Search

Objective: This study describes the prevalence and characteristics of an elevated resting energy expenditure (REE) in patients with chronic obstructive pulmonary disease (COPD).Design and Setting: Patients were consecutively admitted to an in-patient pulmonary rehabilitation centre.Subjects: The study group consisted of 172 (123 males) clinically stable patients with COPD, age mean (s.d.) 64(10) y).Interventions: REE was assessed by indirect calorimetry (ventilated hood) and adjusted for the influence of fat-free mass (FFM; measured by bioelectrical impedance analysis) using the linear regression equations of REE on FFM generated in 92 healthy age-matched subjects (58 males, age 67(8) y) for men and women separately. The predicted REE adjusted for FFM (REEFFM) was obtained by using the FFM of each individual patient in the linear regression equation of REE on FFM generated in the healthy control group.Results: 26% of the patients were hypermetabolic (defined as REE > 110% REEFFM), characterized by a lower age (60 (10) vs 65 (9) y) and a lower total lung capacity (TLC; 122(27)vs 139(28) %pred) compared to normometabolic patients (P < 0.001). The prevalence of FFM-depletion was equal among normo- and hypermetabolic patients: 36% vs 33% respectively. Depleted patients expressed however a significantly higher residual volume/TLC ratio and a lower maximal inspiratory mouth pressure independently of hypermetabolism (P < 0.05). In contrast, on base of the Harris & Benedict (HB) prediction equations, which do not take body composition into account, 54% of the patients were hypermetabolic (REE > 110% REEHB), characterized by a higher age and a lower body mass and FFM (P < 0.05).Conclusions: Hypermetabolism commonly occurs in COPD, characterized by less hyperinflation at rest, in contrast to the suggested contribution of an elevated oxygen cost of breathing (OCB) to hypermetabolism in COPD. The higher hyperinflation at rest in FFM-depleted patients independently of hypermetabolism suggests a higher OCB during activities, contributing to the elevated total daily energy expenditure previously reported in COPD. The HB-equations overestimate the prevalence of hypermetabolism and link hypermetabolism incorrectly to aging and depletion. [ABSTRACT FROM AUTHOR]

The article describes about levels of C reactive protein (CRP) in the healthy controls and patients with clinically stable chronic obstructive pulmonary disease (COPD). The control group used consisted of randomly selected subjects over 50 years of age and living in the same area as the patients. These subjects had no evidence of COPD based on questionnaires and lung function testing, did not exhibit any acute or chronic disease, and were not taking medication. Based on these selection criteria, this group was considered a healthy population control group. Although two of the 23 control subjects had enhanced CRP levels, the reason for which is unknown, they were not excluded in order to prevent bias. Non-parametric tests were used to compare the CRP levels between controls and COPD patients, and therefore the results are not affected by these two outliers.

Objective: The present study focuses on the prevalence of nutritional depletion in relation to functional performance, airflow limitation, experienced dyspnoea and health status in a large multi-center out-patient population with chronic obstructive pulmonary disease (COPD)., Methods: In 39 out-patient centers in The Netherlands, 389 patients with moderate to severe COPD (217 men) were recruited. The study evaluated on the baseline characteristics of the COSMIC study. Measurements included body composition by bioelectrical impedance analysis, dyspnoea by MRC-score, peripheral muscle function by isometric handgrip strength and disease-specific health status by St. George Respiratory Questionnaire., Results: The prevalence of nutritional depletion (defined as body mass index (BMI)

In this overview, the available literature on endocrinological disturbances in chronic obstructive pulmonary disease (COPD) is reviewed, with stress on growth hormone/insulin-like growth factor I (IGF-I), thyroid hormone and the anabolic steroids. In COPD, little is known about circulating growth hormone or IGF-I concentrations. Some authors find a decrease in growth hormone or IGF-I, others an increase. An increase of growth hormone might reflect a nonspecific response of the body to stress (for instance, hypoxaemia). Until now, only one controlled study on growth hormone supplementation has been published, which however did not reveal any functional benefits. Before growth hormone supplementation can be advised as part of the treatment in COPD, further controlled studies must be performed to investigate its functional efficacy. The prevalence of thyroid dysfunction in COPD and its role in pulmonary cachexia has not been extensively studied. So far, there is no evidence that thyroid function is consistently altered in COPD, except perhaps in a subgroup of patients with severe hypoxaemia. Further research is required to more extensively study the underlying mechanisms and consequences of disturbed thyroid function in this subgroup of COPD patients. A few studies have reported the results of anabolic steroid supplementation in chronic obstructive pulmonary disease. Although some studies have discerned that low circulating levels of testosterone are common in males with chronic obstructive pulmonary disease, little is known about the prevalence, the underlying causes or functional consequences of hypogonadism in these patients. The use of systemic glucocorticosteroids and an influence of the systemic inflammatory response have been suggested as contributing to low testosterone levels. It can be hypothesised that low anabolic hormones will reduce muscle mass and eventually result in a diminished muscle function. Further evidence is required before testosterone replacement can be recommended for males with chronic obstructive pulmonary disease.

Previously we reported an impaired energy balance in patients with chronic obstructive pulmonary disease (COPD) during an acute disease exacerbation, but limited data are available on the underlying mechanisms. Experimental and clinical research supports the hypothesis of involvement of the hormone leptin in body weight and energy balance homeostasis. The aim of this study was to investigate the course of the energy balance in relation to leptin and the soluble tumor necrosis factor (TNF) receptors (sTNF-R) 55 and 75, plasma glucose, and serum insulin in patients with severe COPD during the first 7 d of hospitalization for an acute exacerbation (n = 17, 11 men, age mean [SD] 66 [10] yr, FEV(1) 36 [12] %pred). For reference values of the laboratory parameters, blood was collected from 23 (16 men) healthy, elderly subjects. On admission, the dietary intake/resting energy expenditure (REE) ratio was severely depressed (1.28 [0.57]), but gradually restored until Day 7 (1.65 [0. 45], p = 0.005 versus Day 1). Glucose and insulin concentrations were elevated on admission, but on Day 7 only plasma glucose was decreased. The sTNF-Rs were not different from healthy subjects and did not change. Plasma leptin, adjusted for fat mass expressed as percentage of body weight (%FM), was elevated on Day 1 compared with healthy subjects (1.82 [3.85] versus 0.32 [0.72] ng%/ml, p = 0.008), but decreased significantly until Day 7 (1.46 [3.77] ng%/ml, p = 0. 015 versus Day 1). On Day 7, sTNF-R55 was, independently of %FM, correlated with the natural logarithm (LN) of leptin (r = 0.65, p = 0.041) and with plasma glucose (r = 0.81, p = 0.015). In addition, the dietary intake/REE ratio was not only inversely related with LN leptin (-0.74, p = 0.037), but also with sTNF-R55 (r = -0.93, p = 0. 001) on day seven. In conclusion, temporary disturbances in the energy balance were seen during an acute exacerbation of COPD, related to increased leptin concentrations as well as to the systemic inflammatory response. Evidence was found that the elevated leptin concentrations were in turn under control of the systemic inflammatory response, and, presumably, the high-dose systemic glucocorticosteroid treatment.

Nutritional support can increase body weight and physiologic function in COPD, but there are some patients who do not respond to nutritional therapy. The aim of this prospective study was to describe the nonresponse to 8 wk of oral nutritional supplementation therapy (500 to 750 kcal/d extra), implemented in an inpatient pulmonary rehabilitation program, with respect to lung function, body composition, energy balance, and systemic inflammatory profile in 24 (16 male) depleted patients with COPD. On the basis of the weight change after 8 wk, patients were divided into three groups (Group 1: weight gain < 2% of baseline body weight, n = 5; Group 2: weight gain 2 to 5%, n = 9; Group 3: weight gain >/= 5%, n = 10). Although no differences were seen in lung function and body composition, Group 1 was characterized by older age, a lower baseline dietary intake/resting energy expenditure (REE) ratio, and a greater number of users of continuous supplemental oxygen when compared with Group 3. In addition, Group 1 exhibited higher baseline concentrations of fasting glucose and LPS-binding protein than did Groups 2 and 3. The concentrations of the soluble TNF- receptors 55 and 75 were elevated in Groups 1 and 2 when compared with Group 3. Furthermore, a significant, inverse correlation coefficient between baseline dietary intake and soluble intercellular adhesion molecule was revealed (r = -0.50, p = 0.016). On linear regression analysis, age, baseline intake/REE ratio, sTNF-receptor 55, and extracellular/intracellular water (ECW/ICW) ratio were selected as independent, significant parameters contributing to a total explained variation of 78% in weight change after nutritional therapy. In conclusion, nonresponse to nutritional therapy in COPD is associated with ageing, relative anorexia, and an elevated systemic inflammatory response. Further research is needed to investigate whether these factors contribute to eventual disturbances in intermediary metabolism as reflected by the increased glucose concentration and ECW/ICW ratio.

Chronic obstructive pulmonary disease (COPD) is a syndrome of chronic wasting, in part associated with a chronic inflammatory response. The aim of this study was to investigate cross-sectionally and prospectively the potential 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 concentrations of leptin and soluble tumor necrosis factor (TNF) receptors (sTNF-R) 55 and 75 by ELISA were measured in 27 male patients with emphysema and 15 male patients with chronic bronchitis (disease-subtype defined by high-resolution computed tomography [HRCT]). Emphysematous patients were characterized by a lower body mass index due to a lower fat mass (FM) (p = 0.001) and by lower mean (detectable) leptin concentrations (p = 0.020) compared with bronchitic 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). Furthermore, a significant partial correlation coefficient between leptin and sTNF-R55 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 emphysematous depleted male patients with COPD, baseline plasma leptin divided by FM was in addition logarithmically inversely related to baseline dietary intake (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 link in pulmonary cachexia may explain the poor response to nutritional support in some of the cachectic patients with COPD and may open a novel approach in combating this significant comorbidity in COPD. Schols AMWJ, Creutzberg EC, Buurman WA, Campfield LA, Saris WHM, Wouters EFM. Plasma leptin is related to proinflammatory status and dietary intake in patients with chronic obstructive pulmonary disease.

Anabolic steroids may be an additional mode of intervention to promote anabolism and improve clinical outcome in various acute and chronic wasting diseases. The present review discusses the rationale for anabolic steroid treatment in acute and chronic disease, their mechanistic actions, the available clinical trials in acute and chronic disease and their side-effects.