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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">The diagram shows the concept of CES&#46; The presence of a triggering factor in a COPD patient &#40;with its social determinants and comorbidity&#41; leads to the appearance of a CES syndrome&#44; where worsening dyspnea is the final manifestation of various biological and pathophysiological mechanisms&#46; Because of the heterogeneity of symptoms&#44; different biological endotypes and various phenotypic presentations susceptible to specific treatments can be expressed&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">In a position paper published in 1995&#44; the American Thoracic Society &#40;ATS&#41; officially recognized that the exacerbation of chronic obstructive pulmonary disease &#40;COPD&#41; was difficult to define&#44; and that its pathogenesis was still unclear&#46; At the time&#44; the society already mooted the need for a standardized definition that could be universally accepted and useful for clinicians&#44; researchers&#44; and other health providers&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Five years later&#44; responding to that challenge&#44; a group of experts led by Dr&#46; Rodr&#237;guez-Roisin<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> defined exacerbation as <span class="elsevierStyleItalic">&#8220;a sustained worsening of the patient&#39;s condition&#44; from the s</span>table s<span class="elsevierStyleItalic">tate and beyond normal day-to-day variations&#44; that is acute in onset and necessitates a change in regular medication in a patient with underlying COPD&#8221;&#46;</span> It has been 20 years since that initial proposal&#44; and significant advances have been made in the knowledge of COPD&#44; which is now understood as a complex and heterogeneous syndrome requiring an increasingly personalized approach&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> However&#44; the concept&#44; diagnosis&#44; and management of exacerbations have hardly changed&#46; We continue to indiscriminately use short-acting bronchodilators&#44; systemic steroids&#44; and antibiotics with poor outcomes&#46; Therapeutic failures are common&#44; the 30-day readmission rate is 20&#37;&#44; and in-hospital mortality is 5&#37;&#44; increasing to 11&#37; at 3 months&#46; Furthermore&#44; a considerable proportion of patients have persistent exacerbations&#44; we do not have a good classification system&#44; we do not use generalized predictive risk models&#44; admission criteria are not standardized&#44; and clinical trials still define exacerbation or severity based on resource use&#46;<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4&#8211;7</span></a> As a result&#44; scientific results are very heterogeneous and progress is inconsistent&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The origin of this confusion lies in the construction of the definition itself&#44; which fails to identify the underlying biological mechanism&#44; does not recognize the heterogeneity of the clinical picture and&#44; being symptom-based&#44; is very unspecific&#46; Many other concomitant diseases &#40;comorbidities&#41; can also cause the same worsening of symptoms in COPD patients&#46; Heart failure&#44; arrhythmias&#44; ischemic heart disease&#44; anxiety&#44; pulmonary embolism&#44; and pneumonia are diseases that often occur in COPD and present with increased respiratory symptoms&#46; However&#44; by consensus&#44; they are not considered COPD exacerbations&#46; A comprehensive differential diagnosis is needed to rule out these other diseases&#44; but this is not always easy&#46; Pneumonia&#44; for example&#44; is an entity that is typically distinct from exacerbation due to the presence of infiltrates in the pulmonary parenchyma&#46; However&#44; the difference between the two entities is very subtle&#46; Up to one third of COPD patients have infiltrates on computed tomography that are not visible on simple chest X-ray&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> These patients are classified and categorized as COPD exacerbations when they are actually pneumonia&#46; Are they different entities or phases of the same disease&#63; The pulmonary microbiome is practically identical&#44; causative factors are very similar&#44; and clinical expression&#44; prognostic impact&#44; and treatment are also similar&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">8&#44;9</span></a> A similar situation occurs with heart failure&#44; ischemic heart disease&#44; and pulmonary embolism&#44; which often overlap with the exacerbation itself&#46;<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">10&#8211;12</span></a> The direct consequence of all this is confusion&#44; heterogeneous clinical outcomes&#44; scant progress in understanding the underlying mechanisms&#44; and barriers to accessing personalized treatment&#46; A change of strategy is therefore urgent&#46; We need a new definition derived from more objective and specific criteria that&#44; even at the risk of losing some sensitivity&#44; also takes into account the variety of presentations&#44; helps identify biological endotypes&#44; and offers a direct pathway to precision medicine&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">A good reference model is acute coronary disease&#44; the current definition of which is based on 3 essential parameters&#58; 1&#41; a syndrome-based approach &#40;acute coronary syndrome&#41;&#59; 2&#41; a guiding symptom &#40;chest pain&#41;&#59; and 3&#41; objective variables with underlying biological mechanisms &#40;electrocardiographic alterations and biomarkers&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> Using a syndrome-based approach to what we might call COPD exacerbation syndrome &#40;CES&#41; would allow us to take into account all other diseases that can produce similar symptoms that are very hard to differentiate&#46; The advantage of this approach is that differentiated and&#47;or combined clinical endotypes or phenotypes that may potentially have different outcomes and specific therapeutic approaches are taken into account &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Worsening dyspnea emerges as the guiding symptom of CES&#46; Expiratory airflow limitation and dynamic hyperinflation have been described as the main pathophysiological mechanisms&#44; although cardiovascular&#44; muscle&#44; and psychosocial disorders may also be involved&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> Changes in respiratory rate&#44; heart rate and&#47;or gas exchange are also an objective manifestation of underlying pathophysiological changes&#44; so analysis of these parameters may be helpful&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Finally&#44; we need to incorporate biomarkers associated with the underlying biological alteration that help identify and categorize exacerbations and guide treatment&#46; Various&#44; largely unsuccessful&#44; attempts have been made to identify a reference biomarker for diagnosis&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> However&#44; the simultaneous use of different biomarkers may open new avenues&#46; In a multilevel analysis&#44; Noell et al&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a> found that the best biomarker panel to define exacerbation was the combination of circulating neutrophils&#44; C-reactive protein&#44; and dyspnea &#40;area under the curve&#8239;&#61;&#8239;0&#46;97&#41;&#46; Peripheral eosinophilia&#44; procalcitonin&#44; D-dimer or cardiovascular biomarkers such as troponin or N-terminal pro-brain natriuretic peptide &#40;NT-pro-BNP&#41; are some examples of other biomarkers that may be helpful in identifying traits that guide personalization of treatment&#44;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> although none of them has been shown to be sufficiently specific to the disease&#46; In contrast&#44; some alveolar mediators&#44; such as surfactant protein D&#44; may be useful during COPD exacerbations&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">In short&#44; a quarter of a century after the ATS recommendation&#44; we need to change the paradigm and redefine exacerbation by incorporating elements that help improve the specificity of the clinical picture&#44; without losing sensitivity&#46; A syndrome-based approach may better address the heterogeneity of the process&#46; Dyspnea emerges as the guiding symptom&#46; However&#44; given its subjective nature&#44; it would be desirable to include some objective parameters associated with the pathophysiology of the episode&#44; along with biomarkers that help to profile the underlying endotype&#46; Only if we can improve the specificity of the picture will we be able to deepen our understanding of its biological mechanisms&#44; customize treatments&#44; and ultimately mitigate the negative consequences that these episodes generate&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflict of interests</span><p id="par0035" class="elsevierStylePara elsevierViewall">Juan Jos&#233; Soler-Catalu&#241;a has received speaker fees from AstraZeneca&#44; Boehringer Ingelheim&#44; Bial&#44; Ferrer&#44; Laboratorio Esteve&#44; Menarini&#44; Mundipharma&#44; Novartis&#44; Rovi&#44; and TEVA&#59; consultancy fees from AirLiquide&#44; AstraZeneca&#44; Boehringer Ingelheim&#44; Chiesi&#44; Ferrer&#44; GlaxoSmithKline&#44; Laboratorios Esteve&#44; Mundipharma and Novartis&#44; and research assistance from GlaxoSmithKline&#44; Chesi&#44; and Boehringer Ingelheim&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Cristina Miralles Saavedra states that she has no conflict of interests&#46;</p></span></span>"
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Editorial
Exacerbation syndrome in COPD: A paradigm shift
Hacia el síndrome de agudización en la EPOC: un cambio de paradigma
Juan José Soler-Cataluñaa,b,
Corresponding author
jjsoler@telefonica.net

Corresponding author.
, Cristina Mirallesa
a Servicio de Neumología, Hospital Arnau de Vilanova, Valencia, Spain
b Centro de Investigación en Red de Enfermedades Respiratorias (CIBERES), Madrid, Spain
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from the s</span>table s<span class="elsevierStyleItalic">tate and beyond normal day-to-day variations&#44; that is acute in onset and necessitates a change in regular medication in a patient with underlying COPD&#8221;&#46;</span> It has been 20 years since that initial proposal&#44; and significant advances have been made in the knowledge of COPD&#44; which is now understood as a complex and heterogeneous syndrome requiring an increasingly personalized approach&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> However&#44; the concept&#44; diagnosis&#44; and management of exacerbations have hardly changed&#46; We continue to indiscriminately use short-acting bronchodilators&#44; systemic steroids&#44; and antibiotics with poor outcomes&#46; Therapeutic failures are common&#44; the 30-day readmission rate is 20&#37;&#44; and in-hospital mortality is 5&#37;&#44; increasing to 11&#37; at 3 months&#46; Furthermore&#44; a considerable proportion of patients have persistent exacerbations&#44; we do not have a good classification system&#44; we do not use generalized predictive risk models&#44; admission criteria are not standardized&#44; and clinical trials still define exacerbation or severity based on resource use&#46;<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4&#8211;7</span></a> As a result&#44; scientific results are very heterogeneous and progress is inconsistent&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The origin of this confusion lies in the construction of the definition itself&#44; which fails to identify the underlying biological mechanism&#44; does not recognize the heterogeneity of the clinical picture and&#44; being symptom-based&#44; is very unspecific&#46; Many other concomitant diseases &#40;comorbidities&#41; can also cause the same worsening of symptoms in COPD patients&#46; Heart failure&#44; arrhythmias&#44; ischemic heart disease&#44; anxiety&#44; pulmonary embolism&#44; and pneumonia are diseases that often occur in COPD and present with increased respiratory symptoms&#46; However&#44; by consensus&#44; they are not considered COPD exacerbations&#46; A comprehensive differential diagnosis is needed to rule out these other diseases&#44; but this is not always easy&#46; Pneumonia&#44; for example&#44; is an entity that is typically distinct from exacerbation due to the presence of infiltrates in the pulmonary parenchyma&#46; However&#44; the difference between the two entities is very subtle&#46; Up to one third of COPD patients have infiltrates on computed tomography that are not visible on simple chest X-ray&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> These patients are classified and categorized as COPD exacerbations when they are actually pneumonia&#46; Are they different entities or phases of the same disease&#63; The pulmonary microbiome is practically identical&#44; causative factors are very similar&#44; and clinical expression&#44; prognostic impact&#44; and treatment are also similar&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">8&#44;9</span></a> A similar situation occurs with heart failure&#44; ischemic heart disease&#44; and pulmonary embolism&#44; which often overlap with the exacerbation itself&#46;<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">10&#8211;12</span></a> The direct consequence of all this is confusion&#44; heterogeneous clinical outcomes&#44; scant progress in understanding the underlying mechanisms&#44; and barriers to accessing personalized treatment&#46; A change of strategy is therefore urgent&#46; We need a new definition derived from more objective and specific criteria that&#44; even at the risk of losing some sensitivity&#44; also takes into account the variety of presentations&#44; helps identify biological endotypes&#44; and offers a direct pathway to precision medicine&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">A good reference model is acute coronary disease&#44; the current definition of which is based on 3 essential parameters&#58; 1&#41; a syndrome-based approach &#40;acute coronary syndrome&#41;&#59; 2&#41; a guiding symptom &#40;chest pain&#41;&#59; and 3&#41; objective variables with underlying biological mechanisms &#40;electrocardiographic alterations and biomarkers&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> Using a syndrome-based approach to what we might call COPD exacerbation syndrome &#40;CES&#41; would allow us to take into account all other diseases that can produce similar symptoms that are very hard to differentiate&#46; The advantage of this approach is that differentiated and&#47;or combined clinical endotypes or phenotypes that may potentially have different outcomes and specific therapeutic approaches are taken into account &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Worsening dyspnea emerges as the guiding symptom of CES&#46; Expiratory airflow limitation and dynamic hyperinflation have been described as the main pathophysiological mechanisms&#44; although cardiovascular&#44; muscle&#44; and psychosocial disorders may also be involved&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> Changes in respiratory rate&#44; heart rate and&#47;or gas exchange are also an objective manifestation of underlying pathophysiological changes&#44; so analysis of these parameters may be helpful&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Finally&#44; we need to incorporate biomarkers associated with the underlying biological alteration that help identify and categorize exacerbations and guide treatment&#46; Various&#44; largely unsuccessful&#44; attempts have been made to identify a reference biomarker for diagnosis&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> However&#44; the simultaneous use of different biomarkers may open new avenues&#46; In a multilevel analysis&#44; Noell et al&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a> found that the best biomarker panel to define exacerbation was the combination of circulating neutrophils&#44; C-reactive protein&#44; and dyspnea &#40;area under the curve&#8239;&#61;&#8239;0&#46;97&#41;&#46; Peripheral eosinophilia&#44; procalcitonin&#44; D-dimer or cardiovascular biomarkers such as troponin or N-terminal pro-brain natriuretic peptide &#40;NT-pro-BNP&#41; are some examples of other biomarkers that may be helpful in identifying traits that guide personalization of treatment&#44;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> although none of them has been shown to be sufficiently specific to the disease&#46; In contrast&#44; some alveolar mediators&#44; such as surfactant protein D&#44; may be useful during COPD exacerbations&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">In short&#44; a quarter of a century after the ATS recommendation&#44; we need to change the paradigm and redefine exacerbation by incorporating elements that help improve the specificity of the clinical picture&#44; without losing sensitivity&#46; A syndrome-based approach may better address the heterogeneity of the process&#46; Dyspnea emerges as the guiding symptom&#46; However&#44; given its subjective nature&#44; it would be desirable to include some objective parameters associated with the pathophysiology of the episode&#44; along with biomarkers that help to profile the underlying endotype&#46; Only if we can improve the specificity of the picture will we be able to deepen our understanding of its biological mechanisms&#44; customize treatments&#44; and ultimately mitigate the negative consequences that these episodes generate&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflict of interests</span><p id="par0035" class="elsevierStylePara elsevierViewall">Juan Jos&#233; Soler-Catalu&#241;a has received speaker fees from AstraZeneca&#44; Boehringer Ingelheim&#44; Bial&#44; Ferrer&#44; Laboratorio Esteve&#44; Menarini&#44; Mundipharma&#44; Novartis&#44; Rovi&#44; and TEVA&#59; consultancy fees from AirLiquide&#44; AstraZeneca&#44; Boehringer Ingelheim&#44; Chiesi&#44; Ferrer&#44; GlaxoSmithKline&#44; Laboratorios Esteve&#44; Mundipharma and Novartis&#44; and research assistance from GlaxoSmithKline&#44; Chesi&#44; and Boehringer Ingelheim&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Cristina Miralles Saavedra states that she has no conflict of interests&#46;</p></span></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Soler-Catalu&#241;a JJ&#44; Miralles C&#46; Hacia el s&#237;ndrome de agudizaci&#243;n en la EPOC&#58; un cambio de paradigma&#46; Arch Bronconeumol&#46; 2021&#59;57&#58;246&#8211;248&#46;</p>"
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">The diagram shows the concept of CES&#46; The presence of a triggering factor in a COPD patient &#40;with its social determinants and comorbidity&#41; leads to the appearance of a CES syndrome&#44; where worsening dyspnea is the final manifestation of various biological and pathophysiological mechanisms&#46; Because of the heterogeneity of symptoms&#44; different biological endotypes and various phenotypic presentations susceptible to specific treatments can be expressed&#46;</p>"
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ISSN: 15792129
Original language: English
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