Sara Vilà

Colour of sputum is a marker for bacterial colonisation in chronic obstructive pulmonary disease

BackgroundBacterial colonisation in chronic obstructive pulmonary disease (COPD) contributes to airway inflammation and modulates exacerbations. We assessed risk factors for bacterial colonisation in COPD.MethodsPatients with stable COPD consecutively recruited over 1 year gave consent to provide a sputum sample for microbiologic analysis. Bronchial colonisation by potentially pathogenic microorganisms (PPMs) was defined as the isolation of PPMs at concentrations of ≥102 colony-forming units (CFU)/mL on quantitative bacterial culture. Colonised patients were divided into high (>105 CFU/mL) or low (<105 CFU/mL) bacterial load.ResultsA total of 119 patients (92.5% men, mean age 68 years, mean forced expiratory volume in one second [FEV1] [% predicted] 46.4%) were evaluated. Bacterial colonisation was demonstrated in 58 (48.7%) patients. Patients with and without bacterial colonisation showed significant differences in smoking history, cough, dyspnoea, COPD exacerbations and hospitalisations in the previous year, and sputum colour. Thirty-six patients (62% of those colonised) had a high bacterial load. More than 80% of the sputum samples with a dark yellow or greenish colour yielded PPMs in culture. In contrast, only 5.9% of white and 44.7% of light yellow sputum samples were positive (P < 0.001). Multivariate analysis showed an increased degree of dyspnoea (odds ratio [OR] = 2.63, 95% confidence interval [CI] 1.53-5.09, P = 0.004) and a darker sputum colour (OR = 4.11, 95% CI 2.30-7.29, P < 0.001) as factors associated with the presence of PPMs in sputum.ConclusionsAlmost half of our population of ambulatory moderate to very severe COPD patients were colonised with PPMs. Patients colonised present more severe dyspnoea, and a darker colour of sputum allows identification of individuals more likely to be colonised.

Efficacy of moxifloxacin in the treatment of bronchial colonisation in COPD

This study was designed to investigate the efficacy of moxifloxacin for the eradication of bacterial colonisation of the airways in patients with moderate-to-severe chronic obstructive pulmonary disease (COPD). Out of 119 stable patients with COPD screened, 40 (mean age 69 yrs, mean forced expiratory volume in 1 s 50% predicted) were colonised with potentially pathogenic microorganisms (PPMs) and were included in a randomised, double-blind, placebo-controlled trial with moxifloxacin 400 mg daily for 5 days. Eradication rates were 75% with moxifloxacin and 30% with placebo at 2 weeks (p = 0.01). Bacterial persistence at 8 weeks was still higher (not significantly) in the placebo arm (five (25%) out of 20 versus one (5%) out of 20; p = 0.18). The frequencies of acquisition of a new PPM were high and similar in both treatment groups; consequently, the prevalence of colonisation at 8 weeks was also similar between treatment arms. No difference was found in the number of patients with exacerbations during the 5-month follow-up. Only the acquisition of a new PPM during follow-up showed a statistically significant relationship with occurrence of an exacerbation. Moxifloxacin was effective in eradicating PPMs in patients with positive sputum cultures. However, most patients were recolonised after 8 weeks of follow-up. Acquisition of a new strain of bacteria was associated with an increased risk of developing an exacerbation.

Programa de cribado para el déficit de α-antitripsina en pacientes con EPOC mediante el uso de gota de sangre en papel secante

El deficit de α-antitripsina (AAT) es una enfermedad in-fradiagnosticada, por lo que se recomienda establecer pro-gramas de cribado en pacientes con EPOC. Presentamos los resultados de la fase piloto de un programa de cribado del deficit de AAT, con el objetivo de evaluar la tecnica utiliza-da, los circuitos de envio de muestras y los resultados obte-nidos Participaron en el estudio 5 centros, que recogieron du-rante el periodo de un mes muestras de todos los pacientes con EPOC en los que nunca se hubieran determinado las concentraciones plasmaticas de AAT o el fenotipo Pi. Se aplicaron gotas de sangre capilar sobre discos de papel se-cante, que posteriormente se enviaban por correo postal al laboratorio central del estudio. Las muestras se procesaron para la determinacion cuantitativa de los valores de AAT mediante un metodo de inmunonefelometria y, para la de-terminacion del genotipo de AAT, con un analizador de ADN del tipo LightCycler. Se analizaron muestras de 86 pa-cientes con EPOC (76 varones, 10 mujeres) con una edad media de 68,2 anos. En 74 pacientes (86%) se descarto el de-ficit por presentar concentraciones de AAT por encima del punto de corte establecido, aunque uno de ellos fue heteroci-goto MZ por genotipificacion. De los 12 restantes (13,9%), solo 2 individuos presentaban tambien un alelo Z. El resto correspondio a pacientes con concentraciones por debajo del umbral establecido y sin evidencia del alelo Z (10 pacientes; 11,6%). La frecuencia observada del alelo Z (3/172; 1,74%) es muy similar a la encontrada en la poblacion general Los resultados de esta fase inicial permiten comprobar el correcto funcionamiento del circuito utilizado para la obten-cion y envio de las muestras. Es un metodo aplicable, como-do y bien aceptado por los medicos participantes y permite la cuantificacion de AAT, asi como la deteccion del alelo de-ficitario Z en las muestras con una excelente correlacion con las tecnicas estandar que usan muestras de sangre total

Déficit de alfa-1-antitripsina. Situación en España y desarrollo de un programa de detección de casos

Estudios realizados en Espana senalan que un 9% de la poblacion general de entre 40 y 70 anos esta afectada de enfermedad pulmonar obstructiva cronica (EPOC). El humo del tabaco es el factor causal en mas del 90% de los casos; sin embargo, se ha estimado que solo un 10-20% de los fumadores desarrollan EPOC. La causa se puede encontrar en la existencia de factores geneticos o ambientales que modulan el efecto toxico del tabaco. El factor genetico mas conocido es el deficit de alfa-1-antitripsina, que comporta un riesgo aumentado de desarrollar enfisema pulmonar en fumadores. Tanto la Organizacion Mundial de la Salud como la American Thoracic Society/European Respiratory Society en sus recientes normativas recomiendan establecer programas de deteccion del deficit de alfa-1-antitripsina en pacientes con EPOC. Esta estrategia es crucial en Espana, donde la enfermedad esta infradiagnosticada, sobre todo debido a un bajo indice de sospecha entre los medicos.

α1-Antitrypsin Deficiency: Situation in Spain and Development of a Screening Program

Studies undertaken in Spain indicate that 9% of the general population aged between 40 and 70 years is affected by chronic obstructive pulmonary disease (COPD). Although tobacco smoke is the causative factor in more than 90% of cases, it is estimated that only 10% to 20% of smokers develop COPD. This may be explained by the existence of genetic or environmental factors that modulate the toxic effects of tobacco. The best known genetic factor is alpha1-antitrypsin deficiency, which is associated with an increased risk of developing pulmonary emphysema in smokers. The most recent guidelines from both the World Health Organization and the American Thoracic Society/European Respiratory Society recommend the establishment of screening programs for the detection of alpha1-antitrypsin deficiency in patients with COPD. This strategy is crucial in Spain, where the disease is under diagnosed, mainly due to a low index of suspicion among doctors.