Assessing Adherence by Combining the Test of Adherence to Inhalers With Pharmacy Refill Records.

BACKGROUND AND OBJECTIVE: The Global Initiative for Asthma (GINA) recommends the concurrent use of self-report and pharmacy refill data to assess treatment adherence. However, clinical evidence to support this combined approach is limited. Objective: To determine nonadherence to inhaler medication based on a validated questionnaire (Test of Adherence to Inhalers; TAI) and prescription refill data in a community sample of patients with chronic obstructive pulmonary disease (COPD) or asthma. Secondarily, we sought to determine the degree of concordance between these two measures. METHODS: Cross-sectional, observational multicenter study in patients with asthma or COPD. Sociodemographic and clinical data were obtained from clinical records. Refill data were retrieved from electronic pharmacy databases. Participants completed the 12-item TAI during a single visit as part of routine care. Nonadherence was defined as TAI <50 or <80% pharmacy refill rate (PRR) in the previous 6 months. RESULTS: A total of 816 patients (mean age, 60) were included. Nonadherence rates were 58.1% (TAI) and 28.6% (PRR) compared with 64.6% for the combined data (P<.0001). Concordance between the 2 measures was weak (к=0.205). CONCLUSIONS: These findings confirm the GINA recommendations, indicating that concomitant use of the TAI and pharmacy refill data identifies a higher percentage of nonadherent asthma or COPD patients than either instrument alone.

Guía española de la enfermedad pulmonar obstructiva crónica (GesEPOC) 2017: tratamiento farmacológico en fase estable / Spanish guidelines for management of chronic obstructive pulmonary disease (GesEPOC) 2017: pharmacological treatment of stable phase

La enfermedad pulmonar obstructiva crónica (EPOC) presenta una gran heterogeneidad clínica, por lo que su tratamiento se debe individualizar según el nivel de riesgo y el fenotipo. La Guía española de la EPOC (GesEPOC) estableció por primera vez en 2012 unas pautas de tratamiento farmacológico basadas en fenotipos clínicos. Estas pautas han sido adoptadas posteriormente por otras normativas nacionales, y han sido respaldadas por nuevas evidencias publicadas desde entonces. En esta actualización 2017 se ha sustituido la clasificación de gravedad inicial por una clasificación de riesgo mucho más sencilla (bajo o alto riesgo), basándose en la función pulmonar, el grado de disnea y la historia de agudizaciones, y se recomienda la determinación del fenotipo clínico únicamente en pacientes de alto riesgo. Se mantienen los mismos fenotipos clínicos: no agudizador, EPOC-asma (ACO), agudizador con enfisema y agudizador con bronquitis crónica. La base del tratamiento farmacológico de la EPOC es la broncodilatación, y también es el único tratamiento recomendado en pacientes de bajo riesgo. En los pacientes con alto riesgo se añadirán diversos fármacos a los broncodilatadores según el fenotipo clínico. GesEPOC supone una aproximación al tratamiento de la EPOC más individualizado según las características clínicas de los pacientes y su nivel de riesgo o de complejidad.(AU)

The clinical presentation of chronic obstructive pulmonary disease (COPD) varies widely, so treatment must be tailored according to the level of risk and phenotype. In 2012, the Spanish COPD Guidelines (GesEPOC) first established pharmacological treatment regimens based on clinical phenotypes. These regimens were subsequently adopted by other national guidelines, and since then, have been backed up by new evidence. In this 2017 update, the original severity classification has been replaced by a much simpler risk classification (low or high risk), on the basis of lung function, dyspnea grade, and history of exacerbations, while determination of clinical phenotype is recommended only in high-risk patients. The same clinical phenotypes have been maintained: non-exacerbator, asthma-COPD overlap (ACO), exacerbator with emphysema, and exacerbator with bronchitis. Pharmacological treatment of COPD is based on bronchodilators, the only treatment recommended in low-risk patients. High-risk patients will receive different drugs in addition to bronchodilators, depending on their clinical phenotype. GesEPOC reflects a more individualized approach to COPD treatment, according to patient clinical characteristics and level of risk or complexity.(AU)

Inflammatory Asthma Phenotype Discrimination Using an Electronic Nose Breath Analyzer.

BACKGROUND AND OBJECTIVE: Patients with persistent asthma have different inflammatory phenotypes. The electronic nose is a new technology capable of distinguishing volatile organic compound (VOC) breath-prints in exhaled breath. The aim of the study was to investigate the capacity of electronic nose breath-print analysis to discriminate between different inflammatory asthma phenotypes (eosinophilic, neutrophilic, paucigranulocytic) determined by induced sputum in patients with persistent asthma. METHODS: Fifty-two patients with persistent asthma were consecutively included in a cross-sectional proof-of-concept study. Inflammatory asthma phenotypes (eosinophilic, neutrophilic and paucigranulocytic) were recognized by inflammatory cell counts in induced sputum. VOC breath-prints were analyzed using the electronic nose Cyranose 320 and assessed by discriminant analysis on principal component reduction, resulting in cross-validated accuracy values. Receiver operating characteristic (ROC) curves were calculated. RESULTS: VOC breath-prints were different in eosinophilic asthmatics compared with both neutrophilic asthmatics (accuracy 73%; P=.008; area under ROC, 0.92) and paucigranulocytic asthmatics (accuracy 74%; P=.004; area under ROC, 0.79). Likewise, neutrophilic and paucigranulocytic breath-prints were also different (accuracy 89%; P=.001; area under ROC, 0.88). CONCLUSION: An electronic nose can discriminate inflammatory phenotypes in patients with persistent asthma in a regular clinical setting. ClinicalTrials.gov identifier: NCT02026336.

Low-dose theophylline enhances the anti-inflammatory effects of steroids during exacerbations of COPD.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterised by an abnormal inflammatory response mainly to cigarette smoke that flares up during exacerbations of the disease (ECOPD). Reduced activity of histone deacetylases (HDAC) contributes to enhanced inflammation in stable COPD. It was hypothesised that HDAC activity is further reduced during ECOPD and that theophylline, an HDAC activator, potentiates the anti-inflammatory effect of steroids in these patients. A study was performed to investigate HDAC activity during ECOPD and the effects of theophylline on the anti-inflammatory effects of steroids in a randomised single-blind controlled study. METHODS: 35 patients hospitalised with ECOPD and treated according to international guidelines (including systemic steroids) were randomised to receive or not to receive low-dose oral theophylline (100 mg twice daily). Before treatment and 3 months after discharge, HDAC and nuclear factor-kappaB (NF-kappaB) activity in sputum macrophages, the concentration of nitric oxide in exhaled air (eNO) and total antioxidant status (TAS), tumour necrosis factor alpha (TNFalpha), interleukin (IL)-6 and IL8 levels in sputum supernatants were measured. RESULTS: Patients receiving standard therapy showed decreased NF-kappaB activity, eNO concentration and sputum levels of TNFalpha, IL6 and IL8, as well as increased TAS during recovery of ECOPD, but HDAC activity did not change. The addition of low-dose theophylline increased HDAC activity and further reduced IL8 and TNFalpha concentrations. CONCLUSIONS: During ECOPD, low-dose theophylline increases HDAC activity and improves the anti-inflammatory effects of steroids. TRIAL REGISTRATION NUMBER: NCT00671151.

EPOC: ¿una enfermedad inflamatoria obstructiva o sistémica? / COPD: Is it an obstructive inflammatory or systemic disease?

La enfermedad pulmonar obstructiva crónica (EPOC) se caracteriza por una respuesta inflamatoria anómala al humo del tabaco, que se traduce en una afectación pulmonar con obstrucción crónica al flujo aéreo y que también se caracteriza por unas consecuenciassistémicas. La EPOC tiene efectos sistémicos bien reconocidos como la pérdida de peso y otras alteraciones nutricionales, así como disfunción del músculo esquelético, aunque también hay otros no menos importantes como el mayor riesgo cardiovascular,depresión, osteoporosis o, incluso, cáncer. Los mecanismos subyacentes a estos efectos no son bien conocidos, aunque es posible que dichos efectos sistémicos puedan estar en relación,al menos en parte, con la inflamación sistémica que, deforma cada vez más convincente, se demuestra en estos enfermos. El origen de esta inflamación sistémica tampoco es bien conocido y se postula que puede provenir del humo del tabaco, del procesoinflamatorio pulmonar, del músculo esquelético, de la médula ósea o ser consecuencia de la hipoxia crónica de los tejidos. El determinar los mecanismos subyacentes puede ser muy relevante ya que es probable que tratamientos dirigidos a reducir la inflamación sistémica en la EPOC puedan tener un impactoclínico significativo (AU)

No disponible (AU)

Autoinmunidad en la EPOC / No disponible

No disponible

Corticoides en las exacerbaciones de la EPOC: sí, pero menos. Respuesta / Corticosteroids in exacerbations of chronic obstructive pulmonary disease: yes, but less. Reply

No disponible

Empleo de esteroides inhalados en el tratamiento de la EPOC / Inhaled steroids in the treatment of COPD

No disponible

Mecanismos moleculares de los glucocorticoides / Molecular mechanisms of glucocorticoids

No disponible

[Mechanical ventilation in a respiratory ward. Evolution from 1994 to 2000]. / Ventilación mecánica en hospitalización neumológica. Evolución en el período 1994-2000.

OBJECTIVE: To investigate the absolute and relative frequency of mechanical ventilation in the management of patients on a respiratory medicine ward between 1994 and 2000. To describe reasons for admission, mean hospital stay and outcomes. SETTING: A tertiary-care university hospital. METHODS: Observational, descriptive study of a case series. RESULTS: During the study period, 257 admissions involved mechanical ventilation of 132 patients. During that time, there was a progressive increase in the total number of ventilated patients as well as in the relative frequency, such that ventilated patients eventually accounted for 6.1% of all admissions for respiratory care in 2000. Nearly 80% of admissions were related to the service's home mechanical ventilation program, either to initiate and adapt ventilation for new patients or to treat exacerbations or diagnose and treat other medical or surgical problems in already-ventilated patients. Patients transferred from the intensive care unit (ICU) because of weaning difficulties (median ventilation, 31 days) had the highest mean stay. Nine of the 132 patients had to be transferred to the ICU and 18 died while hospitalized (7% of admissions and 13.6% of patients). The patients who died were those who were more acutely and severely ill (acute exacerbation in home-ventilated patients, patients with acute respiratory failure treated initially with non-invasive ventilation and patients transferred from the ICU due to weaning difficulties). CONCLUSIONS: Admissions requiring mechanical ventilation have increased and most are related to the home mechanical ventilation program. The mean stay and the mortality rate were related to the reason for admission.