Search

Background: COPD is a chronic inflammatory disorder with high risk of cardiovascular morbidity and mortality. Adiponectin is a hormone that has anti inflammatory, antidiabetic, and anti atherogenic activities. We investigated the relationship of serum adiponectin to health outcomes in COPD.Methods: We measured adiponectin levels in serum samples from participants of the Lung Health Study, who were smokers with mild to moderate airflow limitation. We determined the relationship of serum adiponectin to hospitalization and mortality using a Cox proportional hazards model and to baseline lung function measurements and bronchial reactivity using multiple regression methods.Results: Serum adiponectin concentrations were inversely related to hospitalizations and mortality from coronary heart disease (hazard ratio [HR], 0.73; 95% CI, 0.62-0.86) and to cardiovascular disease (HR, 0.83; 95% CI, 0.73-0.94) and positively related to deaths from respiratory causes (HR, 2.09; 95% CI, 1.41-3.11). However, serum adiponectin concentrations were not significantly related to total mortality (HR, 1.10; 95% CI, 0.93-1.29) or cancer-related mortality(HR, 1.11; 95% CI, 0.92-1.34). Serum adiponectin concentrations were significantly related to increased bronchial reactivity and an accelerated decline in lung function (both P , .0001). Smoking status had no material influence on serum adiponectin concentrations.Conclusions: Adiponectin is a complex serum biomarker in COPD that is associated with decreased risk of cardiovascular events but increased risk of respiratory mortality. Because serum adiponectin is not significantly influenced by smoking status, it is a very promising biomarker of cardiovascular outcomes in COPD. [ABSTRACT FROM AUTHOR]

Background: Nearly 30% of all exacerbations of COPD do not have a clear etiology. Although pulmonary embolism (PE) can exacerbate respiratory symptoms such as dyspnea and chest pain, and COPD patients are at a high risk for PE due to a variety of factors including limited mobility, inflammation, and comorbidities, the prevalence of PE during exacerbations is uncertain.Methods: A systematic review of the literature was performed to determine the reported prevalence of PE in acute exacerbations of COPD in patients who did and did not require hospitalization. The literature search was performed using MEDLINE, CINAHL, and EMBASE, and complemented by hand searches of bibliographies. Only cross-sectional or prospective studies that used CT scanning or pulmonary angiography for PE diagnosis were included.Results: Of the 2,407 articles identified, 5 met the inclusion criteria (sample size, 550 patients). Overall, the prevalence of PE was 19.9% (95% confidence interval [CI], 6.7 to 33.0%; p = 0.014). In hospitalized patients, the prevalence was higher at 24.7% (95% CI, 17.9 to 31.4%; p = 0.001) than those who were evaluated in the emergency department (3.3%). Presenting symptoms and signs were similar between patients who did and did not have PE.Conclusions: One of four COPD patients who require hospitalization for an acute exacerbation may have PE. A diagnosis of PE should be considered in patients with exacerbation severe enough to warrant hospitalization, especially in those with an intermediate-to-high pretest probability of PE. [ABSTRACT FROM AUTHOR]

Background: Surfactant dysfunction has been implicated in both lung cancer and COPD. This study evaluated the relationship between surfactant protein D (SP-D) and the progression of bronchial dysplasia in heavy smokers.Methods: SP-D and oxidized glutathione levels were determined in samples of BAL fluid from 71 ex-smokers and current heavy smokers who participated in a lung cancer chemoprevention study with inhaled budesonide therapy. Bronchoscopy with biopsies was performed at baseline and was repeated at 6 months. The primary end point was the progression of bronchial dysplasia over 6 months.Results: Log-normalized SP-D levels in BAL fluid were significantly associated with the progression of bronchial dysplasia. A 1-U decrease in log-normalized SP-D levels at baseline was associated with a 3.2-fold increase (95% confidence interval, 1.24 to 8.26) in the risk for progression. Reduced FEV(1) also predicted the progression of bronchial dysplasia (p < 0.05). Additional reductions in BAL fluid SP-D levels over the 6 months further increased the risk of progression (odds ratio, 1.76 for a 1-U decrease in log-normalized SP-D levels in BAL fluid; p = 0.023). Thirty-seven percent of the variation in SP-D levels in BAL fluid was related positively to the subject's FEV(1)/FVC ratio, and inversely to their plasma C-reactive protein levels and number of pack-years of smoking.Conclusion: Reduced SP-D expression in BAL fluid was associated with the progression of bronchial dysplasia. SP-D levels in BAL fluid may serve as a potential biomarker to identify smokers who are at risk of early lung cancer. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular comorbidities have a negative impact on the health status and prognosis of patients with COPD. We determined whether nocturnal noninvasive (positive) mechanical ventilation (NIMV) can improve heart rate variability (HRV), decrease circulating natriuretic peptide levels, and improve functional performance of patients with very advanced COPD., Methods: A randomized, double-blind, parallel controlled trial was conducted in 23 participants with stable but advanced COPD. Participants received standard medical therapy plus nocturnal NIMV or standard medical therapy plus sham NIMV for 3 months., Results: After 3 months of NIMV therapy, the 24-h triangular interpolation of N-N intervals increased from 322 to 473 ms (p = 0.034), the 24-h HRV index (HRVI) increased from 21.8 to 29.9 ms (p = 0.035), nocturnal HRVI increased from 6.1 to 8.0 ms (p = 0.026), and the SD of the average N-N interval increased from 37 to 41 ms (p = 0.020). None of these indexes changed significantly in the control group. Additionally, compared with the control group, the pro-atrial natriuretic peptide levels declined significantly in the NIMV group (p = 0.013)., Conclusions: NIMV applied nocturnally over 3 months may improve HRV, reduce circulating natriuretic peptide levels, and enhance the functional performance of patients with advanced but stable COPD. While not definitive due to small sample size, these data suggest that nocturnal NIMV may reduce the impact of cardiac comorbidities in COPD patients.

Study Objectives: Conditions that give rise to reduced lung function are frequently associated with low-grade systemic inflammation, which may lead to poor cardiovascular outcomes. We sought to determine the relationship between reduced FEV1 and cardiovascular mortality, independent of smoking., Design: Longitudinal population-based study and a meta-analysis of literature., Setting: Representative sample of the general population., Participants: Participants of the first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study who were 40 to 60 years of age at baseline assessment (n = 1,861)., Measurements and Results: We compared the risk of cardiovascular mortality across quintiles of FEV1. Individuals in the lowest FEV1 quintile had the highest risk of cardiovascular mortality (relative risk [RR], 3.36; 95% confidence interval [CI], 1.54 to 7.34). Compared to FEV1 quintile 1, individuals in quintile 5 had a fivefold increase in the risk of death from ischemic heart disease (RR, 5.65; 95% CI, 2.26 to 14.13). We also performed a systematic review of large cohort studies (> 500 participants) that reported on the relationship between FEV1 and cardiovascular mortality (12 studies; n = 83,880 participants). Compared to participants in the highest FEV1 category, those with reduced FEV1 had a higher risk of cardiovascular mortality (pooled RR, 1.77; 95% CI, 1.56 to 1.97)., Conclusions: There is strong epidemiologic evidence to indicate that reduced FEV1 is a marker for cardiovascular mortality independent of age, gender, and smoking history.

Background: Low-grade systemic inflammation is commonly observed in conditions associated with reduced FEV(1). Active cigarette smoking, which is a leading risk factor for decreased FEV(1), can also independently induce systemic inflammation., Study Objectives: To determine the independent contributions of active cigarette smoking and reduced FEV(1) (as well as their potential interactions) on systemic inflammation., Design: Cross-sectional survey., Setting: The US general population., Participants: A total of 7,685 adult participants, >/= 40 years of age, in the Third National Health and Nutrition Examination Survey, who had acceptable data on spirometry and laboratory measurements such as serum C-reactive protein (CRP)., Measurements: The participants were stratified into four equal groups (quartiles) based on the percent predicted FEV(1) values. Each group was further categorized as active smokers or nonsmokers according to serum cotinine level (ie, >/= 10 or < 10 ng/mL). Serum levels of CRP, plasma fibrinogen, blood leukocytes, and platelets were compared across the predicted FEV(1) quartile groups and across smoking status using multiple logistic regression models., Results: We found that active smoking by itself increased the odds of having elevated CRP levels by 63% (adjusted odds ratio [OR], 1.63; 95% confidence interval, 1.28 to 2.09). The adjusted OR for reduced FEV(1) was 2.27 (95% confidence interval, 1.92 to 2.70). Having both risk factors increased the OR to 3.31 (95% confidence interval, 2.73 to 4.02). Similar findings were observed for blood leukocytes and plasma fibrinogen., Conclusion: These findings suggest an additive effect of active smoking and reduced FEV(1) on markers of systemic inflammation and suggest their potential interactions in the pathogenesis of systemic complications observed in patients with poor lung function.

Study Objective: Children from poor families are much more likely to have emergency visits for asthma than those from nonpoor families, which may be related to financial access barriers to good preventive care for the poor. We sought to determine whether in a health-care system that provides free access to outpatient and hospital services, the disparities in the rates of emergency visits for asthma would be less apparent across the income gradient., Design: Longitudinal, population-based study., Setting: Alberta, Canada., Participants: All children born in Alberta, Canada between 1985 and 1988 (n = 90,845) were classified into three mutually exclusive groups based on the reported annual income of their parents from the previous year: very poor, poor, and nonpoor groups., Measurements and Results: We compared the relative risk (RR) of emergency visits for childhood asthma among children of very poor, poor, and nonpoor families using a Cox proportional hazard model during a 10-year follow-up. We found that the very poor children were 23% more likely to have had an emergency visit for asthma than those from nonpoor families (RR, 1.23; 95% confidence interval [CI], 1.14 to 1.33), adjusted for a variety of factors. The poor group, however, had a similar risk of asthma emergency visits as the nonpoor group (RR, 0.97; 95% CI, 0.91 to 1.04). The average number of office visits for asthma was similar between the very poor and nonpoor groups., Conclusions: In a setting of universal access to health care, children of poor and nonpoor families had similar rates of asthma emergency visits; the very poor children, however, continued to experience an excess risk. These findings suggest that a universal health-care system can reduce, but not fully eliminate, the disparities in emergency utilization of asthma across income categories.

Background: Aboriginals in Canada bear a disproportionately higher burden of some chronic illnesses than nonaboriginals. Although there is a greater prevalence of smoking, poor housing, and overcrowding in aboriginal than nonaboriginal communities, the rates of office and emergency visits for asthma and COPD among aboriginals are not well known., Study Objective: To determine whether aboriginals require higher rates of asthma and COPD emergency and office visits than nonaboriginals., Setting: Population-based cohort of people residing in Alberta, Canada (population 2.8 million) between April 1, 1996, and March 31, 1997., Design: Retrospective cohort study., Results: We observed that aboriginals were 2.1 times (95% confidence interval [CI], 2.0 to 2.2) and 1.6 times (95% CI, 1.6 to 1.6) more likely to have an emergency and office visit for asthma or COPD, respectively, when compared to age-matched and sex-matched nonaboriginals. However, they were 55% (95% CI, 52 to 58%) less likely to see a specialist and 66% (95% CI, 63 to 70%) less likely to undergo spirometry than nonaboriginals., Conclusions: These findings indicate that aboriginals bear a disproportionately higher burden of asthma and COPD than nonaboriginals. However, lower use of spirometry and specialist services suggests that there might be access barriers to quality health care for aboriginals in Canada.

Two patients with progressive sarcoidosis who had poor responses and side effects from corticosteroid therapy were treated with cyclosporine. Cyclosporine suppressed conventional markers of inflammation and there was clinical improvement in one patient, but the disease recurred when therapy was discontinued. The second patient who had diabetes mellitus developed unstable glucose metabolism when given cyclosporine. This unstable diabetes mellitus together with side effects of nausea and vomiting resulted in weight loss and inadequate serum therapeutic levels that was associated with a poor therapeutic response to the cyclosporine. The major side effects in both patients were headache and gastrointestinal symptoms, but there was no renal dysfunction. We conclude that while corticosteroids remain the mainstay of sarcoid therapy, when these drugs have not been successful for the skin manifestations of the disease, a trial of cyclosporine may be justified.