Bronchodilator responsiveness has been associated with a subsequent accelerated decline in forced expiratory volume in one second (FEV1). Therefore, bronchodilator responsiveness and total serum immunoglobulin E(IgE) levels were assessed in 184 adult first-degree relatives of probands with severe early-onset chronic obstructive pulmonary disease (COPD) and a control group.Greater bronchodilator responsiveness was found among current smokers or exsmokers who were first-degree relatives of early-onset COPD probands than in currently or exsmoking controls, expressed as increase in FEV1 as a percentage of baseline (5.88.1 versus 2.95.1%, p<0.01), absolute increase in FEV1 from baseline (120130 versus 60110 mL, p<0.05), and increase in FEV1 as a percentage of the predicted value (3.64.1 versus 2.23.9%, p<0.05). However, elevated total serum IgE levels were not found in first-degree relatives of early-onset COPD probands compared with control subjects.The increased bronchodilator responsiveness among currently smoking/exsmoking first-degree relatives of early-onset COPD probands suggests that these individuals may have enhanced susceptibility to the detrimental effects of cigarette smoking. Eur Respir J 1999; 14: 1009±1014. Chronic obstructive pulmonary disease (COPD), the fourth leading cause of death in the USA [1, 2] and a growing international problem, is strongly associated with cigarette smoking [3]. Even though tobacco use is a well-known risk factor for COPD [4], the development of airflow obstruction in response to smoking is highly variable [5], and it has been postulated that individuals may vary in their genetic susceptibility to COPD [3]. In a previous report on individuals without severe a 1 -antitrypsin deficiency, increased risk of airflow obstruction and chronic bronchitis was found in current smokers and exsmokers who were first-degree relatives of probands with severe early-onset COPD, compared with appropriate control subjects [6]. Thus, the findings of the authors and others [7±13] suggest that familial factors, probably genetic, contribute to the development of COPD.Bronchodilator responsiveness, a physiological response that differs from airway responsiveness to bronchoconstrictors, has been associated with a subsequent accelerated decline in forced expiratory volume in one second (FEV1) [14±17]. Thus, bronchodilator responsiveness may be associated with an increased risk of either acquiring COPD or developing the disease at an earlier age in susceptible individuals who smoke.Higher total serum immunoglobulin E (IgE) levels have previously been demonstrated in first degree relatives of PI Z subjects with COPD than in first-degree relatives of PI Z subjects without COPD [18]. This report presents a comparison of bronchodilator responsiveness and total serum IgE levels in 184 adult first-degree relatives of 44 probands with severe early-onset COPD (without severe a 1 -antitrypsin deficiency) and 83 adult control subjects. Methods Study participantsThe screening and enrolment procedures ...
Change in airway responsiveness is used frequently as a clinical as well as an epidemiological tool. Changes in airway responsiveness can be superior to other measures of lung function in that they are more sensitive indicators of an environmental effect. However, normal variation in test results must be defined before change can be interpreted.To characterize annual variability in airways responsiveness, we administered a high-dose methacholine challenge at 1 yr intervals for up to 4 yrs to 105 healthy, nonasthmatic working subjects. Using this high-dose protocol, the majority of tests (83%) produced at least a 20% fall in forced expiratory volume in one second (FEV1), allowing standard calculation of the provocative dose of methacholine causing a 20% fall in FEV1 (PD20).An annual change in methacholine responsiveness by one or more doubling doses was seen in at least 30% of subjects each year. The components of variance of airways responsiveness measures were estimated to allow direct comparison of within-subject and between-subject variability. The within-subject variability in PD20, was markedly greater than the comparable within-subject variability in FEV1. Level of FEV1 and age were both significant determinants of methacholine responsiveness. Comparison of two methods of expressing methacholine responsiveness (PD20 using the full challenge up to 250 mg·mL -1 methacholine, and the dose-response slope using data up to 32 mg·mL -1 methacholine as the maximum dose) had similar annual variability in censored data and mixed-effects models. We then developed an approach to statistical analysis of "right-censored" methacholine challenge data using a maximum likelihood estimation under a censored Gaussian model. These studies of methacholine responsiveness provide normative data on annual test variability in healthy, nonasthmatic working adults, and show that a shorter low-dose challenge has comparable annual variability to a lengthier high-dose challenge.
Background: Weight loss reduces body fat and lean mass, but whether these changes are influenced by macronutrient composition of the diet is unclear. Objective: We determined whether energy-reduced diets that emphasize fat, protein, or carbohydrate differentially reduce total, visceral, or hepatic fat or preserve lean mass. Design: In a subset of participants in a randomized trial of 4 weightloss diets, body fat and lean mass (n = 424; by using dual-energy X-ray absorptiometry) and abdominal and hepatic fat (n = 165; by using computed tomography) were measured after 6 mo and 2 y. Changes from baseline were compared between assigned amounts of protein (25% compared with 15%) and fat (40% compared with 20%) and across 4 carbohydrate amounts (35% through 65%). Results: At 6 mo, participants lost a mean (6SEM) of 4.2 6 0.3 kg (12.4%) fat and 2.1 6 0.3 kg (3.5%) lean mass (both P , 0.0001 compared with baseline values), with no differences between 25% and 15% protein (P 0.10), 40% and 20% fat (P 0.34), or 65% and 35% carbohydrate (P 0.27). Participants lost 2.3 6 0.2 kg (13.8%) abdominal fat: 1.5 6 0.2 kg (13.6%) subcutaneous fat and 0.9 6 0.1 kg (16.1%) visceral fat (all P , 0.0001 compared with baseline values), with no differences between the diets (P 0.29). Women lost more visceral fat than did men relative to total-body fat loss. Participants regained ;40% of these losses by 2 y, with no differences between diets (P 0.23). Weight loss reduced hepatic fat, but there were no differences between groups (P 0.28). Dietary goals were not fully met; self-reported contrasts were closer to 2% protein, 8% fat, and 14% carbohydrate at 6 mo and 1%, 7%, and 10%, respectively, at 2 y. Conclusion: Participants lost more fat than lean mass after consumption of all diets, with no differences in changes in body composition, abdominal fat, or hepatic fat between assigned macronutrient amounts. This trial was registered at clinicaltrials.gov as NCT00072995.Am J Clin Nutr 2012;95:614-25.
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