Plasma levels of amino acids and hypermetabolism in patients with chronic obstructive pulmonary disease

Nutrition ◽  
2001 ◽  
Vol 17 (2) ◽  
pp. 95-99 ◽  
Author(s):  
Takahiro Yoneda ◽  
Masanori Yoshikawa ◽  
Akihiro Fu ◽  
Katsuhiko Tsukaguchi ◽  
Yukinori Okamoto ◽  
...  
Pneumologia ◽  
2019 ◽  
Vol 68 (1) ◽  
pp. 21-26
Author(s):  
Retno AS Soemarwoto ◽  
Andika Chandra Putra ◽  
Syazili Mustofa ◽  
◽  

Abstract Background Chronic mucus hypersecretion is a common feature in chronic obstructive pulmonary disease (COPD) and is associated with epidermal growth factor (EGF) activity. Aberrant EGF and its receptor signalling can cause airway hyperproliferation, increase in mucous cell differentiation and mucus hyperproduction. Furthermore, it can also promote subepithelial fibrosis and excessive collagen deposition in COPD. The objective of this research was to investigate the plasma levels of EGF in smokers with COPD in comparison with clinically healthy smokers. In addition, the relationship between the plasma levels of EGF and clinical features was investigated. Methods A cross-sectional study included 82 clinically stable male patients with mild-to-very severe COPD (mean age: 64.5±8.6 years), and the control group consisted of 86 healthy male smokers (mean age: 61.6±9.5 years). To define COPD, we performed spirometry and classified COPD using Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification. We analyzed the levels of EGF by enzyme-linked immunosorbent assay in plasma. Results The mean serum levels of EGF were significantly lower in smokers with COPD than those in controls (69.30 and 83.82 pg/mL, respectively, p = 0.046). The plasma levels of EGF were significantly different (p = 0.004) between mild COPD and moderate-to-very severe COPD. There were no significant differences between the levels of EGF in plasma of spontaneous sputum producers (COPD patients) vs. nonsputum producers (p = 0.101) and between nonexacerbated COPD and exacerbated COPD patients(p = 0.138). Conclusions There is a significant difference in the plasma levels of EGF in male smokers with COPD as compared with male healthy smokers. Our findings suggest that the plasma levels of EGF may contribute to the pathogenesis of COPD.


1992 ◽  
Vol 83 (5) ◽  
pp. 529-533 ◽  
Author(s):  
Chim C. Lang ◽  
Wendy J. Coutie ◽  
Allan D. Struthers ◽  
D. Paul Dhillon ◽  
John H. Winter ◽  
...  

1. Studies in vitro have recently shown that both atrial natriuretic peptide and brain natriuretic peptide have pulmonary vasorelaxant activity. The purpose of the present study was to evaluate for the first time whether plasma levels of brain natriuretic peptide are elevated in chronic obstructive pulmonary disease. Plasma levels of brain natriuretic peptide and atrial natriuretic peptide were therefore measured in 12 patients admitted with acute hypoxaemic chronic obstructive pulmonary disease [arterial partial pressure of O2, 6.2 ± 0.4 kPa; arterial partial pressure of CO2, 6.9 ± 0.1 kPa; forced expiratory volume in 1 s, 0.6 ± 0.07 litre (27 ± 3% of predicted)]. All but three patients had oedema on admission. 2. Plasma levels of both brain natriuretic peptide and atrial natriuretic peptide were elevated in patients with chronic obstructive pulmonary disease (31.4 ± 4.1 pmol/l and 45.0 ± 8.1 pmol/l, respectively) compared with healthy control subjects (1.7 ± 0.8 pmol/l and 8.0 ± 3.5 pmol/l, respectively). Thus, plasma levels of brain natriuretic peptide and atrial natriuretic peptide in patients with chronic obstructive pulmonary disease were increased by 18.5- and 5.6-fold respectively compared with healthy control subjects. 3. There was a significant inverse correlation between the plasma level of brain natriuretic peptide and the arterial partial pressure of O2 (r = −0.65, r2 = 0.42, P = 0.03), but not between the plasma atrial natriuretic peptide level and the arterial partial pressure of O2 (r2 = 0.07, not significant). The arterial partial pressure of CO2 did not correlate with the plasma level of either brain natriuretic peptide or atrial natriuretic peptide. 4. Thus, plasma levels of brain natriuretic peptide were proportionately higher than those of atrial natriuretic peptide in patients with hypoxaemic chronic obstructive pulmonary disease. Unlike those of atrial natriuretic peptide, plasma levels of brain natriuretic peptide were correlated with the degree of hypoxaemia. Further studies are required to investigate the release and clearance of brain natriuretic peptide in chronic obstructive pulmonary disease, as well as its pulmonary vasodilator activity in vivo.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Sirpa Leivo-Korpela ◽  
Lauri Lehtimäki ◽  
Mari Hämälainen ◽  
Katriina Vuolteenaho ◽  
Lea Kööbi ◽  
...  

COPD (chronic obstructive pulmonary disease) is a common lung disease characterized by airflow limitation and systemic inflammation. Recently, adipose tissue mediated inflammation has gathered increasing interest in the pathogenesis of the disease. In this study, we investigated the role of novel adipocytokines nesfatin-1 and visfatin in COPD by measuring if they are associated with the inflammatory activity, lung function, or symptoms. Plasma levels of NUCB2/nesfatin-1 and visfatin were measured together with IL-6, IL-8, TNF-α, and MMP-9, lung function, exhaled nitric oxide, and symptoms in 43 male patients with emphysematous COPD. The measurements were repeated in a subgroup of the patients after four weeks’ treatment with inhaled fluticasone. Both visfatin and NUCB2/nesfatin-1 correlated positively with plasma levels of IL-6 (r=0.341,P=0.027andrho=0.401,P=0.008, resp.) and TNF-α(r=0.305,P=0.052andrho=0.329,P=0.033, resp.) and NUCB2/nesfatin-1 also with IL-8 (rho=0.321,P=0.036) in patients with COPD. Further, the plasma levels of visfatin correlated negatively with pulmonary diffusing capacity (r=-0.369,P=0.016). Neither of the adipokines was affected by fluticasone treatment and they were not related to steroid-responsiveness. The present results introduce adipocytokines NUCB2/nesfatin-1 and visfatin as novel factors associated with systemic inflammation in COPD and suggest that visfatin may mediate impaired pulmonary diffusing capacity.


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