Pulmonary cachexia, systemic inflammatory profile, and the interleukin 1β −511 single nucleotide polymorphism

Broekhuizen, R.; Grimble, Robert F.; Howell, W. M.; Shale, Dennis J.; Creutzberg, E.C.; Wouters, Emiel F.M.; Schols, A.M.W.J.

doi:10.1093/ajcn/82.5.1059

Cited by 96 publications

(100 citation statements)

References 48 publications

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“…Similarly, Schols and colleagues found that REE, when adjusted for fat-free mass, was higher in patients with COPD who lost weight compared with those whose weight remained stable (23). Serum levels of TNF-a are higher in cachectic patients with COPD compared with noncachectic patients with COPD and healthy control subjects (24,25), and elevations in IL-1 and IL-6 may also play a role in the development of cachexia (26,27). Reductions in circulating levels of testosterone, growth hormone, insulin-like growth factor, and leptin have also been found in cachectic patients with COPD (21,22,25).…”

Section: Discussionmentioning

confidence: 94%

Weight Gain after Lung Reduction Surgery Is Related to Improved Lung Function and Ventilatory Efficiency

Kim

Kretschman

Sternberg

et al. 2012

Am J Respir Crit Care Med

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Rationale: Lung volume reduction surgery (LVRS) is associated with weight gain in some patients, but the group that gains weight after LVRS and the mechanisms underlying this phenomenon have not been well characterized. Objectives: To describe the weight change profiles of LVRS patients enrolled in the National Emphysema Treatment Trial (NETT) and to correlate alterations in lung physiological parameters with changes in weight. . We compared BMI groups and LVRS and medical groups within each BMI stratum with respect to baseline characteristics and percent change in BMI (%DBMI) from baseline. We examined patients with (DBMI > 5%) and without (DBMI , 5%) significant weight gain at 6 months and assessed changes in lung function and ventilatory efficiency (V E/V CO 2 ). Measurements and Main Results: The percent change in BMI was greater in the LVRS arm than in the medical arm in the underweight and normal weight groups at all follow-up time points, and at 12 and 24 months in the overweight group. In the LVRS group, patients with DBMI > 5% at 6 months had greater improvements in FEV 1 (11.53 6 9.31 vs. 6.58 6 8.68%; P , 0.0001), FVC (17.51 6 15.20 vs. 7.55 6 14.88%; P , 0.0001), residual volume (-66.20 6 40.26 vs. -47.06 6 39.87%; P , 0.0001), 6-minute walk distance (38.70 6 69.57 vs. 7.57 6 73.37 m; P , 0.0001), maximal expiratory pressures (12.73 6 49.08 vs. 3.54 6 32.22; P ¼ 0.0205), and V E/V CO 2 (-1.58 6 6.20 vs. 0.22 6 8.20; P ¼ 0.0306) at 6 months than patients with DBMI , 5% at 6 months. Conclusions: LVRS leads to weight gain in nonobese patients, which is associated with improvement in lung function, exercise capacity, respiratory muscle strength, and ventilatory efficiency. These physiological changes may be partially responsible for weight gain in patients who undergo LVRS.

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Section: Discussionmentioning

confidence: 94%

Weight Gain after Lung Reduction Surgery Is Related to Improved Lung Function and Ventilatory Efficiency

Kim

Kretschman

Sternberg

et al. 2012

Am J Respir Crit Care Med

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“…Tumour necrosis factor-a Plasma tumour necrosis factor (TNF)-a and its soluble receptor are increased in COPD patients [13][14][15], and TNF-a is also released from circulating cells in COPD patients with cachexia [16]. Circulating TNF-a appears to be related, at least in part, to hypoxaemia [14].…”

Section: Interleukin-6mentioning

confidence: 99%

“…IL-1b has also been linked to cachexia, but increased plasma concentrations or decreased concentrations of its endogenous antagonist IL-1 receptor antagonist have not been found in COPD, although there is an association between COPD and a polymorphism of the IL-1b gene [15].…”

Section: Il-1bmentioning

confidence: 99%

“…Leptin is an adipokine (cytokine derived from fat cells) that plays an important role in regulating energy balance, and in COPD patients, plasma concentrations tend to be low and there is a loss of the normal diurnal variation [14,15], but its role in cachexia is not certain. By contrast, circulating concentrations of ghrelin, a growth hormone-releasing peptide that increases food intake, is elevated in cachectic patients with COPD [19].…”

Section: Adipokinesmentioning

confidence: 99%

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Systemic manifestations and comorbidities of COPD

Barnes¹,

Celli²

2009

Eur Respir J

1,476

1,113

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Increasing evidence indicates that chronic obstructive pulmonary disease (COPD) is a complex disease involving more than airflow obstruction. Airflow obstruction has profound effects on cardiac function and gas exchange with systemic consequences. In addition, as COPD results from inflammation and/or alterations in repair mechanisms, the ''spill-over'' of inflammatory mediators into the circulation may result in important systemic manifestations of the disease, such as skeletal muscle wasting and cachexia. Systemic inflammation may also initiate or worsen comorbid diseases, such as ischaemic heart disease, heart failure, osteoporosis, normocytic anaemia, lung cancer, depression and diabetes. Comorbid diseases potentiate the morbidity of COPD, leading to increased hospitalisations, mortality and healthcare costs. Comorbidities complicate the management of COPD and need to be evaluated carefully. Current therapies for comorbid diseases, such as statins and peroxisome proliferator-activated receptor-agonists, may provide unexpected benefits for COPD patients. Treatment of COPD inflammation may concomitantly treat systemic inflammation and associated comorbidities. However, new broad-spectrum anti-inflammatory treatments, such as phosphodiesterase 4 inhibitors, have significant side-effects so it may be necessary to develop inhaled drugs in the future. Another approach is the reversal of corticosteroid resistance, for example with effective antioxidants. More research is needed on COPD comorbidities and their treatment.

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“…However, inconsistent results have been reported (Ishii et al, 2000;Asada et al, 2005;Hegab et al, 2005;Broekhuizen et al, 2005;Shi et al, 2006;Danilko et al, 2007;Lee et al, 2008;Trajkov et al, 2009;Liu et al, 2012;Shukla et al, 2012;Sun et al, 2013;Issac et al, 2014), which may be because of differences in ethnicity and sample size between studies, resulting in lower statistical power. Meta-analysis may be useful for pooling independent statistical powers and thus achieving a quantitative understanding of the associations.…”

Section: Introductionmentioning

confidence: 98%

Association of interleukin-1β -511C/T promoter polymorphism with COPD risk: a meta-analysis

Wang

Liu²,

Xu³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Studies examining the role of interleukin (IL)-1β -511C/ T promoter polymorphism in the pathogenesis of chronic obstructive pulmonary disease (COPD) have shown inconsistent results. This metaanalysis was performed to assess the association between the IL-1β -511C/T promoter polymorphism and COPD susceptibility. Published case-control, cross-sectional, and cohort studies from Pubmed, Embase, and China National Knowledge Infrastructure databases were retrieved. Data were extracted and pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Twelve studies with 1692 cases and 2009 controls were included in this meta-analysis. Pooled effect size showed an overall but not significantly decreased risk of IL-1β -511 C/T with COPD susceptibility (OR = 0.89, 95%CI = 0.78-1.01) in a complete overdominant genetic model (TT+CC vs CT), indicating that homozygous individuals (CC and TT) have a decreased risk for COPD compared with heterozygotes (2015) (CT). In subgroup analysis by ethnicity, IL-1β -511C/T was significantly correlated with a decreased risk of COPD in Asians (OR = 0.73, 95%CI = 0.60-0.88, P = 0.001), but not in Caucasians (OR = 1.02, 95%CI = 0.83-1.24, P = 0.46), confirming a protective role of IL-1β -511C/T in COPD in Asians. Moreover, after excluding studies that included populations not in Hardy-Weinberg equilibrium, the pooled results were robust and no publication bias was observed. This meta-analysis suggests that the IL-1β -511C/T promoter polymorphism deceases the risk of COPD in Asians.

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Pulmonary cachexia, systemic inflammatory profile, and the interleukin 1β −511 single nucleotide polymorphism

Abstract: In COPD patients, who are characterized by an elevated systemic inflammatory response, cachexia is not discriminatory for the extent of increase in inflammatory status. This study, however, indicates a potential influence of genetic predisposition on the cachexia process.

Cited by 96 publications

References 48 publications

Weight Gain after Lung Reduction Surgery Is Related to Improved Lung Function and Ventilatory Efficiency

Weight Gain after Lung Reduction Surgery Is Related to Improved Lung Function and Ventilatory Efficiency

Systemic manifestations and comorbidities of COPD

Association of interleukin-1β -511C/T promoter polymorphism with COPD risk: a meta-analysis

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