Typing of chronic obstructive pulmonary disease using high-resolution computed tomography and the association with smoking, airway inflammation, and common comorbidities

Background/aim: This study performed typing of chronic obstructive pulmonary disease (COPD) using high-resolution computed tomography (HRCT) to determine the association with smoking, matrix metalloproteinases, and common comorbidities. Materials and methods: The study enrolled 94 hospitalized patients. Participants were divided into a group of 69 current and former smokers (group A) and a group of 25 that had never smoked (group B). Patients were also divided into 3 categories according to the degree of emphysema and bronchial wall thickness using HRCT to determine the association with levels of matrix metalloproteinase 9 (MMP-9) and TIMP-1, as well as associated comorbidities. These three categories were: type A - no or mild emphysema, with or without bronchial wall thickening; type E - emphysema without bronchial wall thickening; and type M - both emphysema and bronchial wall thickening. Results: The low attenuation area (LAA) scores in group A patients were higher than those in group B (t = 2.86, P < 0.01); correlation analysis showed that smoking was associated with a decline of the forced expiratory volume in 1 s and forced vital capacity ratio (FEV1/ FVC%) and higher LAA scores in patients with COPD (F = 4.46, F = 8.20, P < 0.05). The levels of MMP-9 in group A were higher than those in group B (t = 3.65, P < 0.01). Among COPD patients with more than 3 comorbidities, there were statistically significant differences in both the smoking group and the nonsmoking group (chi-square = 12.08, P < 0.01). When compared to type A patients, who had coincident cardiovascular diseases in the smoking group, patients of type M and E showed statistically significant differences (F = 2.42 and 2.12, P < 0.05). Conclusion: Emphysema was more severe in smokers. Metalloproteinase levels in smokers were higher than those in nonsmokers. Moreover, comorbidities were more severe in smokers.

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  • Ostridge K, Williams N, Kim V, Harden S, Bourne S, Coombs NA, Elkington PT, Estepar RS, Washko G, Staples KJ et al. Distinct emphysema subtypes defined by quantitative CT analysis are associated with specific pulmonary matrix metalloproteinases. Respir Res 2016; 17: 92.
  • Papakonstantinou E, Karakiulakis G, Batzios S, Savic S, Roth M, Tamm M, Stolz D. Acute exacerbations of COPD are associated with significant activation of matrix metalloproteinase 9 irrespectively of airway obstruction, emphysema and infection. Respir Res 2015; 16: 78.
  • Montaño M, Sansores RH, Becerril C, Cisneros J, González-Avila G, Sommer B, Ochoa L, Herrera I, Ramírez-Venegas A, Ramos C. FEV1 inversely correlates with metalloproteinases 1, 7, 9 and CRP in COPD by biomass smoke exposure. Respir Res 2014; 15: 74.
  • Grzela K, Litwiniuk M, Zagorska W, Grzela T. Airway remodeling in chronic obstructive pulmonary disease and asthma: the role of matrix metalloproteinase-9. Arch Immunol Ther Exp 2016; 64: 47-55.
  • Jia TG, Zhao JQ, Liu JH. Serum inflammatory factor and cytokines in AECOPD. Asian Pac J Trop Med 2014; 7: 1005-1008.
  • Smith BM, Austin JH, Newell JD Jr, D’Souza BM, Rozenshtein A, Hoffman EA, Ahmed F, Barr RG. Pulmonary emphysema subtypes on computed tomography: the MESA COPD study. Am J Med 2014; 127: 94.e7-23.
  • Foster WL Jr, Pratt PC, Roggli VL, Godwin JD, Halvorsen RA Jr, Putman CE. Centrilobular emphysema: CT-pathologic correlation. Radiology 1986; 159: 27-32.
  • Hruban RH, Meziane NA, Zerhouni EA. Resolution computed tomography of inflation-fixed lungs pathologic-radiologic correlation of centriobular emphysema. Am Rev Respir Dis 1987; 136: 935-940.
  • Vestbo J, Hurd SS, Agustí AG, Jones PW, Vogelmeier C, Anzueto A, Barnes PJ, Fabbri LM, Martinez FJ, Nishimura M et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am J Respir Crit Care Med 2013; 187: 347- 365.
  • Tan WC, Sin DD, Bourbeau J, Hernandez P, Chapman KR, Cowie R, FitzGerald JM, Marciniuk DD, Maltais F, Buist AS et al. Characteristics of COPD in never-smokers and ever- smokers in the general population: results from the CanCOLD study. Thorax 2015; 70: 822-829.
  • Kitaguchi Y, Fujimoto K, Kubo K, Honda T. Characteristics of COPD phenotypes classified according to the findings of HRCT. Respir Med 2006; 100: 1742-1752.
  • Roberts HR, Wells AU, Milne DG, Rubens MB, Kolbe J, Cole PJ, Hansell DM. Airflow obstruction in bronchiectasis: correlation between computed tomography features and pulmonary function tests. Thorax 2000; 55: 198-204.
  • Singh S, Loke YK, Enright PL, Furberg CD. Mortality associated with tiotropium mist inhaler in patients with chronic obstructive pulmonary disease: systematic review and meta-analysis of randomised controlled trials. BMJ 2011; 342: d3215.
  • Hong Y, Ji W, An S, Han SS, Lee SJ, Kim WJ. Sex differences of COPD phenotypes in nonsmoking patients. Int J Chron Obstruct Pulmon Dis 2016; 11: 1657-1662.
  • Sun XW, Gu SY, Li QY, Ren L, Shen JM, Wan HY, Huang SG, Deng WW. Pulmonary function parameters in high-resolution computed tomography phenotypes of chronic obstructive pulmonary disease. Am J Med Sci 2015; 349: 228-233.
  • Saetta M, Kim WD, Izquierdo JL, Ghezzo H, Cosio MG. Extent of centriobular and panacinar emphysema in smokers’ lungs: pathological and mechanical implications. Eur Respir J 1994; 7: 664-671.
  • Shin IS, Shin NR, Park JW, Jeon CM, Hong JM, Kwon OK, Kim JS, Lee IC, Kim JC, Oh SR et al. Melatonin attenuates neutrophil inflammation and mucus secretion in cigarette smoke-induced chronic obstructive pulmonary diseases via suppression of Erk-Sp1 signaling. J Pineal Res 2015; 58: 50-60.
  • Dar KA, Shahid M, Mubeen A, Bhargava R, Ahmad Z, Ahmad I, Islam N. The role of noninvasive methods in assessing airway inflammation and structural changes in asthma and COPD. Monaldi Arch Chest Dis 2012; 77: 8-18.
  • Kwiatkowska S, Noweta K, Zieba M, Nowak D, Bialasiewicz P. Enhanced exhalation of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in patients with COPD exacerbations: a prospective study. Respiration 2012; 804: 231- 241.
  • Linder R, Rönmark E, Pourazar J, Behndig A, Blomberg A, Lindberg A. Serum metalloproteinase-9 is related to COPD severity and symptoms - cross-sectional data from a population based cohort-study. Respir Res 2015; 16: 28.
  • Divo M, Cote C, de Torres JP, Casanova C, Marin JM, Pinto- Plata V, Zulueta J, Cabrera C, Zagaceta J, Hunninghake G et al. Comorbidities and risk of mortality in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2012; 186: 155-161.
  • Barnes PJ, Celli BR. Systemic manifestations and comorbidities of COPD. Eur Respir J 2009; 33: 1165-1185.
  • Celli BR, Locantore N, Yates J, Tal-Singer R, Miller BE, Bakke P, Calverley P, Coxson H, Crim C, Edwards LD et al. Inflammatory biomarkers improve clinical prediction of mortality in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2012; 185: 1065-1072.
  • Selvarajah S, Todd I, Tighe PJ, John M, Bolton CE, Harrison T, Fairclough LC. Multiple circulating cytokines are coelevated in chronic obstructive pulmonary disease. Mediators Inflamm 2016; 2016: 3604842.
  • Marques-Vidal P, Bastardot F, von Känel R, Paccaud F, Preisig M, Waeber G, Vollenweider P. Association between circulating cytokine levels, diabetes and insulin resistance in a population- based sample (CoLaus study). Clin Endocrinol 2013; 78: 232- 241.