Plasma leptin is related to proinflammatory status and dietary intake in patients with chronic obstructive pulmonary disease

Citation
Amwj. Schols et al., Plasma leptin is related to proinflammatory status and dietary intake in patients with chronic obstructive pulmonary disease, AM J R CRIT, 160(4), 1999, pp. 1220-1226
Citations number
40
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073449X → ACNP
Volume
160
Issue
4
Year of publication
1999
Pages
1220 - 1226
Database
ISI
SICI code
1073-449X(199910)160:4<1220:PLIRTP>2.0.ZU;2-O
Abstract
Chronic obstructive pulmonary disease (COPD) is a syndrome of chronic wasti ng, in part associated with a chronic inflammatory response. The aim of thi s study was to investigate cross-sectionally and prospectively the potentia l role of leptin in relation to systemic inflammation in the regulation of the energy balance in COPD. Body composition by deuterium dilution, resting energy expenditure (REE) by indirect calorimetry, and plasma concentration s of leptin and soluble tumor necrosis factor (TNF) receptors (sTNF-R) 55 a nd 75 by ELISA were measured in 27 male patients with emphysema and 15 male patients with chronic bronchitis (disease-subtype defined by high-resoluti on computed tomography [HRCT]). Emphysematous patients were characterized b y a lower body mass index due to a lower fat mass (FM) (p = 0.001) and by l ower mean (detectable) leptin concentrations (p = 0.020) compared with bron chitic patients. Leptin was exponentially related to FM in emphysema (r = 0 .74, p < 0.001) and in chronic bronchitis (r = 0.80, p = 0.001). Furthermor e, a significant partial correlation coefficient between leptin and sTNF-R5 5 adjusted for FM and oral corticosteroid use was seen in emphysema (r = 0. 81, p < 0.001) but not in chronic bronchitis. In 17 predominantly emphysema tous depleted male patients with COPD, baseline plasma leptin divided by FM was in addition logarithmically inversely related to baseline dietary inta ke (r = -0.50, p = 0.047) and to the degree of weight change after 8 wk of nutritional support (r = -0.60, p = 0.017). This proposed cytokine-leptin l ink in pulmonary cachexia may explain the poor response to nutritional supp ort in some of the cachectic patients with COPD and may open a novel approa ch in combating this significant comorbidity in COPD.