Editorial
Chronic obstructive pulmonary disease and metabolic syndrome: traveling with bad companies
Enfermedad pulmonar obstructiva crónica y síndrome metabólico: viajar en mala compañía
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López Andreu, C. López Rodríguez" "autores" => array:2 [ 0 => array:4 [ "nombre" => "F.R." "apellidos" => "López Andreu" "email" => array:1 [ 0 => "frlopezandreu@gmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "C." "apellidos" => "López Rodríguez" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Servicio de Medicina Interna, Hospital General Universitario Reina Sofía, Murcia, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Servicio de Medicina Interna, Hospital General Universitario Reina Sofía, Murcia, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Enfermedad pulmonar obstructiva crónica y síndrome metabólico: viajar en mala compañía" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Chronic obstructive pulmonary disease (COPD) is a common, preventable and treatable clinical entity characterized by persistent respiratory symptoms including dyspnea, cough and expectoration, along with chronic airflow restriction due to airway or alveolar disorders, commonly caused by exposure to harmful gases and microparticles. The main risk factor is cigarette smoke, but exposure to biomass fuel and atmospheric contamination can be involved in the development of COPD.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Given that COPD only affects approximately 50% of heavy smokers, there must be individual factors that include genetic predisposition, lung development disorders and age.</p><p id="par0010" class="elsevierStylePara elsevierViewall">COPD is a serious public health problem that affects up to 10% of the population older than 45 years, exceeding 50% among heavy smokers and is the third leading cause of death worldwide.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">In recent years, research efforts have focused mainly on the following aspects: establishing phenotypic groups that enable a more accurate adjustment of the prognosis and treatment; a better understanding of the underlying pathophysiological process and of the factors that perpetuate it, making the disease incurable once it has been established; and changing the natural history of the disease by the presence of various comorbidities and adverse effects of the treatments. Identifying and properly assessing the extrapulmonary manifestations of COPD is also essential.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">American Heart Association/National Heart, Lung and Blood Institute and Consensus Statement defines metabolic syndrome (MS) as the combination of 3 or more of the following risk factors: abdominal obesity, increased triglyceride levels, reduced HDL-cholesterol levels, arterial hypertension and increased fasting blood glucose levels.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> MS entails a notably increased cardiovascular risk, which exceeds the merely additive.<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4,5</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">This issue of <span class="elsevierStyleSmallCaps">Revista Clínica Española</span> presents the study by Sepúlveda et al.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> that assessed the impact of MS in patients with COPD by analyzing various markers related to oxidation processes, as well as pulmonary function tests and symptom severity. The study included 74 patients (39 with COPD) separated into 4 groups: COPD with MS, COPD without MS, controls with MS and controls without MS. The authors measured advanced oxidation protein products, paraoxonase-1, catalase activity, sulfhydryl groups and lipid hydroperoxides. The authors, who mentioned their small sample size as a study limitation, concluded that greater COPD severity (according to the GOLD guidelines<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a>), greater impairment in pulmonary function tests and the combination with MS were related to increased oxidative stress, indicating as well the presence of increased comorbidity assessed with the Charlson index.<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7,8</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Due to their anatomical characteristics, the lungs are especially vulnerable to oxidative stress in the environment. The lungs are also permanently exposed to endogenous sources due to mitochondrial respiration and mediators of the inflammatory response against viral and bacterial infections. There are various environmental sources, including tobacco smoke. Once the pathological process of COPD has been established, smoking cessation does not halt the increase in oxidative stress or the disease progression.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Reactive oxygen species of mitochondrial origin, epithelial cells, smooth muscle cells and various inflammatory cells are also involved in this process.</p><p id="par0035" class="elsevierStylePara elsevierViewall">A recent study by Fischer et al.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> emphasized the importance of the balance between oxidants and antioxidants and the role of tobacco in breaking this delicate equilibrium, making it difficult to separate the direct impact of tobacco from that derived from the associated inflammatory response. In a similar sense, the study by Ye et al.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> concluded that serum modulator-1 levels of reactive oxygen species are high in patients with COPD and are associated with functional impairment, inflammation and oxidative stress. Sanders et al.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> highlighted the role of the receptor for advanced glycation end products, a cell membrane receptor capable of recognizing ligands generated in tobacco combustion and that has been implicated in the pathogenesis of COPD. Their study demonstrated that deletion or pharmacologic inhibition of the receptor for advanced glycation end products can prevent the development of tobacco-related emphysema.</p><p id="par0040" class="elsevierStylePara elsevierViewall">As part of this panoramic approach, we should mention the recent study by Papakonstantinou et al.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> on the role of hyaluronic acid and its degradation products in the pulmonary pathophysiology and airway remodeling in COPD, which found a direct correlation between serum hyaluronic acid levels and disease severity or the presence of exacerbations.</p><p id="par0045" class="elsevierStylePara elsevierViewall">Equally important are the therapeutic implications of this oxidant/antioxidant imbalance because we do not have treatments that can reverse or at least slow the progression of COPD. In contrast to the behavior of the inflammatory component in asthma, the response to inhaled steroids provides a scarce benefit for the inflammatory component of COPD. Oral N-acetyl-cysteine also showed no net benefit on disease progression or the frequency of exacerbations.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> In this scenario, directing resources to the effective prevention of the disease and the development of effective drugs to reverse or at least stop the evolutionary process of the disease is essential. It is also essential to further the studies on identifying those markers of oxidative process that could be useful in daily clinical practice as indicators of activity or prognostic factors.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Returning to the adverse effects in patients with COPD, both in terms of the rate of oxidative stress and clinical manifestations, attributable to the coexistence of MS (the subject of the study under discussion), the results of the study are supported by a similar study by Díez-Manglano et al.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> who found diagnostic criteria for MS in up to 60% of patients with severe or highly severe COPD. We can therefore conclude that the concomitant presence of the 2 diseases is, undoubtedly, “traveling in bad company”.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: López Andreu FR, López Rodríguez C. Enfermedad pulmonar obstructiva crónica y síndrome metabólico: viajar en mala compañía. Rev Clin Esp. 2019;219:492–493.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:13 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:1 [ "referenciaCompleta" => "Global Initiative for Chronic Obstructive Lung Disease. 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