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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Although not formally considered a clinical practice guideline&#44; the Global Strategy for the Diagnosis&#44; Management&#44; and Prevention of Chronic Obstructive Lung Disease &#40;GOLD&#41; documents have led the recommendations for the management of COPD in the world since 2001&#46; The 2019 version<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">1</span></a> has been a significant change in the disease management strategy with some key points which represent both a novelty in disease management and also current challenges that should focus future research&#46; Specifically&#44; one of the major changes has been the differentiation between initial and follow-up pharmacological treatments&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Firstly&#44; GOLD 2019 is strongly based on eosinophil blood count&#46; Interestingly&#44; although the evidence is consistent showing a better response to inhaled corticosteroids &#40;ICS&#41; with increased blood eosinophils&#44; we must keep in mind that all this evidence comes from post hoc&#44; secondary pre-specified&#44; and data modelling analyses&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">2</span></a> Therefore&#44; although it is possible that blood eosinophil counts may help clinicians estimate the likelihood of a beneficial preventive response to ICS&#44; in daily clinical practice it should probably not be considered as a standalone decision-making parameter&#46; In fact&#44; in a population of COPD patients not overlapping with asthma&#44; the blood eosinophil count and percent has not been found to be associated with lung function changes&#44; quality of life&#44; exacerbation frequency&#44; or response to ICS&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a> Accordingly&#44; GOLD 2019 states that there is insufficient evidence to recommend that blood eosinophils should be used to predict future exacerbation risk on an individual basis in COPD patients&#46; Rather&#44; different approaches have been proposed to wisely use blood eosinophils count for treatment selection including the clinical context&#44;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">4</span></a> the persistence over time<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">5</span></a> or the combination with exhaled biomarkers&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">6</span></a> Altogether&#44; we understand that the message behind including eosinophil blood count is to identify ICS responders &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#44; which is probably a more complex debate that should focus future research&#46; More importantly&#44; the predictor value of blood eosinophils to identify ICS responders will help determine whether this is a strong biomarker or just simply another bystander of COPD&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">7</span></a> This ICS responder might as well match with the concept of asthma-COPD overlap as defined by the Spanish guideline &#40;GesePOC&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">8&#44;9</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">Secondly&#44; GOLD 2019 considers the de-escalation of ICS if pneumonia&#44; inappropriate original indication or the lack of response to ICS&#46; However&#44; beyond the debate on the difficulties in defining some of these concepts&#44; the possibility of de-escalation in patients with a well-controlled disease in terms of exacerbations or symptoms is not specifically considered in the document&#46; The decrease in the number of exacerbations for a prolonged time poses a clinical scenario that challenges the necessity of continuing with ICS&#44; even if correctly prescribed initially&#46; Different studies have consistently shown that it is safe to withdraw ICS in patients without previous exacerbations<a class="elsevierStyleCrossRefs" href="#bib0125"><span class="elsevierStyleSup">10&#44;11</span></a> and recent studies start to point out that ICS prescription could potentially be temporally intensified in determined clinical contexts&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">12</span></a> Therefore&#44; the discussion whether&#44; in a patient receiving ICS&#44; not having exacerbation is due to the effect of the ICS or because of the natural expression of the disease needs further scrutiny&#46; On the other hand&#44; the possibility of de-scalation of double bronchodilator therapy to single bronchodilation in patients with symptoms control has not been explored in the literature and should be evaluated in the future&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Thirdly&#44; switching medication between drugs of the same family represents another interesting debate&#46; Although the GOLD 2019 document suggest considering switching inhaled device or molecules if symptoms are not well-controlled with two long-acting bronchodilators&#44; this idea could potentially be considered in every step of the scalation process&#46; Beyond the potential improvement in the management of a new inhaler after the switch&#44; there is a rationale behind on the specific therapeutic response in a particular patient&#46; Different cross-over studies have clearly showed that different patients respond differently to the same drug&#46;<a class="elsevierStyleCrossRefs" href="#bib0140"><span class="elsevierStyleSup">13&#44;14</span></a> Therefore&#44; besides the classical statement that the inhaler device technique and treatment adherence should be guaranteed before escalating&#44; future research should focus on the individual response to inhaled drugs even within the same family&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Finally&#44; clinicians should keep in mind that COPD patients do suffer from many other comorbidities which determine the disease presentation and the therapeutic response&#46; Therefore&#44; the potential impact of comorbidities should always be kept in mind in an escalation strategy to improve symptoms or prevent exacerbations&#46; GesEPOC identifies the frequent exacerbator as one relevant clinical phenotype&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">8</span></a> Interestingly&#44; there are a number of comorbid conditions that may impact on exacerbation risk &#40;e&#46;g&#46; cardiovascular disease&#44; gastro-esophageal reflux&#44; bronchiectasis&#44; or vitamin D deficiency&#41;&#44; and none of these are treated with ICS&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">15</span></a> Therefore&#44; future research should focus on exploring an algorithm to systematically study COPD patients with persistent exacerbations with the final aim to provide the best approach for each case&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">With these debates in mind&#44; an alternative comprehensive scheme combining GOLD 2019 strategy with GesEPOC approach could be built from the GOLD 2019 follow-up treatment algorithm &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>a&#41;&#46; This figure starts from the premise that a patient might initiate therapy with a long-acting muscarinic antagonist &#40;LAMA&#41; or a combination of a long-acting &#946;<span class="elsevierStyleInf">2</span> agonist &#40;LABA&#41; with an ICS&#44; as suggested by both GOLD 2019 and GesEPOC&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">1&#44;8</span></a> Thereof&#44; the escalation process would be based on phenotypic clinical presentation with the symptomatic&#44; frequent exacerbator and ICS-responder patient as drivers of the change&#44; as GesEPOC recommends&#46; Interestingly and although the evidence is not as strong for both endpoints&#44; when this approach is built&#44; the recommended escalation strategy is the same for symptoms improvement and preventing exacerbations&#46; Therefore&#44; this diagram could be simplified in a 2<span class="elsevierStyleHsp" style=""></span>&#237;<span class="elsevierStyleHsp" style=""></span>2 table combining the initial treatment &#40;either a LAMA or a LABA&#47;ICS&#41; and being ICS responder or not &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>b&#41;&#46; Consequently&#44; it seems that the real challenge for research is to identify the ICS responder rather than the specific clinical endpoint to improve&#46; Different initiatives have been discussed in the literature to identify these patients&#44; including bronchial reversibility&#44; the blood eosinophil count&#44; the co-expression with asthma&#44; bronchial hyperresponsiveness&#44; or Th2 biomarkers&#44; to name a few examples&#46; Here&#44; GOLD 2019 focuses on eosinophil blood count and GesEPOC on a definition of asthma-COPD overlap&#46; Future research should focus on the identification of individual therapeutic response&#46; This knowledge will allow us to advance in precision medicine in COPD and provide the best therapeutic approach for the individual patient&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">JLLC has received honoraria over the last three years for lecturing&#44; scientific advice&#44; participation in clinical studies or writing for publications for &#40;alphabetical order&#41;&#58; AstraZeneca&#44; Boehringer Ingelheim&#44; Chiesi&#44; CSL Behring&#44; Esteve&#44; Ferrer&#44; Gebro&#44; GlaxoSmithKline&#44; Grifols&#44; Menarini&#44; Novartis&#44; Rovi and Teva&#46; JJSC has received fees as speaker of AstraZeneca&#44; Boehringer Ingelheim&#44; Bial&#44; Ferrer&#44; Esteve&#44; Menarini&#44; Mundipharma&#44; Novartis&#44; Rovi and TEVA&#59; Consulting fees for AirLiquide&#44; AstraZeneca&#44; Boehringer Ingelheim&#44; Chiesi&#44; Ferrer&#44; GlaxoSmithKline&#44; Esteve&#44; Mundipharma&#44; and Novartis and research grants from GlaxoSmithKline and Boehringer Ingelheim&#46; MM has received speaker fees from AstraZeneca&#44; Boehringer Ingelheim&#44; Chiesi&#44; Cipla&#44; AstraZeneca&#44; Menarini&#44; Rovi&#44; Bial&#44; Zambon&#44; CSL Behring&#44; Grifols and Novartis&#44; consulting fees from AstraZeneca&#44; Boehringer Ingelheim&#44; Chiesi&#44; GlaxoSmithKline&#44; Bial&#44; Gebro Pharma&#44; CSL Behring&#44; Laboratorios Esteve&#44; Ferrer&#44; Mereo Biopharma&#44; Verona Pharma&#44; TEVA&#44; pH Pharma&#44; Novartis and Grifols and research grants from GlaxoSmithKline and Grifols&#46;</p></span></span>"
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Editorial
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease 2019 Report: Future Challenges
Informe 2019 sobre la estrategia global de diagnóstico, manejo y prevención de la enfermedad pulmonar obstructiva crónica: futuros desafíos
Josèc) Luis López-Camposa,b,
Corresponding author
lopezcampos@separ.es

Corresponding author.
, Juan Josèc) Soler-Cataluñac, Marc Miravitllesd
a Unidad Mèc)dico-Quirúrgica de Enfermedades Respiratorias, Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío/Universidad de Sevilla, Sevilla, Spain
b Centro de Investigación Biomèc)dica en Red de Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III, Madrid, Spain
c Servicio de Neumología, Hospital de Arnau de Villanova, Valencia, Spain
d Servicio de Neumología, Hospital Universitari Vall d
tm)Hebron/Vall d
tm)Hebron Institut de Recerca, Barcelona, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Although not formally considered a clinical practice guideline&#44; the Global Strategy for the Diagnosis&#44; Management&#44; and Prevention of Chronic Obstructive Lung Disease &#40;GOLD&#41; documents have led the recommendations for the management of COPD in the world since 2001&#46; The 2019 version<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">1</span></a> has been a significant change in the disease management strategy with some key points which represent both a novelty in disease management and also current challenges that should focus future research&#46; Specifically&#44; one of the major changes has been the differentiation between initial and follow-up pharmacological treatments&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Firstly&#44; GOLD 2019 is strongly based on eosinophil blood count&#46; Interestingly&#44; although the evidence is consistent showing a better response to inhaled corticosteroids &#40;ICS&#41; with increased blood eosinophils&#44; we must keep in mind that all this evidence comes from post hoc&#44; secondary pre-specified&#44; and data modelling analyses&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">2</span></a> Therefore&#44; although it is possible that blood eosinophil counts may help clinicians estimate the likelihood of a beneficial preventive response to ICS&#44; in daily clinical practice it should probably not be considered as a standalone decision-making parameter&#46; In fact&#44; in a population of COPD patients not overlapping with asthma&#44; the blood eosinophil count and percent has not been found to be associated with lung function changes&#44; quality of life&#44; exacerbation frequency&#44; or response to ICS&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a> Accordingly&#44; GOLD 2019 states that there is insufficient evidence to recommend that blood eosinophils should be used to predict future exacerbation risk on an individual basis in COPD patients&#46; Rather&#44; different approaches have been proposed to wisely use blood eosinophils count for treatment selection including the clinical context&#44;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">4</span></a> the persistence over time<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">5</span></a> or the combination with exhaled biomarkers&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">6</span></a> Altogether&#44; we understand that the message behind including eosinophil blood count is to identify ICS responders &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#44; which is probably a more complex debate that should focus future research&#46; More importantly&#44; the predictor value of blood eosinophils to identify ICS responders will help determine whether this is a strong biomarker or just simply another bystander of COPD&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">7</span></a> This ICS responder might as well match with the concept of asthma-COPD overlap as defined by the Spanish guideline &#40;GesePOC&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">8&#44;9</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">Secondly&#44; GOLD 2019 considers the de-escalation of ICS if pneumonia&#44; inappropriate original indication or the lack of response to ICS&#46; However&#44; beyond the debate on the difficulties in defining some of these concepts&#44; the possibility of de-escalation in patients with a well-controlled disease in terms of exacerbations or symptoms is not specifically considered in the document&#46; The decrease in the number of exacerbations for a prolonged time poses a clinical scenario that challenges the necessity of continuing with ICS&#44; even if correctly prescribed initially&#46; Different studies have consistently shown that it is safe to withdraw ICS in patients without previous exacerbations<a class="elsevierStyleCrossRefs" href="#bib0125"><span class="elsevierStyleSup">10&#44;11</span></a> and recent studies start to point out that ICS prescription could potentially be temporally intensified in determined clinical contexts&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">12</span></a> Therefore&#44; the discussion whether&#44; in a patient receiving ICS&#44; not having exacerbation is due to the effect of the ICS or because of the natural expression of the disease needs further scrutiny&#46; On the other hand&#44; the possibility of de-scalation of double bronchodilator therapy to single bronchodilation in patients with symptoms control has not been explored in the literature and should be evaluated in the future&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Thirdly&#44; switching medication between drugs of the same family represents another interesting debate&#46; Although the GOLD 2019 document suggest considering switching inhaled device or molecules if symptoms are not well-controlled with two long-acting bronchodilators&#44; this idea could potentially be considered in every step of the scalation process&#46; Beyond the potential improvement in the management of a new inhaler after the switch&#44; there is a rationale behind on the specific therapeutic response in a particular patient&#46; Different cross-over studies have clearly showed that different patients respond differently to the same drug&#46;<a class="elsevierStyleCrossRefs" href="#bib0140"><span class="elsevierStyleSup">13&#44;14</span></a> Therefore&#44; besides the classical statement that the inhaler device technique and treatment adherence should be guaranteed before escalating&#44; future research should focus on the individual response to inhaled drugs even within the same family&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Finally&#44; clinicians should keep in mind that COPD patients do suffer from many other comorbidities which determine the disease presentation and the therapeutic response&#46; Therefore&#44; the potential impact of comorbidities should always be kept in mind in an escalation strategy to improve symptoms or prevent exacerbations&#46; GesEPOC identifies the frequent exacerbator as one relevant clinical phenotype&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">8</span></a> Interestingly&#44; there are a number of comorbid conditions that may impact on exacerbation risk &#40;e&#46;g&#46; cardiovascular disease&#44; gastro-esophageal reflux&#44; bronchiectasis&#44; or vitamin D deficiency&#41;&#44; and none of these are treated with ICS&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">15</span></a> Therefore&#44; future research should focus on exploring an algorithm to systematically study COPD patients with persistent exacerbations with the final aim to provide the best approach for each case&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">With these debates in mind&#44; an alternative comprehensive scheme combining GOLD 2019 strategy with GesEPOC approach could be built from the GOLD 2019 follow-up treatment algorithm &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>a&#41;&#46; This figure starts from the premise that a patient might initiate therapy with a long-acting muscarinic antagonist &#40;LAMA&#41; or a combination of a long-acting &#946;<span class="elsevierStyleInf">2</span> agonist &#40;LABA&#41; with an ICS&#44; as suggested by both GOLD 2019 and GesEPOC&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">1&#44;8</span></a> Thereof&#44; the escalation process would be based on phenotypic clinical presentation with the symptomatic&#44; frequent exacerbator and ICS-responder patient as drivers of the change&#44; as GesEPOC recommends&#46; Interestingly and although the evidence is not as strong for both endpoints&#44; when this approach is built&#44; the recommended escalation strategy is the same for symptoms improvement and preventing exacerbations&#46; Therefore&#44; this diagram could be simplified in a 2<span class="elsevierStyleHsp" style=""></span>&#237;<span class="elsevierStyleHsp" style=""></span>2 table combining the initial treatment &#40;either a LAMA or a LABA&#47;ICS&#41; and being ICS responder or not &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>b&#41;&#46; Consequently&#44; it seems that the real challenge for research is to identify the ICS responder rather than the specific clinical endpoint to improve&#46; Different initiatives have been discussed in the literature to identify these patients&#44; including bronchial reversibility&#44; the blood eosinophil count&#44; the co-expression with asthma&#44; bronchial hyperresponsiveness&#44; or Th2 biomarkers&#44; to name a few examples&#46; Here&#44; GOLD 2019 focuses on eosinophil blood count and GesEPOC on a definition of asthma-COPD overlap&#46; Future research should focus on the identification of individual therapeutic response&#46; This knowledge will allow us to advance in precision medicine in COPD and provide the best therapeutic approach for the individual patient&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">JLLC has received honoraria over the last three years for lecturing&#44; scientific advice&#44; participation in clinical studies or writing for publications for &#40;alphabetical order&#41;&#58; AstraZeneca&#44; Boehringer Ingelheim&#44; Chiesi&#44; CSL Behring&#44; Esteve&#44; Ferrer&#44; Gebro&#44; GlaxoSmithKline&#44; Grifols&#44; Menarini&#44; Novartis&#44; Rovi and Teva&#46; JJSC has received fees as speaker of AstraZeneca&#44; Boehringer Ingelheim&#44; Bial&#44; Ferrer&#44; Esteve&#44; Menarini&#44; Mundipharma&#44; Novartis&#44; Rovi and TEVA&#59; Consulting fees for AirLiquide&#44; AstraZeneca&#44; Boehringer Ingelheim&#44; Chiesi&#44; Ferrer&#44; GlaxoSmithKline&#44; Esteve&#44; Mundipharma&#44; and Novartis and research grants from GlaxoSmithKline and Boehringer Ingelheim&#46; MM has received speaker fees from AstraZeneca&#44; Boehringer Ingelheim&#44; Chiesi&#44; Cipla&#44; AstraZeneca&#44; Menarini&#44; Rovi&#44; Bial&#44; Zambon&#44; CSL Behring&#44; Grifols and Novartis&#44; consulting fees from AstraZeneca&#44; Boehringer Ingelheim&#44; Chiesi&#44; GlaxoSmithKline&#44; Bial&#44; Gebro Pharma&#44; CSL Behring&#44; Laboratorios Esteve&#44; Ferrer&#44; Mereo Biopharma&#44; Verona Pharma&#44; TEVA&#44; pH Pharma&#44; Novartis and Grifols and research grants from GlaxoSmithKline and Grifols&#46;</p></span></span>"
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Article information
ISSN: 15792129
Original language: English
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