Access the full text.
Sign up today, get DeepDyve free for 14 days.
Loading next page...
/lp/pubmed-central/sarcopenia-correlates-with-systemic-inflammation-in-copd-68RGhkRP7y
References
References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.
- Publisher
- Pubmed Central
- Copyright
- © 2017 Byun et al. This work is published and licensed by Dove Medical Press Limited
- ISSN
- 1176-9106
- eISSN
- 1178-2005
- DOI
- 10.2147/COPD.S130790
- Publisher site
- See Article on Publisher Site
Abstract
Journal name: International Journal of COPD Article Designation: Original Research Year: 2017 Volume: 12 Running head verso: Byun et al International Journal of COPD Dovepress Running head recto: Sarcopenia and systemic inflammation in COPD open access to scientific and medical research DOI: http://dx.doi.org/10.2147/COPD.S130790 Open access Full Text article O r I g I nal r esear C h Sarcopenia correlates with systemic inflammation in COPD Min Kwang Byun Background: Muscle wasting and chronic inflammation are predominant features of patients with COPD. Systemic inflammation is associated with an accelerated decline in lung function. eun n a Cho In this study, the prevalence of sarcopenia and the relationships between sarcopenia and systemic Joon Chang inflammations in patients with stable COPD were investigated. Chul Min ahn 1 Materials and methods: In a cross-sectional design, muscle strength and muscle mass were hyung Jung Kim measured by handgrip strength (HGS) and bioelectrical impedance analysis in 80 patients with Division of Pulmonology, Department stable COPD. Patients ($40 years old) diagnosed with COPD were recruited from outpatient of Internal Medicine, g angnam severance hospital, Division of clinics, and then COPD stages were classified. Sarcopenia was defined as the presence of both Pulmonology, Department of Internal low muscle strength (by HGS) and low muscle mass (skeletal muscle mass index [SMMI]). Medicine, s everance h ospital, Yonsei Levels of circulating inflammatory biomarkers (IL-6 and high-sensitivity TNF α [hsTNFα]) University College of Medicine, seoul, south Korea were measured. Results: Sarcopenia was prevalent in 20 (25%) patients. Patients with sarcopenia were older, had lower body mass index, and a higher percentage of cardiovascular diseases. In addition, they had significantly higher modified Medical Research Council scores and lower 6-minute walk distance than those without sarcopenia. HGS was significantly correlated with age, modified Medical Research Council score, and COPD Assessment Test scores. Both HGS and SMMI had associations with IL-6 and hsTNFα (HGS, r=-0.35, P=0.002; SMMI, r=-0.246, P=0.044) level. In multivariate analysis, old age, lower body mass index, presence of cardiovascular comorbidities, and higher hsTNFα levels were significant determinants for sarcopenia in patients with stable COPD. Conclusion: Sarcopenia is very common in patients with stable COPD, and is associated with more severe dyspnea-scale scores and lower exercise tolerance. Systemic inflammation could be an important contributor to sarcopenia in the stable COPD population. Keywords: sarcopenia, muscle wasting, handgrip strength, systemic inflammation, COPD Introduction COPD is a leading cause of morbidity and mortality worldwide. It is characterized by persistent, progressive limitations in airflow, which are usually associated with enhanced airway and lung-inflammatory responses to noxious particles or gases. Systemic inflammation is associated with an accelerated decline in lung function, 2,3 and is heightened during episodes of exacerbation. Systemic inflammation is now Correspondence: hyung Jung Kim a recognized risk factor for other complications commonly observed in patients with Division of Pulmonology, Department of 4 5 6 7 Internal Medicine, gangnam severance COPD, including atherosclerosis, cachexia, anorexia, and osteoporosis. It is present hospital, Yonsei University College of not only in acutely exacerbated COPD but also in stable COPD. Medicine, 211 eonju-ro, Dogok-dong, gangnam-gu, seoul 06273, south Korea Muscle wasting is another characteristic feature of COPD, and evaluation of both Tel +82 2 2019 3316 muscle quality and quantity are essential. Physical inactivity is involved in the early Fax +82 2 3463 3882 email [email protected] loss of muscle function in COPD, and muscle wasting can further decrease physical submit your manuscript | www.dovepress.com International Journal of COPD 2017:12 669–675 Dovepress © 2017 Byun et al. This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you http://dx.doi.org/10.2147/COPD.S130790 hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). Byun et al Dovepress activity, exercise tolerance, and quality of life. Previous of active lung disease, diagnosis of bronchial asthma, lung studies have reported that muscle wasting is closely associ- resection or transplantation, presence of severe cardiovascu- ated with higher rates of COPD exacerbation and lower lar disease, an episode of COPD exacerbation within the last 10,11 survival rates. The BODE index (body mass index [BMI], month, inability to perform a 6MWD test due to severe dysp- obstruction of airways as measured by forced expiratory nea, lower-leg trauma, severe muscle weakness, and inability volume in 1 second [FEV ], dyspnea as measured by the to read or understand informed consent documents. All con- modie fi d Medical Research Council [mMRC] dyspnea scale, senting subjects completed a Korean version of the COPD and exercise capacity as measured by 6-minute walk dis- Assessment Test (CAT) questionnaire (GlaxoSmithKline, tance [6MWD]) was originally designed to predict mortality London, UK). Subjects were evaluated using the mMRC in COPD. It also demonstrates the prognostic signic fi ance of dyspnea scale and postbronchodilator FEV in a pulmonary muscle mass and exercise capacity (as assessed by BMI and function test (Vmax 229; SensorMedics, Yorba Linda, CA, 6MWD) in predicting long-term outcomes. This concept USA), 6MWD, muscle measurements, and venous blood recently den fi ed as sarcopenia a clinical syndrome comprised sampling at a single visit. We evaluated history of exacerba- of multiple factors, including physical inactivity, malnutri- tions in the last year, the BODE index, and disease severity 13,14 tion, inflammation, and chronic illness. The European according to a 2011 GOLD revision; the revised document Working Group on Sarcopenia in Older People (EWGSOP) recommends assessment of symptoms, lung function, and recommends using the presence of both low muscle mass risk of exacerbation. and low muscle function (strength or performance) for the This study was performed in accordance with the diagnosis of sarcopenia. Declaration of Helsinki and South Korean good clinical Initially, sarcopenia used to describe age-related loss of practice guidelines. All protocols were approved by the muscle mass and power. However, catabolic inflammatory institutional review board of Gangnam Severance Hospital processes often observed in chronic illnesses can enhance (3-2011-0300). sarcopenia. As such, it has recently been recognized as a Measurement of muscle mass and muscle syndrome in various chronic conditions. Also, in the COPD population the prevalence of sarcopenia is reported to be strength 15%, and is associated with impaired lung function and poor Muscle mass was quantified with BIA (Body Composition health status. No studies, however, have yet shown a direct Analysis 1000; MediGate, Seoul, South Korea). Height (cm), association between sarcopenia and levels of inflammatory body weight (kg), and BMI (kg/m ) were also measured. biomarkers in this group. We measured muscle mass and Fat mass index (FMI) and fat-free mass index (FFMI) were muscle strength in South Korean patients with stable COPD calculated as fat mass or fat-free mass (FFM) divided by the to determine the prevalence of sarcopenia using handgrip square of the patient’s height (kg/height ). Skeletal muscle strength (HGS) and bioelectrical impedance analysis (BIA). mass index (SMMI) was calculated as skeletal muscle mass In addition, we evaluated relationships between sarcopenia, (SMM) divided by the square of patient’s height (kg/height ). biomarkers of systemic inflammation, disease severity, and Low MM was defined as having an SMMI at least two stan - other clinical features. dard deviations (SDs) below normal sex-specific means in young persons. Data were compared with the 2008–2011 Materials and methods Korean National Health and Nutrition Examination Survey study design and populations IV and V, a nationally representative survey conducted by the Patients ($40 years old) diagnosed with COPD accord- South Korean Ministry of Health and Welfare. To determine ing to the Global Initiative for Chronic Obstructive Lung muscle strength, HGS was measured using a Jamar handheld Disease (GOLD) and attending outpatient clinics between dynamometer (Patterson Medical, Warrenville, IL, USA), June 2012 and June 2014 at Gangnam Severance Hospital the reliability of which has been previously established in were considered eligible. Investigators explained the aim and community-dwelling older adults. Subjects were seated with protocol of the study to patients who fulfilled the inclusion shoulders at 0° adduction and neutral rotation, elbows at 90° criteria. Written informed consent and medical history were flexion, and forearms in neutral position. Three trials were obtained at the visit. This was a cross-sectional study, and performed with a rest period of 1 minute between trials, and all measurements were completed at a single visit for each average values were recorded. Low muscle strength was participants. Exclusion criteria were age ,40 years, presence defined as HGS values #30 kg in men and #20 kg in women. submit your manuscript | www.dovepress.com International Journal of COPD 2017:12 Dovepress Dovepress Sarcopenia and systemic inflammation in COPD Table 1 Baseline characteristics of study subjects According to the recommendation of the EWGSOP, sarcopenia was defined when patients had both low MM Variable Total With Without P-value (n=80) sarcopenia sarcopenia (assessed by decreased SMMI lower than cutoff values) and (n=20, 25%) (n=60, 75%) low muscle strength (measured by low HGS values). age (years) 68.4±8.9 73.1±8 66.8±8.7 0.006 Male (%) 67 (83.8) 17 (85) 50 (83.3) 0.585 Measurement of dyspnea and quality BMI (kg/m ) 23.3±3.2 21.1±1.7 24.1±3.2 ,0.001 of life Comorbidities (%) Diabetes 20 (25) 6 (30) 14 (23.3) 0.374 The mMRC dyspnea scale, which uses a 0–4 scoring system, hypertension 38 (47.5) 12 (60) 26 (43.3) 0.181 was used to assess shortness of breath. To assess functional Cardiovascular 19 (23.8) 10 (50) 9 (15) 0.003 status and exercise capacity, we used patients’ 6MWD, disease Tuberculosis 26 (32.5) 6 (30) 20 (33.3) 0.507 which measures the distance that a patient can quickly walk Bronchiectasis/ 19 (23.8) 3 (15) 16 (26.7) 0.228 along a corridor. Using these data, we measured patients’ emphysema BODE index. The BODE index ranges from 0 to 10 points, Body composition and strength with higher scores indicating a greater risk of death in Whr 0.92±0.04 0.90±0.16 0.91±0.05 0.464 Fat mass (kg) 15.7±5.3 13.8±3.6 16.4±5.6 0.056 COPD. To evaluate quality of life, we used the Korean FMI (kg/m ) 5.8±1.9 5.1±1.4 6±2.1 0.087 version of the CAT, as previously mentioned. This question- Body fat (%) 24.6±5.9 24.1±5.1 24.7±6.5 0.729 naire consists of eight questions scored on a 0–5 scale. FFM (kg) 47.4±6.9 42.8±4.6 49±7.4 ,0.001 FFMI (kg/m ) 17.4±1.6 15.9±1 17.9±1.5 ,0.001 Measurement of biomarkers of systemic sMM (kg) 25.9±4.7 22.8±3.5 27±4.6 0.001 sMMI (kg/m ) 9.5±1.2 8.5±0.8 9.8±1.1 ,0.001 inflammation hgs (kg) 30.6±9.3 25.4±6.1 32.9±9.8 0.002 Venous blood was drawn from subjects, and circulating levels Pulmonary function* of biomarkers of systemic ina fl mmation were measured using FeV (%) 61.2±14.3 58±13.9 62.3±13.9 0.253 a high-sensitivity TNFα (hsTNFα) enzyme-linked immuno- FeV /FVC (%) 51±12.9 46.1±13 52.6±12.8 0.05 sorbent assay kit (Quantikine ; R&D Systems, Minneapolis, gOlD stage, 2011 revised (%) 0.624 a 24 (30) 4 (20) 20 (33.3) MN, USA) and a chemiluminescence assay to measure IL-6 B 31 (38.8) 9 (45) 22 (36.7) (Immulite 2000; Siemens, Munich, Germany). C 5 (6.2) 2 (10) 3 (5) D 20 (25) 5 (25) 15 (25) statistical analyses # Notes: *Postbronchodilator; according to 2011 gOlD revision. Data expressed as mean ± standard deviation or n (%). Statistical analyses were performed using SPSS software Abbreviations: BMI, body mass index; Whr, waist:hip ratio; FMI, fat mass index; (version 23.0; IBM, Armonk, NY, USA). All data are expressed FFM, fat-free mass; FFMI, FFM index; sMM, skeletal muscle mass; sMMI, sMM index; hgs, handgrip strength; FeV , forced expiratory volume in 1 second; FVC, forced as means ± SD or medians with interquartile ranges. The vital capacity; gOlD, global Initiative for Chronic Obstructive lung Disease. Kolmogorov–Smirnov test was used to analyze normality of distribution. For skewed data, including serum IL-6, natural log values were used. Continuous variables are described as patients. Patients with sarcopenia were significantly older, means ± SD, and Student’s t-test was used for comparative showed lower BMI values, and had a higher percentage of analysis. Categorical variables were analyzed using χ and cardiovascular disease. FFM, FFMI, SMM, and SMMI were t-tests with 95% confidence intervals (CIs). Pearson’s cor - markedly decreased in sarcopenic patients with BIA. HGS relation analysis was used to determine relationships among was also lower in patients with sarcopenia. There was no HGS, SMMI, and other clinical or ina fl mmatory parameters. significant difference in COPD severity between patients Multiple logistic regression analysis was performed to find with and without sarcopenia. significant determinants of sarcopenia. P,0.05 was deemed Clinical outcomes associated with to indicate statistical significance. sarcopenia Results Table 2 shows that compared with patients without sarcopenia, Patient characteristics patients with sarcopenia had significantly more severe symp - Table 1 shows 80 patients with stable COPD were included. toms of dyspnea and higher mMRC scores, but CAT scores Subjects were 68.4±8.9 (range 42–88) years old and were not signic fi antly different between the two groups. These 83.8% (67) were male. Sarcopenia was prevalent in 20 (25%) patients exhibited poorer exercise tolerance, as indicated by submit your manuscript | www.dovepress.com International Journal of COPD 2017:12 Dovepress Byun et al Dovepress Table 2 Clinical outcomes according to presence or absence of Table 3 Correlations among HGS, SMMI, and inflammatory sarcopenia biomarkers Variable With Without P-value Variable HGS SMMI sarcopenia sarcopenia Coefficient P-value Coefficient P-value (n=20, 25%) (n=60, 75%) age -0.415 ,0.001 -0.074 0.527 mMrC score 0.95±0.86 0.62±0.71 0.044 BMI 0.001 0.998 0.852 ,0.001 0–1 15 (75%) 51 (85%) 0.059 hgs 1 – 0.427 ,0.001 2–4 5 (25%) 9 (15%) FFMI 0.346 0.002 0.99 ,0.001 CaT score 15 (7–22) 14 (8.75–21.25) 0.678 FMI -0.325 0.004 0.275 0.017 ,10 6 (30) 26 (43.3) 0.216 sMMI 0.427 ,0.001 1 – $10 14 (70) 34 (56.7) FeV * -0.103 0.367 0.018 0.88 BODe index 3 (0–6) 1 (0–4) 0.001 FeV /FVC* -0.13 0.367 0.079 0.498 6MWD (m) 350.8±78 389.3±66.9 0.042 mMrC score -0.346 0.002 -0.062 0.595 acute exacerbations 9 (45) 22 (36.7) 0.343 6MWD 0.44 ,0.001 0.015 0.899 $1/year (n) BODe index -0.216 0.045 -0.257 0.026 Inflammatory biomarkers CaT score -0.236 0.048 -0.132 0.275 Il-6* 1.36±0.81 0.64±0.69 0.044 Il-6 -0.273 0.018 -0.227 0.048 hsTnF α* 0.72±1.01 -0.03±1.16 0.013 -0.35 0.002 -0.246 0.044 hsTnF α Notes: *log-transformed value. all data expressed as mean ± sD or n (%) except Notes: *Postbronchodilator; log-transformed value. for CaT score, BODe index, and number of acute exacerbation in the previous year Abbreviations: BMI, body mass index; hgs , handgrip strength; FFMI, fat-free mass (median with inter-quartile ranges). index; FMI, fat mass index; sMMI, skeletal muscle mass index; FeV , forced expiratory Abbreviations: mMRC, modified Medical Research Council; CAT, COPD Asses volume in 1 second; FVC, forced vital capacity; mMRC, modie fi d Medical Research sment Test; 6MWD, 6-minute walk distance; hsTnF α, high-sensitivity TnF α; Council; 6MWD, 6-minute walk distance; CaT, COPD assessment Test; hsTnF α, BODE, body (mass index), (airflow) obstruction, dyspnea, exercise (capacity); SD, high-sensitivity TnF α; BODE, body (mass index), (airo fl w) obstruction, dyspnea, standard deviation. exercise (capacity). the shorter 6MWD values. The median score in the BODE was not associated with sarcopenia. As a systemic inflamma - index was also significantly higher in patients with sarcope - tory biomarker, hsTNFα levels showed significant negative nia. There was no significant difference in the frequency correlations with the presence of sarcopenia in our analysis. of acute exacerbation of COPD between the two groups. In multivariate analysis, significant determinants for the Among inflammatory biomarkers, hsTNF α (P=0.013) and presence of sarcopenia in patients with stable COPD were IL-6 (P=0.044) levels were signic fi antly higher in patients old age (odds ratio [OR] 1.19, 95% CI 1.03–1.36), low BMI with sarcopenia than patients without sarcopenia. (OR 0.52, 95% CI 0.35–0.78), presence of previous cardio- vascular disease (OR 4.66, 95% CI 1.01–18.31), and higher Correlations among hgs, sMM, and hsTNFα levels (OR 1.99, 95% CI 1.04–3.81). inflammatory biomarkers As shown in Table 3, HGS showed positive correlations Discussion with FFMI, SMMI, and 6MWD and significant negative To summarize, the prevalence of sarcopenia in South Korean correlations with age, FMI, mMRC score, CAT scores, patients with stable COPD was 25%, which was consis- IL-6, and hsTNFα; SMMI positively correlated with BMI, tent with previous studies reporting prevalence rates of 17–19 HGS, FFMI, and FMI, and negatively correlated with BODE 20%–40%. Patients with sarcopenia tended to be older, index, IL-6, and hsTNFα. have a higher percentage of cardiovascular comorbidity, more Figure 1 shows HGS (r=-0.35, P=0.002) and SMMI severe mMRC dyspnea scores, higher BODE index scores, (r=0.246, P=0.044) levels were very closely associated with and lower exercise tolerance in the 6MWD than those without hsTNFα as a systemic inflammatory parameter. In addition, sarcopenia. Sarcopenia in male and female patients was 25.4% values for the BODE index tended to correlate with HGS (17 of 67) and 23.1% (three of 13). There was no difference and SMMI. However, FEV did not correlate with HGS or in sex. The proportion of male sex among COPD patients was SMMI in this study. far higher in our study. However, it was not different from other South Korean COPD data. According to the representa- Factors associated with sarcopenia in tive South Korean COPD cohort data of nearly 1,000 COPD patients with COPD patients, 91.2% were male, higher than our data. As shown in Table 4, cardiovascular disease, a common MM measured by SMMI correlated with BMI and body- comorbidity in patients with COPD, was associated with the composition parameters, whereas muscle strength assessed presence of sarcopenia. GOLD classic fi ation (revised in 2011) by HGS significantly correlated with mMRC dyspnea scale, submit your manuscript | www.dovepress.com International Journal of COPD 2017:12 Dovepress Dovepress Sarcopenia and systemic inflammation in COPD +LJKVHQVLWLYLW\71) +LJKVHQVLWLYLW\71) ± ± U ± U ± 3 3 +DQGJULSVWUHQJWK NJ 6NHOHWDOPXVFOHPDVVLQGH[ NJP Figure 1 Correlation of handgrip strength and skeletal muscle mass index with high-sensitivity TnF α. Abbreviation: TnF α, Tumor necrosis factor alpha. CAT score, and 6MWD as COPD clinical parameters. Low are currently unknown. The presence of systemic inflam - HGS and SMMI showed positive correlations with the BODE mation, however, is closely associated with complications 23,24 25,26 index. These results suggest sarcopenia is closely correlated that affect prognosis, such as weight loss, cachexia, 27,28 with the BODE index, predicting higher risk of mortality. and cardiovascular disease. In a review of inflammatory Consistent with our findings, Swallow et al reported that markers in patients with COPD, CRP, b fi rinogen, leukocytes, muscle strength is important in patient prognosis. A recent TNFα, IL-6, and IL-8 levels were significantly elevated study of patients with stable COPD using prospective multi- in patients with COPD compared with healthy controls. center data also found that HGS correlated signic fi antly with In this study, we assessed correlations of sarcopenia with mortality. Therefore, HGS might provide critical prognostic the systemic inflammatory biomarkers IL-6 and hsTNF α. information for patients with COPD. Muscle strength assessed by HGS and MM measured by In addition, the presence of sarcopenia was highly associ- SMMI showed significant correlations with levels of IL-6 ated with levels of systemic inflammation. The mechanisms and hsTNFα. In multivariate analysis, higher hsTNFα was by which patients with COPD develop systemic ina fl mmation a significant determinant for the presence of sarcopenia. The strength of this study was that most of patients in our study had milder COPD severity (GOLD A/B, 68.8%) and Table 4 Factors associated with sarcopenia all patients had stable status, not exacerbated, and signifi - Variable Sarcopenia cant correlations of HGS and SMMI with levels of systemic Univariate analysis Multivariate analysis inflammatory biomarkers is a noteworthy result. OR (95% CI) P-value OR (95% CI) P-value In the elderly and patients with COPD, physical inactivity age Years 1.11 (1.03–1.22) 0.009 1.19 (1.03–1.36) 0.017 is a key factor in the development of sarcopenia and a predic- sex tor of mortality and disability. The causes and prevalence Male vs female 1.13 (0.28–4.6) 0.861 – – of systemic inflammation and the mechanisms by which it BMI kg/m 0.63 (0.48–0.82) 0.001 0.52 (0.35–0.78) 0.001 leads to muscle wasting in COPD patients are uncertain. Diabetes Previous studies have suggested that severe muscle wast- Presence 1.41 (0.38–3.02) 0.552 – – 24,30 ing can lead to cachexia during systemic inflammation. Cardiovascular disease We found that various factors were associated with sarcope- Presence 5.66 (1.8–12.65) 0.003 4.66 (1.01–18.31) 0.048 gOlD stage nia, including age, BMI, and systemic inflammation. COPD a–B 1 – – severity, however, was not associated with the presence or C–D 1.26 (0.43–3.67) 0.676 – – absence of sarcopenia in this study, and the frequency of hsTnF α* 1.81 (1.1–2.99) 0.019 1.99 (1.04–3.81) 0.038 acute exacerbations of COPD was not different between the Notes: *log-transformed value. Multivariate logistic analysis was performed after adjusting for age, sex, BMI, and diabetes. two groups. Considering the clinical complexity of COPD, Abbreviations: OR, odds ratio; CI, confidence interval; BMI, body mass index; GOLD, global Initiative for Chronic Obstructive lung Disease; hsTnF α, high-sensitivity TnF α. however, we propose that multiple biomarkers are required submit your manuscript | www.dovepress.com International Journal of COPD 2017:12 Dovepress α Byun et al Dovepress 11. Schols AM, Soeters PB, Dingemans AM, Mostert R, Frantzen PJ, to characterize pathogenic factors and clinical outcomes in Wouters EF. Prevalence and characteristics of nutritional depletion in this disease. patients with stable COPD eligible for pulmonary rehabilitation. Am Rev There are several limitations to our study. We utilized a Respir Dis. 1993;147(5):1151–1156. 12. Celli BR, Cote CG, Marin JM, et al. The body-mass index, airflow cross-sectional design, the study population was small, and obstruction, dyspnea, and exercise capacity index in chronic obstructive recruitment was limited to outpatient clinics at a single tertiary pulmonary disease. N Engl J Med. 2004;350(10):1005–1012. 13. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, et al. Sarcopenia – European hospital. Sample composition in terms of disease severity consensus on definition and diagnosis: report of the European Work - according to GOLD stage and FEV was not well balanced. ing Group on Sarcopenia in Older People. Age Ageing. 2010;39(4): 412–423. 14. Kalyani RR, Corriere M, Ferrucci L. Age-related and disease-related Conclusion muscle loss: the effect of diabetes, obesity, and other diseases. Lancet Nearly a quarter of South Korean patients with stable COPD Diabetes Endocrinol. 2014;2(10):819–829. 15. [No authors listed]. ATS statement: guidelines for the six-minute walk have sarcopenia, and sarcopenic patients presented with test. Am J Respir Crit Care Med. 2002;166(1):111–117. more severe dyspnea, showed lower exercise tolerance, and 16. [No authors listed]. Lung function testing: selection of reference predicted poor prognosis. In addition, sarcopenia was highly values and interpretative strategies. Am Rev Respir Dis. 1991;144(5): 1202–1218. associated with levels of systemic inflammation. The pres - 17. Jones SE, Maddocks M, Kon SS, et al. Sarcopenia in COPD: prevalence, ence of systemic inflammation was a main determinant of clinical correlates and response to pulmonary rehabilitation. Thorax. 2015;70(3):213–218. sarcopenia in a stable COPD population. 18. Marquis K, Debigare R, Lacasse Y, et al. Midthigh muscle cross- sectional area is a better predictor of mortality than body mass index Acknowledgment in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2002;166(6):809–813. The authors are grateful for statistical support provided by the 19. Wagner PD. Possible mechanisms underlying the development of Medical Research Supporting Section of Yonsei University cachexia in COPD. Eur Respir J. 2008;31(3):492–501. 20. Lee JY, Chon GR, Rhee CK, et al. Characteristics of patients with College of Medicine. chronic obstructive pulmonary disease at the first visit to a pulmonary medical center in Korea: the Korea COPD Subgroup Study team cohort. Disclosure J Korean Med Sci. 2016;31(4):553–560. 21. Swallow EB, Reyes D, Hopkinson NS, et al. Quadriceps strength pre- The authors report no conflicts of interest in this work. dicts mortality in patients with moderate to severe chronic obstructive pulmonary disease. Thorax. 2007;62(2):115–120. 22. Burtin C, Ter Riet G, Puhan MA, et al. Handgrip weakness and mortality References risk in COPD: a multicentre analysis. Thorax. 2016;71(1):86–87. 1. Vestbo J, Hurd SS, Agustí AG, et al. Global strategy for the diagnosis, 23. de Godoy I, Donahoe M, Calhoun WJ, Mancino J, Rogers RM. Elevated management, and prevention of chronic obstructive pulmonary disease: TNF-α production by peripheral blood monocytes of weight-losing GOLD executive summary. Am J Respir Crit Care Med. 2013;187(4): COPD patients. Am J Respir Crit Care Med. 1996;153(2):633–637. 347–365. 24. Eid AA, Ionescu AA, Nixon LS, et al. Ina fl mmatory response and body 2. Donaldson GC, Seemungal TA, Patel IS, et al. Airway and systemic composition in chronic obstructive pulmonary disease. Am J Respir Crit inflammation and decline in lung function in patients with COPD. Chest. Care Med. 2001;164(8 Pt 1):1414–1418. 2005;128(4):1995–2004. 25. Schols AM. Pulmonary cachexia. Int J Cardiol. 2002;85(1):101–110. 3. Hurst JR, Donaldson GC, Perera WR, et al. Use of plasma biomarkers 26. Agustí AG, Noguera A, Sauleda J, Sala E, Pons J, Busquets X. Systemic at exacerbation of chronic obstructive pulmonary disease. Am J Respir effects of chronic obstructive pulmonary disease. Eur Respir J. 2003; Crit Care Med. 2006;174(8):867–874. 21(2):347–360. 4. Ross R. Atherosclerosis: an ina fl mmatory disease. N Engl J Med. 1999; 27. Hole DJ, Watt GC, Davey-Smith G, Hart CL, Gillis CR, Hawthorne VM. 340(2):115–126. Impaired lung function and mortality risk in men and women: findings 5. Kotler DP. Cachexia. Ann Intern Med. 2000;133(8):622–634. from the Renfrew and Paisley prospective population study. BMJ. 1996; 6. Johnson PM, Vogt SK, Burney MW, Muglia LJ. COX-2 inhibition 313(7059):711–716. attenuates anorexia during systemic inflammation without impairing 28. Schünemann HJ, Dorn J, Grant BJ, Winkelstein W Jr, Trevisan M. cytokine production. Am J Physiol Endocrinol Metab. 2002;282(3): Pulmonary function is a long-term predictor of mortality in the general E650–E656. population: 29-year follow-up of the Buffalo Health Study. Chest. 2000; 7. Raisz LG. Physiology and pathophysiology of bone remodeling. Clin 118(3):656–664. Chem. 1999;45(8 Pt 2):1353–1358. 29. Steiner MC. Sarcopaenia in chronic obstructive pulmonary disease. 8. Gan WQ, Man SF, Senthilselvan A, Sin DD. Association between chronic Thorax. 2007;62(2):101–103. obstructive pulmonary disease and systemic ina fl mmation: a systematic 30. Schols AM, Buurman WA, van den Brekel AJ, Dentener MA, Wouters review and a meta-analysis. Thorax. 2004;59(7):574–580. EF. Evidence for a relation between metabolic derangements and 9. Barnes PJ, Celli BR. Systemic manifestations and comorbidities of increased levels of inflammatory mediators in a subgroup of patients with COPD. Eur Respir J. 2009;33(5):1165–1185. chronic obstructive pulmonary disease. Thorax. 1996;51(8):819–824. 10. Vestbo J, Prescott E, Almdal T, et al. Body mass, fat-free body mass, 31. Cazzola M, Novelli G. Biomarkers in COPD. Pulm Pharmacol Ther. and prognosis in patients with chronic obstructive pulmonary disease 2010;23(6):493–500. from a random population sample: findings from the Copenhagen City Heart Study. Am J Respir Crit Care Med. 2006;173(1):79–83. submit your manuscript | www.dovepress.com International Journal of COPD 2017:12 Dovepress Dovepress Sarcopenia and systemic inflammation in COPD International Journal of COPD Dovepress Publish your work in this journal The International Journal of COPD is an international, peer-reviewed This journal is indexed on PubMed Central, MedLine and CAS. The journal of therapeutics and pharmacology focusing on concise rapid manuscript management system is completely online and includes a reporting of clinical studies and reviews in COPD. Special focus is given very quick and fair peer-review system, which is all easy to use. Visit to the pathophysiological processes underlying the disease, intervention http://www.dovepress.com/testimonials.php to read real quotes from programs, patient focused education, and self management protocols. published authors. Submit your manuscript here: http://www.dovepress.com/international-journal-of-chronic-obstructive-pulmonary-disease-journal submit your manuscript | www.dovepress.com International Journal of COPD 2017:12 Dovepress
Journal
International Journal of Chronic Obstructive Pulmonary Disease – Pubmed Central
Published: Feb 20, 2017