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Abstract Background: The role of hyaluronic acid plus hypertonic saline (HA+HS) as a mucoactive treatment in patients with bronchiectasis is still unknown. This study evaluated whether HA+HS solution enhances similar sputum quantity with better safety profile than HS alone in patients with bronchiectasis. Methods: In this double-blind randomized crossover trial, three solutions (7% HS; 0.1% HA +7%HS; and 0.9% isotonic saline, IS) were compared in outpatients with bronchiectasis and chronic sputum expectoration. Participants inhaled each solution across four consecutive sessions. All sessions, except on session 3, also included 30 minutes of airway clearance technique. A 7-day washout period was applied. Sputum weight was collected during the sessions (primary outcome) as well as during a 24-hour follow-up. The Leicester Cough Questionnaire (LCQ) and lung function were measured before/after each treatment arm. Safety was assessed by the monitoring of adverse events (AEs). Results: Twenty-eight patients with bronchiectasis (mean age of 64.0 (17.9) and FEV1% 60.9 (24.6) of predicted) were recruited. HS and HA+HS promoted similar expectoration during sessions, both being greater than IS [median difference HS vs. IS 3.7 g (95% CI 0.5–6.9); HA+HS vs. IS 3.2 g (95%CI 0.5–5.9)]. Sputum expectorated exclusively during the ACT period was similar across all treatment arms [HS vs. IS −0.3 g (95% CI −1.7 to 0.9); HA+HS vs. IS 0.0 g (95% CI −1.3 to 1.4); HS vs. HA+HS 0.0 g (95% CI −1.2 to 0.4)]. Sputum collected over the 24-hour follow-up tended to be lower for HS and HA+HS compared with IS [HS vs. IS −1.7 g (95% CI −4.2 to 0.0); HA+HS vs. IS −1.1 g (95%CI −3.6 to 0.7)]. No differences in LCQ or lung function were observed. Most severe AEs were reported using HS. Conclusion: HS and HA+HS were more effective on sputum expectoration than IS in patients with bronchiectasis, reporting HA+HS better safety profile than HS.

There is controversy regarding the significance of radiological consolidation in the context of COPD exacerbation (eCOPD). While some studies into eCOPD exclude these cases, consolidation is a common feature of eCOPD admissions in real practice. This study aims to address the question of whether consolidation in eCOPD is a distinct clinical phenotype with implications for management decisions and outcomes. The European COPD Audit was carried out in 384 hospitals from 13 European countries between 2010 and 2011 to analyze guideline adherence in eCOPD. In this analysis, admissions were split according to the presence or not of consolidation on the admission chest radiograph. Groups were compared in terms of clinical and epidemiological features, existing treatment, clinical care utilized and mortality. 14,111 cases were included comprising 2,714 (19.2%) with consolidation and 11,397 (80.8%) without. The risk of radiographic consolidation increased with age, female gender, cardiovascular diseases, having had two or more admissions in the previous year, and sputum color change. Previous treatment with inhaled steroids was not associated. Patients with radiographic consolidation were significantly more likely to receive antibiotics, oxygen and non-invasive ventilation during the admission and had a lower survival from admission to 90-day follow-up. Patients admitted for COPD exacerbation who have radiological consolidation have a more severe illness course, are treated more intensively by clinicians and have a poorer prognosis. We recommend that these patients be considered a distinct subset in COPD exacerbation.

Background: The bronchial mucosa is protected by a specialized immune system focused on the prevention of colonization and infection by potentially pathogenic microorganisms (PPMs). Immunoglobulin A (IgA) is the principal antibody involved in this mechanism. A defective immune barrier may facilitate the recurrent presence of PPMs in COPD. Purpose: The aim of this study was to determine IgA-mediated bronchial specific immune responses against Pseudomonas aeruginosa in stable patients with severe disease. Methods: COPD patients with good-quality sputum samples obtained during stability were included and classified according to the presence or absence of chronic bronchial colonization by P. aeruginosa. Levels of specific IgA for P. aeruginosa in sputum were determined by ELISA and expressed as ratios, using the pooled level of 10 healthy subjects as reference (optical density450 patient/control). Results: Thirty-six stable COPD patients were included, 15 of whom had chronic colonization by P. aeruginosa. Levels of specific IgA against P. aeruginosa in stable non-colonized patients were lower than those in healthy subjects (IgA ratio: median =0.15 [interquartile range {IQR} 0.05-0.36]). Colonized patients had higher levels, (1.56 [IQR 0.59-2.79]) (p,0.001, Mann- Whitney U test), with figures equivalent but not exceeding the reference value. Conclusion: IgA-based immune response against P. aeruginosa was low in severe COPD patients. Levels of specific IgA against this microorganism were higher in colonized patients, but did not attain clear-cut levels above the reference. An impaired local response against P. aeruginosa may favor chronic colonization and recurrent infections in severe COPD.

Background Previous studies have identified lung, sputum or blood transcriptomic biomarkers associated with the severity of airflow limitation in COPD. Yet, it is not clear whether the lung pathobiology is mirrored by these surrogate tissues. The aim of this study was to explore this question. Methods We used Weighted Gene Co-expression Network Analysis (WGCNA) to identify shared pathological mechanisms across four COPD gene-expression datasets: two sets of lung tissues (L1 n  = 70; L2 n  = 124), and one each of induced sputum (S; n  = 121) and peripheral blood (B; n = 121). Results WGCNA analysis identified twenty-one gene co-expression modules in L1. A robust module preservation between the two L datasets was observed (86%), with less preservation in S (33%) and even less in B (23%). Three modules preserved across lung tissues and sputum (not blood) were associated with the severity of airflow limitation. Ontology enrichment analysis showed that these modules included genes related to mitochondrial function, ion-homeostasis, T cells and RNA processing. These findings were largely reproduced using the consensus WGCNA network approach. Conclusions These observations indicate that major differences in lung tissue transcriptomics in patients with COPD are poorly mirrored in sputum and are unrelated to those determined in blood, suggesting that the systemic component in COPD is independently regulated. Finally, the fact that one of the preserved modules associated with FEV1 was enriched in mitochondria-related genes supports a role for mitochondrial dysfunction in the pathobiology of COPD.

The bronchial mucosa is protected by a specialized immune system focused on the prevention of colonization and infection by potentially pathogenic microorganisms (PPMs). Immunoglobulin A (IgA) is the principal antibody involved in this mechanism. A defective immune barrier may facilitate the recurrent presence of PPMs in COPD. The aim of this study was to determine IgA-mediated bronchial specific immune responses against in stable patients with severe disease. COPD patients with good-quality sputum samples obtained during stability were included and classified according to the presence or absence of chronic bronchial colonization by . Levels of specific IgA for in sputum were determined by ELISA and expressed as ratios, using the pooled level of 10 healthy subjects as reference (optical density patient/control). Thirty-six stable COPD patients were included, 15 of whom had chronic colonization by . Levels of specific IgA against in stable non-colonized patients were lower than those in healthy subjects (IgA ratio: median =0.15 [interquartile range {IQR} 0.05-0.36]). Colonized patients had higher levels, (1.56 [IQR 0.59-2.79]) ( <0.001, Mann-Whitney test), with figures equivalent but not exceeding the reference value. IgA-based immune response against was low in severe COPD patients. Levels of specific IgA against this microorganism were higher in colonized patients, but did not attain clear-cut levels above the reference. An impaired local response against may favor chronic colonization and recurrent infections in severe COPD.

The case is presented of an 81-years old man from a rural area who had been a farmer, a coffee harvester 50 years beforehand and a gardener in Bogotá for 22 years. He consulted because of abdominal pain having 10 days' evolution, localized towards the mesogastrium and epigastrium. He was also suffering from dyspnoea and productive cough. Background: chronic obstructive pulmonary disease, smoking 25 packets/year, he had received oral prednisone and inhaled beclomethasone on occasions, including during his last hospitalization. Physical examination revealed signs of undernourishment, tachycardia, tachypnoea; stertors at the base of the right hemithorax; abdomen: soft, depressible with pain on deep palpation of the epigastrium and right hypochondrium. He was admitted suffering from systemic inflammatory response syndrome (SIRS) dueto tachycardia, tachypnoea, 37,600 leukocytosis and 52%-60% eosinophilia, Ig E: 180 UI/ ml. Strongyloides stercoralis rabditiform larvae appeared in sputum and fecal material. Thoracic radiography revealed right pleural leakage; hepatic echography was normal, endoscopy of upper digestive routes revealed gastritis and duodenitis. Treatment was started with 200 mg/Kg/dose ivermectin with clinical and laboratory follow-up and satisfactory clinical evolution. Se presenta un caso de un hombre de 81 años natural de zona rural, agricultor, recolector de café 50 años atrás y jardinero por 22 años en Bogotá. Consultó por dolor abdominal de 10 días de evolución, localizado hacia mesogastrio y epigastrio. Además, disnea, tos productiva. Antecedentes: enfermedad pulmonar obstructiva crónica, cor pulmonale, fumador de 25 paquetes /año, había recibido prednisona oral y beclometasona inhalada en diversas ocasiones incluso en la última hospitalización. En el examen físico presentó signos de desnutrición, taquicardia, taquipnea; estertores en base del hemitórax derecho; abdomen: blando, depresible con dolor a la palpación profunda en epigastrio e hipocondrio derecho. Ingresó con síndrome de respuesta inflamatoria sistémica por taquicardia, taquipnea, leucocitosis 37.600 y eosinofilia 52-60%, Ig E: 180 UI/ ml. Se evidenciaron larvas rabditiformes de Strongyloides stercoralis en esputo y materia fecal. La radiografía de tórax mostró derrame pleural derecho, la ecografía hepática fue normal, la endoscopia de vías digestivas altas evidenció gastritis y duodenitis. Se inició tratamiento con ivermectina 200 mg/ Kg/dosis, con seguimiento clínico y de laboratorio con evolución clínica satisfactoria.

Se presenta un caso de un hombre de 81 años natural de zona rural, agricultor, recolector de café 50 años atrás y jardinero por 22 años en Bogotá. Consultó por dolor abdominal de 10 días de evolución, localizado hacia mesogastrio y epigastrio. Además, disnea, tos productiva. Antecedentes: enfermedad pulmonar obstructiva crónica, cor pulmonale, fumador de 25 paquetes /año, había recibido prednisona oral y beclometasona inhalada en diversas ocasiones incluso en la última hospitalización. En el examen físico presentó signos de desnutrición, taquicardia, taquipnea; estertores en base del hemitórax derecho; abdomen: blando, depresible con dolor a la palpación profunda en epigastrio e hipocondrio derecho. Ingresó con síndrome de respuesta inflamatoria sistémica por taquicardia, taquipnea, leucocitosis 37.600 y eosinofilia 52-60%, Ig E: 180 UI/ ml. Se evidenciaron larvas rabditiformes de Strongyloides stercoralis en esputo y materia fecal. La radiografía de tórax mostró derrame pleural derecho, la ecografía hepática fue normal, la endoscopia de vías digestivas altas evidenció gastritis y duodenitis. Se inició tratamiento con ivermectina 200 mg/Kg/dosis, con seguimiento clínico y de laboratorio con evolución clínica satisfactoria.