Search

Chronic obstructive pulmonary disease (COPD) is an entity with a heterogeneous presentation. For this reason, attempts have been made to characterize different phenotypes and endotypes to enable a more individualized approach. The aim of the Biomarkers in COPD (BIOMEPOC) project is to identify useful biomarkers in blood to improve the characterization of patients. Clinical data and blood samples from a group of patients and healthy controls will be analyzed. The project will consist of an exploration phase and a validation phase. Analytical parameters in blood will be determined using standard techniques and certain 'omics' (transcriptomics, proteomics, and metabolomics). The former will be hypothesis-driven, whereas the latter will be exploratory. Finally, a multilevel analysis will be conducted. Currently, 269 patients and 83 controls have been recruited, and sample processing is beginning. Our hope is to use the results to identify new biomarkers that, alone or combined, will allow a better characterization of patients.

Iron deficiency affects exercise capacity because of the critical role iron plays in the optimal functioning of skeletal muscle metabolism. We hypothesized that intravenous iron may improve exercise tolerance, quality of life (QoL), and daily physical activity (DPA) in patients with chronic obstructive pulmonary disease (COPD).This was a placebo-controlled, single-blind, parallel-group, randomized clinical trial. Iron deficiency was defined as a ferritin level100ng/mL or a ferritin level between 100 and 299ng/mL with a transferrin saturation20%, with or without mild anaemia. Patients were randomized at a 2:1 ratio to receive intravenous ferric carboxymaltose or placebo. The primary objective was to investigate whether intravenous iron replacement improved endurance time from baseline by at least 33%. The secondary objectives were to evaluate impact on QoL using the COPD Assessment Test (CAT) and on DPA by accelerometry.We included 66 patients, 44 (66.7%) in the intervention group and 22 (33.3%) in the placebo group. Among patients receiving ferric carboxymaltose, 23 (52.3%) achieved the primary endpoint compared to 4 (18.2%) in the placebo group [p=0.009; relative risk 3.12, (95% CI, 1.19-8.12)]. CAT score decreased -3 (-6.0-1.3) points from baseline in the intervention group (p=0.007), in contrast to placebo group [-1 (-4.0-2.3) points, p=0.236] with no differences in DPA and adverse events in both groups.Iron replacement improved exercise capacity and QoL in stable COPD patients with iron deficiency. The treatment was well tolerated.EudraCT 2016-001238-89.

Altres ajuts: This study has been supported by Spanish Ministry of Science and Innovation, Sociedad Española de Neumología y Cirugía Torácica (SEPAR) 2018 & 2020. Lung cancer (LC) risk increases in patients with chronic respiratory diseases (COPD). MicroRNAs and redox imbalance are involved in lung tumorigenesis in COPD patients. Whether systemic alterations of those events may also take place in LC patients remains unknown. Our objectives were to assess the plasma levels of microRNAs, redox balance, and cytokines in LC patients with/without COPD. MicroRNAs (RT-PCR) involved in LC, oxidized DNA, MDA-protein adducts, GSH, TEAC, VEGF, and TGF-beta (ELISA) were quantified in plasma samples from non-LC controls (n = 45), LC-only patients (n = 32), and LC-COPD patients (n = 91). In LC-COPD patients compared to controls and LC-only, MDA-protein adduct levels increased, while those of GSH decreased, and two patterns of plasma microRNA were detected. In both LC patient groups, miR-451 expression was downregulated, while those of microRNA-let7c were upregulated, and levels of TEAC and TGF-beta increased compared to the controls. Correlations were found between clinical and biological variables. A differential expression profile of microRNAs was detected in patients with LC. Moreover, in LC patients with COPD, plasma oxidative stress levels increased, whereas those of GSH declined. Systemic oxidative and antioxidant markers are differentially expressed in LC patients with respiratory diseases, thus implying its contribution to the pathogenesis of tumorigenesis in these patients.

In COPD patients, non-anemic iron deficiency (NAID) is a common systemic manifestation. We hypothesized that in COPD patients with NAID, iron therapy may improve systemic oxidative stress. The FACE (Ferinject assessment in patients with COPD and iron deficiency to improve exercise tolerance) study was a single-blind, unicentric, parallel-group, placebo-controlled clinical trial (trial registry: 2016-001238-89). Sixty-six patients were enrolled (randomization 2:1): iron arm, n = 44 and placebo arm, n = 22, with similar clinical characteristics. Serum levels of 3-nitrotyrosine, MDA-protein adducts, and reactive carbonyls, catalase, superoxide dismutase (SOD), glutathione, Trolox equivalent antioxidant capacity (TEAC), and iron metabolism biomarkers were quantified in both groups. In the iron-treated patients compared to placebo, MDA-protein adducts and 3-nitrotyrosine serum levels significantly declined, while those of GSH increased and iron metabolism parameters significantly improved. Hepcidin was associated with iron status parameters. This randomized clinical trial evidenced that iron replacement elicited a decline in serum oxidative stress markers along with an improvement in GSH levels in patients with stable severe COPD. Hepcidin may be a surrogate biomarker of iron status and metabolism in patients with chronic respiratory diseases. These findings have potential clinical implications in the management of patients with severe COPD.

The phenotypic characteristics of chronic obstructive pulmonary disease (COPD) in individuals younger than 50 years of age (early COPD) are not well defined. This prospective, multi-centre, case-control study sought to describe these characteristics and compare them with those of smokers (>= 10 pack-years) of similar age with normal spirometry (controls). We studied 92 cases (post-bronchodilator forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC), In part, by CIBERES, SEPAR, FIS (CP16/00039, PI17/00369, PI18/01008) and an unrestricted grant from Boehringer-Ingelheim. Funding information for this article has been deposited with the Crossref Funder Registry.

Introduction: Patients with Chronic Obstructive Pulmonary Diseases (COPD) have skeletal muscle dysfunction. In these patients, skeletal muscle dysfunction has impact on the quality of life and mortality. However, its relevance is unknown in other chronic respiratory diseases such as bronchiectasis, which shares some deleterious factors with COPD. Accordingly, our aim was to describe the structure and function of skeletal muscle ( vastus lateralis ) in patients with non-cystic fibrosis bronchiectasis (non-CF BCH), valuing its relationship with exercise capacity and physical activity. Methods: 29 patients with non-CF BCH and 8 healthy subjects of similar age were recruited. Anthropometry, body composition (bioimpedance), health-related quality of life (QoL, Quittner9s questionnaire), physical activity (accelerometer), exercise capacity (6 minute walking test), lung function, and respiratory and limb muscle function were assessed in all subjects. In addition, open biopsies of the vastus lateralis were obtained for the analysis of structural signs of muscle damage/regeneration (McGowan technique) and fiber typing. Results: Patients with non-CF BCH showed a moderate obstructive pattern, nutritional disorders (decreased a 13% in fat-free mass index), decreased exercise capacity and physical activity compared to controls. In addition, skeletal muscle strength was also lower in the group of patients, however, no structural alterations were observed in the vastus lateralis . Conclusion: Patients with non-CF BCH have shown skeletal muscle dysfunction that could limit their daily activities and exercise capacity. However, they do not depict changes in the structure of the skeletal muscle.

Introduction: Inspiratory muscle strength is usually assessed thorough the determination of static mouth pressure (PImax). However, since this manoeuvre presents certain problems, alternative techniques have been developed over the last few years. One of the most promising is determination of sniff nasal inspiratory pressure (SNIP). Aim: To evaluate SNIP assessment as an alternative for the evaluation of the inspiratory muscle strength. Methods: Subjects were consecutively included and assigned to one of three different groups: control (8), COPD patients (23) and patients with neuromuscular disorders (21). Different maximal inspiratory pressures were determined: (a) dynamic in the esophagus (maximal sniff Pes, reference variable), (b) PImax, and (c) SNIP. Results: Both SNIP and MIP showed an excellent correlation with Pes (r=0.835 and 0.752, respectively, P