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Purpose: We compared pulmonary function indices and quantitative CT parameters of airway remodeling, air trapping, and emphysema in asthmatic patients and patients with COPD and asthma-COPD overlap (ACO) and explored their relationships with airflow limitation. Patients and Methods: Patients with asthma (n=48), COPD (n=52), and ACO (n=30) and controls (n=54) who completed pulmonary function tests and HRCT scans were retrospectively enrolled in our study. Quantitative CT analysis software was used to assess emphysema (LAA%), airway wall dimensions (wall area (WA), luminal area (LA), and wall area percentage (WA%)), and air trapping ((relative volume change of -860 HU to -950 HU (RVC-860 to-950) and the expiration-to-inspiration ratio of the mean lung density (MLDE/I))). Differences in pulmonary function and HRCT parameters were compared among the groups. Spearman correlation analysis and regression analysis were utilized to explore structureâfunction relationships. Results: The LAA% in COPD and ACO patients was significantly greater than that in asthmatic patients and controls. The WA% and WA in COPD and ACO patients were greater than those in controls, whereas the WA% and LA between asthmatic patients and controls reached statistical significance. The RVC-860 to -950 levels decreased in the following order: ACO, COPD, and asthma. RVC-860 to -950 independently predicted FEV1% in asthmatic patients; LAA% and MLDE/I in COPD patients; and LAA%, WA% and RVC-860 to -950 in ACO patients. Conclusion: Comparable emphysema was observed in patients with COPD and ACO but not in asthmatic patients. All patients exhibited proximal airway remodeling. The bronchi were thickened outward in COPD and ACO patients but are thickened inward in asthmatic patients. Furthermore, air trapping in ACO patients was the most severe among all the groups. Indirect lung densitometry measurements might be more predictive of the degree of airflow limitation than direct airway measurements in obstructive airway diseases.
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Remodelación de las Vías Aéreas (Respiratorias) , Síndrome de Superposición de la Enfermedad Pulmonar Obstructiva Crónica-Asmática , Asma , Pulmón , Valor Predictivo de las Pruebas , Enfermedad Pulmonar Obstructiva Crónica , Enfisema Pulmonar , Humanos , Masculino , Femenino , Persona de Mediana Edad , Pulmón/fisiopatología , Pulmón/diagnóstico por imagen , Estudios Retrospectivos , Asma/fisiopatología , Asma/diagnóstico por imagen , Asma/complicaciones , Enfermedad Pulmonar Obstructiva Crónica/fisiopatología , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico por imagen , Enfermedad Pulmonar Obstructiva Crónica/complicaciones , Anciano , Enfisema Pulmonar/fisiopatología , Enfisema Pulmonar/diagnóstico por imagen , Volumen Espiratorio Forzado , Síndrome de Superposición de la Enfermedad Pulmonar Obstructiva Crónica-Asmática/fisiopatología , Síndrome de Superposición de la Enfermedad Pulmonar Obstructiva Crónica-Asmática/diagnóstico por imagen , Tomografía Computarizada por Rayos X , Adulto , Capacidad Vital , Pruebas de Función Respiratoria , Tomografía Computarizada MultidetectorRESUMEN
The objective of the study was to evaluate the effect of photobiomodulation (PBM) with laser on the inflammatory process in an experimental in vitro model of ACO. The groups were: (1) human bronchial epithelial cells (BEAS-2B); (2) BEAS-2B cells treated with dexamethasone; (3) BEAS-2B cells irradiated with laser; (4) BEAS-2B cells stimulated with cigarette smoke extract (CSE) + House Dust Mite (HDM); (5) BEAS-2B cells stimulated with CSE + HDM and treated with dexamethasone; (6) BEAS-2B cells incubated with CSE + HDM and irradiated with laser. After 24 h, cytokines were quantified. There was a reduction in TNF-α, IL-1ß, IL-6, IL-4, IL-5, IL-13, IL-17, IL-21, IL-23, and an increase in IL-10 and IFN-γ in cells from the laser-irradiated ACO group compared to only ACO group. With these results, we can suggest that photobiomodulation acts in the modulation of inflammation observed in ACO, and may be a treatment option.
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Chronic Obstructive Pulmonary Disease (COPD) is a complex pulmonary condition characterized by chronic airflow limitation. Within the spectrum of COPD, distinct overlap conditions exist, including Asthma-COPD Overlap (ACO), COPD-Obstructive Sleep Apnea (COPD-OSA), Combined Pulmonary Fibrosis and Emphysema (CPFE), and Bronchiectasis-COPD Overlap (BCO). This review provides a comprehensive overview of the clinical and therapeutic implications of these conditions, highlighting the differences in complications compared with COPD alone in addition to the diagnostic challenges of identifying these conditions. Therapeutically tailored approaches are necessary for COPD overlap conditions considering the unique complications that may arise. Optimal pharmacological management, disease-specific interventions, and comprehensive patient-centered care are crucial components of treatment strategies. This review provides insights for healthcare professionals by enhancing their understanding and management of these conditions. This emphasizes the importance of accurate diagnosis and individualized treatment plans, considering the specific complications associated with each COPD overlap condition.
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BACKGROUND: Despite clinical implications, the pathogenesis of mucus plugging in asthma, chronic obstructive pulmonary disease (COPD), and asthma-COPD overlap (ACO) remains unclear. We hypothesized that distinct airway microbiomes might affect mucus plugging differently among ACO, asthma, and COPD and among different extents of airway eosinophilic inflammation. METHODS: The sputum microbiome, sputum cell differential count, and mucus plug score on computed tomography were cross-sectionally evaluated in patients with chronic airflow limitation. RESULTS: Patients with ACO, asthma, or COPD were enrolled (n = 56, 10, and 25). Higher mucus plug scores were associated with a greater relative abundance of the phylum Proteobacteria (rho = 0.29) only in patients with ACO and a greater relative abundance of the phylum Actinobacteria (rho = 0.46) only in patients with COPD. In multivariable models including only patients with ACO, the presence of mucus plugs was associated with a greater relative abundance of the phylum Proteobacteria and the genus Haemophilus, independent of smoking status, airflow limitation, and emphysema severity. Moreover, the mucus score was associated with a greater relative abundance of the genus Streptococcus (rho = 0.46) in patients with a high sputum eosinophil count (n = 22) and with that of the genus Haemophilus (rho = 0.46) in those with a moderate sputum eosinophil count (n = 26). CONCLUSIONS: The associations between mucus plugging and the microbiome in ACO differed from those in COPD and asthma. Greater relative abundances of the phylum Proteobacteria and genus Haemophilus may be involved in mucus plugging in patients with ACO and moderate airway eosinophilic inflammation.
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Asma , Microbiota , Moco , Enfermedad Pulmonar Obstructiva Crónica , Esputo , Tomografía Computarizada por Rayos X , Humanos , Enfermedad Pulmonar Obstructiva Crónica/microbiología , Enfermedad Pulmonar Obstructiva Crónica/complicaciones , Esputo/microbiología , Asma/microbiología , Asma/complicaciones , Asma/diagnóstico , Masculino , Femenino , Persona de Mediana Edad , Anciano , Moco/microbiología , Estudios TransversalesRESUMEN
Lactic acidosis is associated with poorer clinical outcomes in critical care. The causes of this condition are divided into two groups: type A (tissue hypoxia) and type B (metabolic abnormalities). Of these, drug-induced lactic acidosis is categorized as type B and is often overlooked due to clinicians' poor awareness. We herein report a rare case of drug-induced lactic acidosis due to excessive use of a long-acting beta agonist (LABA) in a patient with asthma-chronic obstructive pulmonary disease overlap exacerbation. He initially presented with markedly elevated lactate and metabolic acidosis with unknown etiology. A detailed medical interview revealed that he had inhaled a large amount of LABA on the day of admission, which led to our final diagnosis. The patient's respiratory status and lactate levels gradually improved with the appropriate use of inhalation therapy. While there have been many recent reports of lactic acidosis caused by short-acting beta agonists, our case suggests that excessive use of LABAs may also lead to lactic acidosis. Clinicians should be aware of the possibility that LABAs can cause lactic acidosis because poor awareness of the condition may lead to inappropriate patient care.
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Síndrome de Superposición de la Enfermedad Pulmonar Obstructiva Crónica-Asmática , Humanos , Femenino , Prevalencia , Masculino , Persona de Mediana Edad , Síndrome de Superposición de la Enfermedad Pulmonar Obstructiva Crónica-Asmática/diagnóstico , Síndrome de Superposición de la Enfermedad Pulmonar Obstructiva Crónica-Asmática/epidemiología , Anciano , Pulmón/fisiopatología , Asma/epidemiología , Asma/diagnóstico , Estudios de Cohortes , Adulto , Enfermedad Pulmonar Obstructiva Crónica/epidemiología , Enfermedad Pulmonar Obstructiva Crónica/diagnósticoAsunto(s)
Asma , Progresión de la Enfermedad , Enfermedad Pulmonar Obstructiva Crónica , Humanos , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/fisiopatología , Enfermedad Pulmonar Obstructiva Crónica/complicaciones , Asma/diagnóstico , Asma/fisiopatologíaRESUMEN
BACKGROUND: Asthma-COPD overlap (ACO) is a distinct and intricate respiratory condition that requires specific attention and management. The objective of this cohort study was to examine the epidemiological characteristics of ACO, explore the association between ACO and all-cause mortality, and investigate the potential mediating role of depressive symptoms in this association. METHODS: This retrospective cohort study used data from the National Health and Nutrition Examination Survey (NHANES) 2005-2018 and National Death Index (NDI) 2019. A total of 22,745 participants were included: 705 with ACO, 2352 with asthma-only, 853 with COPD-only, and 18,835 without asthma or COPD. The non-ACO group (N = 22,040) referred to the individuals without ACO. Statistical tests were employed to assess differences in some characteristics between the ACO group and the other groups. Cox proportional hazards models were applied to evaluate the relationship between ACO and all-cause mortality, estimating hazard ratios (HR) with 95% confidence intervals. Mediation analysis was conducted to investigate the potential mediating effects of depressive symptoms on the association of ACO with all-cause mortality. RESULTS: The prevalence of ACO was 3.10% in our study population. Compared to the non-ACO participants, the ACO participants exhibited significantly different characteristics, including higher age, a lower family income-to-poverty ratio, a higher body mass index, higher rates of comorbidities i.e., hypertension, diabetes, hyperlipidemia, cardiovascular disease, and cancer, poorer dietary habits, and a higher rate of depressive disorders. Compared to the participants without ACO, the participants with ACO exhibited a significant increase in all-cause mortality (HR = 1.908, 95%CI 1.578-1.307, p < 0.001). The proportions mediated by depressive symptoms for ACO -associated all-cause mortality were 8.13% (CI: 4.22%-14.00%, p < 0.001). CONCLUSIONS: This study revealed a strong relationship between ACO and all-cause mortality and uncovered a potential psychological mechanism underlying this relationship. Our study indicates the possible necessity of offering comprehensive care to ACO patients, encompassing early detection, lifestyle guidance, and mental health support. Nevertheless, due to the limitations in the study design and the dataset, the results should be interpreted with caution.
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Depresión , Encuestas Nutricionales , Humanos , Masculino , Femenino , Persona de Mediana Edad , Estudios Retrospectivos , Depresión/epidemiología , Adulto , Anciano , Estados Unidos/epidemiología , Síndrome de Superposición de la Enfermedad Pulmonar Obstructiva Crónica-Asmática/epidemiología , Síndrome de Superposición de la Enfermedad Pulmonar Obstructiva Crónica-Asmática/mortalidad , Causas de Muerte , Asma/epidemiología , Asma/mortalidad , Enfermedad Pulmonar Obstructiva Crónica/epidemiología , Enfermedad Pulmonar Obstructiva Crónica/mortalidad , PrevalenciaRESUMEN
BACKGROUND AND OBJECTIVE: Endothelial dysfunction has been widely recognized in chronic airway diseases, including chronic obstructive pulmonary disease (COPD) and asthma; however, it remains unclear in asthma-COPD overlap (ACO). Neopterin (NP), a metabolite of guanosine triphosphate, is a novel biomarker for identifying the increased risk of adverse cardiovascular events. This study aims to investigate the association of NP with endothelial dysfunction and impaired lung function in COPD, asthma, and ACO patients. METHODS: A total of 77 subjects were prospectively recruited. All the participants underwent lung function test, endothelial function evaluation, including pulse wave velocity (PWV) and flow-mediated dilation (FMD), and blood sample detection. Moreover, the effect of NP on endothelial cells (ECs) in anoxic environments was assessed in vitro. RESULTS: Endothelial function was significantly decreased in the COPD and ACO patients compared with that in the healthy controls (P < 0.05). Forced expiratory volume in 1 s (FEV1) was negatively correlated with PWV and positively correlated with FMD (P < 0.05). NP was significantly increased in patients with chronic respiratory diseases compared with that in the control group, with COPD being the highest, followed by asthma, and ACO as the last (P < 0.05). The plasma level of NP exhibited negative correlations with FEV1 and positive correlations with PWV (P < 0.05). In vitro, a high level of NP increased the reactive oxygen species (ROS) and decreased the mitochondrial membrane potential (ΔΨm) of ECs dose-dependently in a hypoxic environment (P < 0.05). CONCLUSION: NP was related to disease severity of chronic airway diseases and involved in the pathogenesis of endothelial dysfunction. A high NP level may contribute to endothelial dysfunction by increasing the oxidative stress of ECs dose-dependently in a hypoxic environment. Our findings may provide a novel evaluation and therapeutic target for endothelial dysfunction related to chronic airway diseases.
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Asma , Enfermedad Pulmonar Obstructiva Crónica , Humanos , Neopterin , Células Endoteliales/metabolismo , Análisis de la Onda del Pulso , Pulmón/metabolismo , Volumen Espiratorio ForzadoRESUMEN
There are few studies on the relationship between dietary habits and asthma-COPD overlap (ACO). In this study, we aimed to investigate the association between dietary inflammation index (DII) score and ACO. Data from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2020. The DII score was first calculated and the demographic characteristics of the grouping based on the DII quartile were assessed. The weighted logistic regression model was used to study the relationship between DII and ACO. Subgroup analysis was used to further explore the differences in different subgroups. Restricted cubic spline (RCS) plot was used to show the general trend of DII score and disease risk, and threshold effect analysis was used to determine the inflection point. In a comparison of baseline characteristics, the highest ACO prevalence was found in the fourth quartile array of people in DII. An adjusted weighted logistic regression model showed that DII was positively correlated with the incidence of ACO. Subgroup analysis showed that the association was more pronounced in women, non-Hispanics, people with cardiovascular disease, and people without diabetes. The RCS graph shows that overall, the risk of ACO increases with the increase of DII score. Threshold effect analysis showed that the inflection point was 3.779, and the risk was more significant after the DII score was greater than the inflection point value (OR 2.001, 95% CI 1.334-3.001, P < 0.001). Higher DII scores were positively associated with ACO risk. These results further support diet as an intervention strategy for ACO prevention and treatment.
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Asma , Enfermedad Pulmonar Obstructiva Crónica , Humanos , Femenino , Encuestas Nutricionales , Inflamación/epidemiología , Inflamación/diagnóstico , Dieta/efectos adversos , Asma/epidemiología , Enfermedad Pulmonar Obstructiva Crónica/epidemiologíaRESUMEN
Purpose: Chronic obstructive pulmonary disease (COPD) phenotypes may introduce different characteristics that need to be known to improve treatment. Respiratory oscillometry provides a detailed analysis and may offer insight into the pathophysiology of COPD. In this paper, we used this method to evaluate the differences in respiratory mechanics of COPD phenotypes. Patients and Methods: This study investigated a sample of 83 volunteers, being divided into control group (CG = 20), emphysema (n = 23), CB (n = 20) and asthma-COPD overlap syndrome (ACOS, n = 20). These analyses were performed before and after bronchodilator (BD) use. Functional capacity was evaluated using the GlittreADL test, handgrip strength and respiratory pressures. Results: Initially it was observed that oscillometry provided a detailed description of the COPD phenotypes, which was consistent with the involved pathophysiology. A correlation between oscillometry and functional capacity was observed (r=-0.541; p = 0.0001), particularly in the emphysema phenotype (r = -0.496, p = 0.031). BD response was different among the studied phenotypes. This resulted in an accurate discrimination of ACOS from CB [area under the receiver operating curve (AUC) = 0.84] and emphysema (AUC = 0.82). Conclusion: These results offer evidence that oscillatory indices may enhance the comprehension and identification of COPD phenotypes, thereby potentially improving the support provided to these patients.
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Asma , Enfisema , Enfermedad Pulmonar Obstructiva Crónica , Enfisema Pulmonar , Humanos , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/tratamiento farmacológico , Pulmón , Oscilometría/métodos , Fuerza de la Mano , Volumen Espiratorio Forzado , Broncodilatadores/uso terapéutico , Fenotipo , Rendimiento Físico FuncionalRESUMEN
Objectives: Asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) patients experience a lower quality of life, frequent exacerbations, and worse pulmonary function. Environmental management is essential in a complex chronic condition, as pollutant exposure can worsen symptoms and increase morbidity and mortality. We aimed to identify evidence that informs nursing interventions in promoting self-management of air quality in asthmatic people with COPD. Methods: We conducted an integrative review in March of 2023. We searched the databases CINAHL, MEDLINE, Academic Search Complete, Cochrane Database of Systematic Reviews (CDSR), Scopus, Web of Science, Joanna Briggs Institute (JBI) Evidence-Based Practice Database, and Google Scholar. We included articles whose participants were adults with asthma, COPD, or both; the intervention was air quality management and the outcome of any exacerbations. We excluded editorials, letters, commentaries, opinion papers, position papers, study protocols, conference abstracts, and reviews. Data extraction and synthesis were performed, categorizing interventions according to nursing actions. Methodological quality assessment was conducted using the JBI Critical Appraisal Checklist tools. The review protocol was registered at Open Science Framework (https://doi.org/10.17605/OSF.IO/5Y4KW). Results: We included five articles from different countries. The interventions promoting air quality self-management for individuals with asthma and COPD included vigilance interventions (health professional regular visits, assessment of symptoms), monitoring interventions (measurement of indoor and outdoor trigger factors), and educational interventions (air quality alerts, allergen avoidance). Policy interventions such as smoke-free policies and comprehensive strategies to improve air quality were also identified. These areas of focus represent critical components of nurses' interventions and can integrate the fundamental patterns of knowing in nursing. Although the studies reveal heterogeneous interventions and the methodological quality is variable, these interventions showed potential for preventing exacerbations, reducing emergency department visits, and minimizing hospitalizations. Conclusions: The study emphasizes the need for a comprehensive approach involving nurses in multidisciplinary teams to air quality self-management. They can use these results to inform their interventions and ways of knowing, benefiting individuals with asthma and COPD. Further research is needed to expand the evidence base and refine these interventions.
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BACKGROUND: There is no uniform standard for a strongly positive bronchodilation test (BDT) result. In addition, the role of bronchodilator response in differentiating between asthma, chronic obstructive pulmonary disease (COPD), and asthma-COPD overlap (ACO) in patients with a positive BDT result is unclear. We explored a simplified standard of a strongly positive BDT result and whether bronchodilator response combined with fractional exhaled nitric oxide (FeNO) can differentiate between asthma, COPD, and ACO in patients with a positive BDT result. METHODS: Three standards of a strongly positive BDT result, which were, respectively, defined as post-bronchodilator forced expiratory volume in 1-s responses (ΔFEV1) increasing by at least 400 mL + 15% (standard I), 400 mL (standard II), or 15% (standard III), were analyzed in asthma, COPD, and ACO patients with a positive BDT result. Receiver operating characteristic curves were used to determine the optimal values of ΔFEV1 and FeNO. Finally, the accuracy of prediction was verified by a validation study. RESULTS: The rates of a strongly positive BDT result and the characteristics between standards I and II were consistent; however, those for standard III was different. ΔFEV1 ≥ 345 mL could predict ACO diagnosis in COPD patients with a positive BDT result (area under the curve [AUC]: 0.881; 95% confidence interval [CI] 0.83-0.94), with a sensitivity and specificity of 90.0% and 91.2%, respectively, in the validation study. When ΔFEV1 was < 315 mL combined with FeNO < 28.5 parts per billion, patients with a positive BDT result were more likely to have pure COPD (AUC: 0.774; 95% CI 0.72-0.83). CONCLUSION: The simplified standard II can replace standard I. ΔFEV1 and FeNO are helpful in differentiating between asthma, COPD, and ACO in patients with a positive BDT result.
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Asma , Enfermedad Pulmonar Obstructiva Crónica , Humanos , Asma/diagnóstico , Asma/tratamiento farmacológico , Pruebas Respiratorias , Broncodilatadores/farmacología , Broncodilatadores/uso terapéutico , Volumen Espiratorio Forzado , Prueba de Óxido Nítrico Exhalado Fraccionado , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/tratamiento farmacológicoRESUMEN
BACKGROUND: Among patients with chronic obstructive pulmonary disease (COPD), some have features of both asthma and COPD-a condition categorized as asthma-COPD overlap (ACO). Our aim was to determine whether asthma- or COPD-related microRNAs (miRNAs) play a role in the pathogenesis of ACO. METHODS: A total of 22 healthy subjects and 27 patients with ACO were enrolled. We selected 6 miRNAs that were found to correlate with COPD and asthma. The expression of miRNAs and target genes was analyzed using quantitative reverse-transcriptase polymerase chain reaction. Cell apoptosis and intracellular reactive oxygen species production were evaluated using flow cytometry. In vitro human monocytic THP-1 cells and primary normal human bronchial epithelial (NHBE) cells under stimuli with cigarette smoke extract (CSE) or ovalbumin (OVA) allergen or both were used to verify the clinical findings. RESULTS: We identified the upregulation of miR-125b-5p in patients with ACO and in THP-1 cells stimulated with CSE plus OVA allergen. We selected 16 genes related to the miR-125b-5p pathway and found that IL6R and TRIAP1 were both downregulated in patients with ACO and in THP-1 cells stimulated with CSE plus OVA. The percentage of late apoptotic cells increased in the THP-1 cell culture model when stimulated with CSE plus OVA, and the effect was reversed by transfection with miR-125b-5p small interfering RNA (siRNA). The percentage of reactive oxygen species-producing cells increased in the NHBE cell culture model when stimulated with CSE plus OVA, and the effect was reversed by transfection with miR-125b-5p siRNA. In NHBE cells, siRNA transfection reversed the upregulation of STAT3 under CSE+OVA stimulation. CONCLUSIONS: Our study revealed that upregulation of miR-125b-5p in patients with ACO mediated late apoptosis in THP-1 cells and oxidative stress in NHBE cells via targeting IL6R and TRIAP1. STAT3 expression was also regulated by miR-125b-5p.
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Apoptosis , Asma , MicroARNs , Enfermedad Pulmonar Obstructiva Crónica , Humanos , Alérgenos , Apoptosis/genética , Asma/genética , Asma/complicaciones , Péptidos y Proteínas de Señalización Intracelular/metabolismo , MicroARNs/metabolismo , Estrés Oxidativo/genética , Enfermedad Pulmonar Obstructiva Crónica/metabolismo , Especies Reactivas de Oxígeno , Receptores de Interleucina-6/metabolismo , ARN Interferente Pequeño/metabolismo , Masculino , AncianoRESUMEN
Background: Airway microbiota in asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) remains unknown. Objective: This study with ACO-enriched population aimed to clarify airway microbiota in ACO and in mixed granulocytic inflammation, often detected in ACO and chronic airway diseases. Methods: This is an observational cross-sectional study. Patients with asthma with airflow limitation, ACO, and COPD were enrolled. Blood tests, pulmonary function, exhaled nitric oxide, and sputum tests were conducted. Sputum microbiota was evaluated using the 16S rRNA gene sequencing technique. Results: A total of 112 patients (13 asthma, 67 ACO, and 32 COPD) were examined. There were no significant differences in α-diversity among the 3 diseases. The relative abundances of phylum Bacteroidetes, class Bacteroidia, and genus Porphyromonas were associated with decreased eosinophilic inflammation, and were significantly lower in ACO than in COPD. In a comparison of sputum inflammatory subtypes, the proportion of Haemophilus was numerically highest in the mixed granulocytic subtype, followed by the neutrophilic subtype. Likewise, the proportion of Haemophilus was the highest in the intermediate-high (2%-8%) sputum eosinophil group and lowest in the severe (≥8%) eosinophil group. Clinically, Haemophilus proportion was associated with sputum symptoms. Finally, the proportion of Streptococcus was associated with higher blood eosinophil counts and most severe airflow limitation. Conclusions: Bacteroidia and Porphyromonas abundances in sputum are associated with the eosinophil-low phenotype, and ACO may be characterized by a decrease in these taxa. A mild elevation in sputum eosinophil does not preclude the presence of Haemophilus, which should be noted in the management of obstructive airway diseases.
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Background: Despite the increasing use of biologics in severe asthma, there is limited research on their use in asthma-chronic obstructive pulmonary disease overlap (ACO). We compared real-world treatment responses to biologics in ACO and asthma. Methods: We conducted a multicenter, retrospective, cohort study using data from the Precision Medicine Intervention in Severe Asthma (PRISM). ACO was defined as post-bronchodilator forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) <0.7 and a smoking history of >10 pack-years. Physicians selected biologics (omalizumab, mepolizumab, reslizumab, benralizumab, and dupilumab) based on each United States Food & Drug Administration (FDA) approval criteria. Results: After six-month treatment with biologics, both patients with ACO (N = 13) and asthma (N = 81) showed positive responses in FEV1 (10.69 ± 17.17 vs. 11.25 ± 12.87 %, P = 0.652), Asthma Control Test score (3.33 ± 5.47 vs. 5.39 ± 5.42, P = 0.290), oral corticosteroid use (-117.50 ± 94.38 vs. -115.06 ± 456.85 mg, P = 0.688), fractional exhaled nitric oxide levels (-18.62 ± 24.68 vs. -14.66 ± 45.35 ppb, P = 0.415), sputum eosinophils (-3.40 ± 10.60 vs. -14.48 ± 24.01 %, P = 0.065), blood eosinophils (-36.47 ± 517.02 vs. -363.22 ± 1294.59, P = 0.013), and exacerbation frequency (-3.07 ± 4.42 vs. -3.19 ± 5.11, P = 0.943). The odds ratio for exacerbation and time-to-first exacerbation showed no significant difference after full adjustments, and subgroup analysis according to biologic type was also showed similar results. Conclusions: Biologics treatment response patterns in patients with ACO and asthma were comparable, suggesting that biologics should be actively considered for ACO patients as well.
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Background: Studies on the prevalence of wheezing in both the asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) and non-ACO groups, as well as the clinical characteristics of wheezing patients in each group, are rare. We examined the prevalence of wheezing in ACO patients and non-ACO patients, respectively. In addition, we aimed to determine clinical characteristics of patients with wheezing compared to those without wheezing in the ACO and non-ACO groups. Methods: We analyzed the data from the Korean COPD Subgroup Study (KOCOSS), a multicenter prospective cohort. We classified patients into four groups according to whether they were ACO patients or had self-reported wheezing based on the patient's answer to the COPD-specific version of St. George's Respiratory Questionnaire (SGRQ-C): ACO with wheezing, ACO without wheezing, non-ACO with wheezing, and non-ACO without wheezing. Clinical characteristics and exacerbations during 1-year follow up were compared among four groups. Results: Wheezing was present in about 56% of patients in the ACO and non-ACO groups. In both groups, patients with wheezing exhibited more severe symptoms, worse lung function, and a higher risk of exacerbation than those without wheezing. There was no association between blood eosinophil count and wheezing in both the ACO and non-ACO groups. During 1-year follow-up, the ACO with wheezing group experienced exacerbations the most frequently, followed by the non-ACO with wheezing group. Moreover, wheezing was an independent predictor of the risk of exacerbation in patients with COPD, irrespective of both the ACO phenotype and the severity of airflow limitation. The exacerbation risk was higher in COPD patients who experienced wheezing more frequently. Conclusions: Wheezing, reflecting more prominent airflow limitation and predicting exacerbation development, may serve as a severe phenotype of COPD rather than being indicative of an ACO phenotype.
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Background: IL-17 is a modulator of the inflammatory response and is implicated in lung remodeling in both asthma and chronic obstructive pulmonary disease (COPD). Well as and probably in patients with asthma-COPD overlap (ACO). Methods: In this study, we evaluated the response of the airways and alveolar septa to anti-IL-17 treatment in an ACO model. Fifty-six male BALB/c mice were sensitized with ovalbumin (OVA group), received porcine pancreatic elastase (PPE group), or both (ACO group). Mice were then treated with either anti-IL-17 monoclonal antibody or saline. We evaluated hyperresponsiveness, bronchoalveolar lavage fluid (BALF) cell counts, and mean alveolar diameter. We quantified inflammatory, response, extracellular matrix remodeling, oxidative stress markers, and signaling pathway markers. Results: Anti-IL-17 treatment in the ACO anti-IL-17 group reduced the maximum response of respiratory system Rrs, Ers, Raw, Gtis, this when compared to the ACO group (p<0.05). There was a reduction in the total number of inflammatory cells, neutrophils, and macrophages in the BALF in the ACO anti-IL-17 group compared to the ACO group (p<0.05). There was attenuated dendritic cells, CD4+, CD8+, FOXP3, IL-1ß, IL-2, IL-6, IL-13, IL-17, IL-33 in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p<0.05). We observed a reduction of MMP-9, MMP-12, TIMP-1, TGF-ß, collagen type I in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p < 0.05). We also observed a reduction of iNOS and 8-iso-PGF2α in the airways and in the alveolar septum was reduced in the ACO anti-IL-17group compared to the ACO group (p < 0.05). Regarding the signaling pathways, NF-kB, ROCK-1, and ROCK-2 in the airway and alveolar septum were attenuated in the ACO anti-IL-17 group when compared to the ACO group (p<0.05). Conclusions: Our results suggest that inhibiting IL-17 modulates cell-associated cytokine production in lung tissue, extracellular matrix remodeling, and oxidative stress in ACO through the modulation of NF-kB and FOXP3.