pacientes y método: Grupo estudio y control sin patología. Realización de espirometría con test broncodilatador, recogida de CAE y extracción sanguínea previa al abandono del tabaco. Análisis estadístico con SPSS 11.0. Resultados: Se incluyeron 51 pacientes (60,8% fumadores), un 56,9% mujeres, con una edad media de 39,88 años. Los fumadores tenían un consumo medio de 21,68 cigarrillos/día y una edad media de inicio de 15,77 años. Los fumadores tenían valores significativamente más elevados de TNF-α en suero (p<0,043); los valores en CAE no mostraban diferencias. De los parámetros de consumo de tabaco, solo la edad de inicio y el TNF-α plasmático guardaban correlación. De la función pulmonar, solo la capacidad vital forzada y el volumen espirado durante el primer segundo guardaban relación con el TNF-α plasmático. Conclusiones: Los fumadores tienen valores más elevados de TNF-α en suero. La cuantía de años de consumo de tabaco influye en los valores de TNF-α plasmáticos. Existe una discreta relación de la función pulmonar con los valores de TNF-α en suero. Los valores de TNF en CAE no muestran diferencias ni correlaciones significativas (AU)

Background and objectives: Smoking creates an inflammation that leads to lose of lung function. Tumor necrosis factor alpha (TNF-α) is a cytokine that plays an important role in the pathogenesis of chronic obstructive pulmonary disease. There is a need to develop methods for an early detection of an impaired lung function in smokers. We aimed to show that smokers have higher levels of TNF-α in serum and exhaled breath condensate (EBC). We also analysed the influence of sex, age and weight on TNF-α, and determined the association between smoking, pulmonary function and TNF-α.Patients and methods: Prospective study of smokers and non-smokers without any known disease. Respiratory function tests, EBC and blood samples were performed before smoking cessation. Statistical analysis: SPSS 11.0. Results: Fifty-one patients (60.8% smokers), 56.9% females, mean age 39.88 years old. Smokers initiated at an age of 15.77 years; the mean of cigarettes/day was 21.68. Significant differences in TNF-α serum levels between smokers and non-smokers were observed (P<.043). Differences did not reach significance for EBC. For tobacco consumption data, only age at smoking initiation and serum TNF-α levels had a correlation. A significant relation between TNF-α serum levels and forced expiratory volume in one second and forced vital capacity was found. Conclusions: Smokers show higher TNF-α levels in serum. Number of years of smoking has an influence on TNF-α levels. There is a modest corelation between pulmonary function and plasma TNF-α levels, but not for EBC (AU)

[Tumor necrosis factor as an early marker of inflammation in healthy smokers]. / Factor de necrosis tumoral como marcador de inflamación precoz en fumadores sanos.

BACKGROUND AND OBJECTIVES: Smoking creates an inflammation that leads to lose of lung function. Tumor necrosis factor alpha (TNF-α) is a cytokine that plays an important role in the pathogenesis of chronic obstructive pulmonary disease. There is a need to develop methods for an early detection of an impaired lung function in smokers. We aimed to show that smokers have higher levels of TNF-α in serum and exhaled breath condensate (EBC). We also analysed the influence of sex, age and weight on TNF-α, and determined the association between smoking, pulmonary function and TNF-α. PATIENTS AND METHODS: Prospective study of smokers and non-smokers without any known disease. Respiratory function tests, EBC and blood samples were performed before smoking cessation. STATISTICAL ANALYSIS: SPSS 11.0. RESULTS: Fifty-one patients (60.8% smokers), 56.9% females, mean age 39.88 years old. Smokers initiated at an age of 15.77 years; the mean of cigarettes/day was 21.68. Significant differences in TNF-α serum levels between smokers and non-smokers were observed (P<.043). Differences did not reach significance for EBC. For tobacco consumption data, only age at smoking initiation and serum TNF-α levels had a correlation. A significant relation between TNF-α serum levels and forced expiratory volume in one second and forced vital capacity was found. CONCLUSIONS: Smokers show higher TNF-α levels in serum. Number of years of smoking has an influence on TNF-α levels. There is a modest correlation between pulmonary function and plasma TNF-α levels, but not for EBC.

[Etanercept as a possible trigger of fatal pulmonary fibrosis]. / Fibrosis pulmonar mortal, con etanercept como posible desencadenante.

Pulmonary fibrosis can be caused by external agents, including certain drugs. For some time now, tumor necrosis factor antagonists such as etanercept have been used to treat certain autoimmune diseases. Fibrosis caused by medication responds to withdrawal of the drug and treatment with corticosteroids. Very rarely, fibrosis is irreversible. We present the case of a patient who developed pulmonary fibrosis after initiating treatment with etanercept. The clinical course was fulminant despite withdrawal of the drug and high doses of corticosteroids.

Fibrosis pulmonar mortal, con etanercept como posible desencadenante / Etanercept as a possible trigger of fatal pulmonary fibrosis

La fibrosis pulmonar es una enfermedad que puede estar causada por agentes externos como determinados fármacos. Desde hace un tiempo se utilizan fármacos antagonistas del factor de necrosis tumoral (TNF) para ciertas enfermedades autoinmunitarias, siendo un ejemplo de estos fármacos el etanercept. Las fibrosis secundarias a medicamentos se caracterizan por la respuesta a la retirada del fármaco y a esteroides. En muy raras ocasiones se produce una fibrosis irreversible. Presentamos el caso de un paciente que desarrolló una fibrosis pulmonar tras iniciar tratamiento con etanercept y que tuvo un curso clínico nefasto a pesar de la retirada del anti-TNF y dosis altas de esteroides

Pulmonary fibrosis can be caused by external agents, including certain drugs. For some time now, tumor necrosis factor antagonists such as etanercept have been used to treat certain autoimmune diseases. Fibrosis caused by medication responds to withdrawal of the drug and treatment with corticosteroids. Very rarely, fibrosis is irreversible. We present the case of a patient who developed pulmonary fibrosis after initiating treatment with etanercept. The clinical course was fulminant despite withdrawal of the drug and high doses of corticosteroids (AU)