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1.
Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. Tobacco smoking is established as a major risk factor, but emerging evidence suggests that other risk factors are important, especially in developing countries. An estimated 25–45% of patients with COPD have never smoked; the burden of non-smoking COPD is therefore much higher than previously believed. About 3 billion people, half the worldwide population, are exposed to smoke from biomass fuel compared with 1·01 billion people who smoke tobacco, which suggests that exposure to biomass smoke might be the biggest risk factor for COPD globally. We review the evidence for the association of COPD with biomass fuel, occupational exposure to dusts and gases, history of pulmonary tuberculosis, chronic asthma, respiratory-tract infections during childhood, outdoor air pollution, and poor socioeconomic status. 相似文献
2.
Chronic obstructive pulmonary disease (COPD) is an increasing cause of morbidity and mortality worldwide, and it has been strongly correlated to tobacco smoking. While a number of studies have concentrated on smokers only, recent published data demonstrate that at least one fourth of patients with COPD are non-smokers, and that the burden of COPD in non-smokers is also higher than previously believed. Risk factors of COPD in non-smokers may include genetic factors, long-standing asthma, outdoor air pollution (from traffic and other sources), environmental smoke exposure (ETS), biomass smoke, occupational exposure, diet, recurrent respiratory infection in early childhood, tuberculosis and so on. In Asian region, indoor/outdoor air pollution and poor socioeconomic status may play important roles in the pathogenesis of non-smoking-related COPD. The prevalence of COPD among never smokers varies widely across nations. Such a variation may arise from several aspects, including study design, definition of COPD, diagnostic criteria, age and gender distribution of the studied population, local risk factors and socioeconomic status. More investigations and efforts are required to elucidate the involved factors and their shared contributions to non-smoking-related COPD so as to achieve better estimation and reduction of the burden of this neglected entity worldwide. 相似文献
3.
BACKGROUND AND OBJECTIVE: Although the association between COPD and smoking status (non-smoking, ex-smoking and current smoking) and indoor air pollution in Chinese populations is well established, the link between COPD and the number of cigarettes smoked has not been examined. This study investigated the relationship between the total amount of cigarettes smoked (TACS) and indoor air pollution, with the risk of COPD among urban and rural Chinese adults. METHODS: A nested case-control study was performed using data collected in a large community survey (N = 29 319) conducted between October 2000 and March 2001 in Nanjing, China. The exposure to indoor respiratory pollutants of cooking and heating materials and to passive cigarette smoke was compared in patients diagnosed with COPD (n = 1743) and controls matched for age, gender and residence (n = 1743). RESULTS: The smoking rate among COPD patients was significantly higher than that among the controls. After controlling for possible confounders, the adjusted odds ratios for COPD increased across TACS tertiles: from lower (OR = 1.40, 95% confidence interval (CI): 1.09-1.79), to middle (OR = 1.55, 95% CI: 1.21-1.99), and upper (OR = 1.77, 95% CI: 1.37-2.29). Among smokers, women were significantly more likely to develop COPD than men (OR = 1.20, 95% CI: 1.02-1.41). There were no significant associations between COPD and domestic fuels used, kitchen ventilation or passive smoking. Heating in winter with coal was weakly but positively linked with COPD among non-smokers overall, among women non-smokers, and specifically for women living in urban as well as rural areas. CONCLUSIONS: A clear dose-response relationship exists between cigarette smoking and COPD; compared with men, women smokers were more susceptible to COPD. Exposure to other respiratory pollutants in the home was not significantly associated with the diagnosis of COPD. 相似文献
4.
W K Lam N W White M M Chan-Yeung 《The international journal of tuberculosis and lung disease》2004,8(9):1045-1057
In industrialised countries, lung cancer is the most common form of cancer among males and it is growing among females. For both sexes, rates reflect smoking behaviours. The pattern appears to be different in Asia, particularly in China, where lung cancer rates in men reflect high smoking rates but high rates among non-smoking women appear to be related to other factors. The incidence of lung cancer is low in most African countries, but it is increasing. In addition to tobacco smoking, a number of etiological factors have been identified for lung cancer: indoor exposure to environmental tobacco smoke, cooking oil vapour, coal burning, or radon, outdoor air pollution and occupational exposure to asbestos and other carcinogens. Recent studies have shown that dietary factors may be important, with high consumption of vegetables and fruits being protective while preserved food and fatty food are harmful, and certain infections such as Mycobacterium tuberculosis, human papilloma virus and Microsporum canis are associated with a high risk of lung cancer. Among non-smokers, the probable role of genetic predisposition in lung cancer by increasing the individual's susceptibility to environmental carcinogens is currently being studied actively. As the single most important cause for lung cancer is tobacco smoke and, with increased sales, a major epidemic is predicted for both Asia and Africa, all health care professionals, government health authorities and national and international health organisations must join in a concerted effort against tobacco. 相似文献
5.
Epidemiology of chronic obstructive pulmonary disease. 总被引:3,自引:0,他引:3
Chronic obstructive pulmonary disease (COPD) is a leading cause of world-wide mortality and disability. On average approximately 5-15% of adults in industrialized countries have COPD defined by spirometry. In 1990, COPD was considered to be at the twelfth position world-wide as a cause of combined mortality and disability but is expected to become the fifth cause by the year 2020. COPD has a chronic long-lasting course characterized by irreversible decline of forced expiratory volume in one second (FEV1), increasing presence of dyspnoea and other respiratory symptoms, and progressive deterioration of health status. After diagnosis the 10-yr survival rate is approximately 50% with more than one-third of patients dying due to respiratory insufficiency. Several environmental exposures such as air pollution increase the risk of death in COPD patients. The aetiology of COPD is overwhelmingly dominated by smoking although many other factors could play a role. Particular genetic variants are likely to increase the susceptibility to environmental factors although little is known about which are the relevant genes. There is clear evidence about the role of the alpha-1-antitrypsin but the fraction of COPD attributable to the relevant variants is only 1%. Phenotypic traits that are considered to play a role in the development of COPD include sex, with females being at a higher risk, bronchial responsiveness and atopy. There is strong causal evidence regarding the relationship between smoking and COPD with decline in FEVI levelling off after smoking cessation. Passive smoking has been found to be associated with a small though statistically significant decline in FEV1. Other risk factors that are likely to be relevant in the development of COPD are occupation, low socioeconomic status, diet and possibly some environmental exposures in early life. Although there is accumulating evidence that oxygen therapy, pharmacological treatment and rehabilitation may improve the course of chronic obstructive pulmonary disease, preventing smoking continues to be the most relevant measure, not only to prevent chronic obstructive pulmonary disease, but also to arrest its development. 相似文献
6.
Significant cardiac morbidity and mortality exists in patients with COPD. Shared risk factors include age, smoking history and exposure to air pollution and passive smoke. Although the inappropriate under-prescribing of β-blockers contributes, it is now appreciated that the observed cardiac risk is not only due to smoking and conventional cardiovascular risk factors, but also other independent factors. A number of hypotheses exist for the increased cardiovascular morbidity and mortality seen in COPD including inflammation, pulmonary hypertension, lung hyperinflation and shared genetics models. Mounting evidence from large randomised controlled trials suggests that COPD treatment may be cardio-protective. We review the current evidence supporting the aforementioned hypotheses and how their modulation may prevent cardiovascular morbidity and mortality in COPD. The persisting underdiagnosis of COPD may have significant consequences. Further mechanistic studies identifying the onset and impact of individual interventions will develop our understanding of this emerging and highly relevant clinical field. 相似文献
7.
Alessia Comandini Paola Rogliani Alfredo Nunziata Mario Cazzola Giacomo Curradi Cesare Saltini 《Respiratory medicine》2009,103(11):1592-1613
Cigarette smoking has been causally linked several diseases, primarily lung cancer and chronic obstructive lung disease (COPD). The diagnosis of COPD currently involves an assessment of smoking and/or occupational exposures, a history of cough, sputum and dyspnea and spirometric measures of airflow obstruction and since spirometric measures take long follow up times to detect significant changes, surrogate measures of outcome capable of predicting long-term health changes have been sought for. These include biomarkers of oxidative stress, inflammation and tissue damage in sputum, bronchoalveolar lavage, exhaled breath and serum. Published biomarker studies have not always accurately compared patients with COPD with age-matched cigarette smokers and non-smoking normal subjects without significant airflow limitation, also comparable for other exposures. Consequently, the interpretation of biomarker association studies is somewhat difficult. The purpose of this narrative review is to summarize publications reporting cellular, soluble or volatile marker of obstructive lung disease in populations of healthy non-smokers and healthy smokers, in order to determine whether the biomarkers examined could be specifically associated with exposure to tobacco smoke rather than with inflammation and airway hyper-reactivity. As induced sputum has been the most widely used investigative tool, this review has been aimed at assessing induced sputum biomarkers, referring to lung biopsy, bronchoalveolar lavage and exhaled breath markers as supporting evidence for biomarkers associations identified with induced sputum studies. 相似文献
8.
AIMS: The objectives of this study are to identify the relationship between ethnic identity and tobacco use, and to examine the mediating effects of peer and sibling smoking and acculturation. DESIGN AND MEASUREMENTS: Data were drawn from a cross-sectional survey of 3400 Toronto students, sampled from 30 schools between 1998 and 2000. Primary ethnic identity was based on adolescents' self-identification of their ethnic heritage condensed to 12 groups for analysis. Tobacco use was measured as a dichotomy, predicting non-smoking in the past year. Multivariate logistic regression models were employed to test for baseline differences in non-smoking by ethnic identity. Subsequent models adjusted for controls (age, gender, social class, religious attendance, educational achievement) and introduced mediators. FINDINGS: Results indicated that smoking varied among adolescents of differing ethnic identities. Adolescents of western European, eastern European and southern European ethnicity were considerably less likely to be non-smokers, while Chinese, South Asian and East Indian and West Indian youth were more inclined to be non-smokers. The discrepancies in rates of non-smoking among western European and South Asian and East Indian adolescents were explained by a combination of peer and sibling smoking and acculturation; among southern European and eastern European youth via peer and sibling smoking; and by neither peer and sibling smoking nor acculturation for Chinese and West Indian youth. CONCLUSIONS: This paper demonstrates that disparities in tobacco use among certain ethnic groups can be explained by peer and sibling smoking and acculturation; however, for other ethnic groups, knowledge of the processes that account for differences in tobacco use remains less clear. 相似文献
9.
Magnesium is one of the most important factors for regulation of inflammatory response as well as muscle function, and COPD is a multicomponent disease characterized by abnormal inflammatory response of the lungs with systemic muscle dysfunction. Because polymorphonuclear (PMN) cells are significantly represented in the pathogenesis of COPD, concentrations of total (tMg) and ionised magnesium (iMg) were determined in plasma and isolated PMN cells in 46 patients in stable phase of COPD (past smokers, current smokers, and non-smokers), 24 healthy smokers and 37 healthy non-smokers. In the same samples concentrations of total (tCa) and ionised calcium (iCa) were determined, due to the antagonism of magnesium towards calcium. We found decreased biological active iMg in PMN compared to the group of healthy non-smokers (5.42, 1.98-17.31 micromol/10(9) cells vs. 7.50, 3.27-15.15 micromol/10(9) cells, p < 0.05). In the plasma and isolated PMN of the patients the ratio of total calcium/total magnesium (tCa/tMg) was significantly increased (2.89, 2.15-3.86 and 1.19, 0.07-9.87) compared to the group of healthy non-smokers (2.65, 2.19-3.44 and 0.67, 0.14-2.40, p < 0.05) and to the group of healthy smokers (2.58, 2.26-3.24 and 0.66, 0.14-2.85, p < 0.05). In the group of patients the concentration of tCa was significantly increased in all samples compared to the healthy group of non-smokers and healthy smokers. The results of univariant logistic regression analysis for smoking, concentration of tCa and ratio of tCa/tMg in PMN showed high odds ratio for COPD status. These results raise a possibility that intracellular polymorphonuclear value of magnesium could be a distinctive marker for COPD risk disclosure among smokers. 相似文献
10.
In 1986, a random sample of 400 males was examined at one of the Moscow enterprises. A registry developed at the enterprise was used to study risk factors for coronary heart disease such as arterial hypertension, smoking, obesity, and morbidity accompanied by temporary disability in 1986. The analysis showed that the major CHD risk factors: smoking, arterial hypertension, and obesity were significantly related to temporary disability parameters. The more "limited" criteria for hypertension, the closer relationship was to temporary disability in terms of both cardiovascular and other diseases. With these diseases, disability parameters in cases and days per 100 workers were significantly higher in smokers and ex-smokers than in non-smokers. The most relative risk for temporary disability was found in the ex-smokers as compared to smokers and non-smokers. The subjects with obesity were demonstrated to be at higher risk for temporary disability due to cardiovascular disease than those without it. No relation was found between temporary disability parameters and obesity for total morbidity. 相似文献
11.
BACKGROUND: The imbalance between oxidants and antioxidants is thought to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). METHODS: Biomarkers of lipid oxidation such as thiobarbituric reactive substances (TBARs), total reduced glutathione (GSH) were estimated in chronic smokers with and without COPD, and non-smokers. RESULTS: The following subjects (all males) were studied: (i) chronic smokers (32.5 +/- 8.6 pack years) with stable COPD (n = 20; mean age 47.2 +/- 7.8 years); (ii) chronic smokers (6.3 +/- 1.9 pack years) without COPD (n = 20; mean age 35.3 +/- 4.5 years); and (iii) non-smokers (n = 20; mean age 37.5 +/- 5.5 years). The mean TBARs levels (nmol of malondialdehyde per ml of plasma) were higher among smokers with COPD (5.72 +/- 1.02) when compared with smokers without COPD (4.85 +/- 0.97) and non-smokers (2.58 +/- 0.56) (p < 0.001). The mean GSH levels (micromol/mg of protein) were significantly higher in non-smokers (0.163 +/- 0.113) compared to smokers with COPD (0.083 +/- 0.05) and those without COPD (0.050 +/- 0.051) (p < 0.001). There was no statistically significant difference in the plasma GSH levels among smokers with and without COPD (p > 0.05). CONCLUSIONS: Our observations demonstrate increased lipid peroxidation because of oxidative stress due to smoking. 相似文献
12.
Tatlicioğlu T 《Tüberküloz ve toraks》2007,55(3):303-318
Chronic obstructive pulmonary disease (COPD) is an important health problem in all countries of the world with its high and steadily increasing mortality, morbidity and prevalence. The disease has long been ignored due to the fact that smoking which is known as an important factor in the development of the disease could not be taken under control throughout the world and due to misperceptions that the disease is progressive and irreversible. In recent years with the understanding that COPD is a global health problem and that it creates increasing socioeconomic burden, the disease became the focus of scientific circles and pharmaceutical industry. Together with better understanding of the disease and the significant advances in its treatment, COPD patients are being approached more optimistically, while the disease is being defined and treated more comprehensively. Yet, it is a fact that COPD has not yet been fully understood and discussions regarding how to define and treat the disease are ongoing. Our knowledge about the risk factors other than smoking responsible from development of COPD, the pathogenesis of the disease, its clinical course, phenotypes, comorbidities and treatment is limited. Currently we have important advances in the treatment of COPD such as the use of long acting anticholinergics and beta- 2-agonists, inhaled steroids and non-pharmaceutical treatments like pulmonary rehabilitation that have to be in use throughout the life time of the patient as main components of therapy. However, in response to severe socioeconomic burden of the disease, in addition to using the available treatment options in full scope there needs to be new therapeutic possibilities that could modify the disease course as well as more effective smoking cessation strategies. We also need new and effective paradigms while trying to understand the pathobiology and the clinical course of COPD and evaluating the benefits of treatment approaches. In future, the development of new treatment paradigms that can make comprehensive use of our knowledge about COPD pathophysiology will gain utmost importance. Thus, the disease will be better treated while treatment effects will be better assessed. 相似文献
13.
Lindberg A Bjerg A Bjerg-Bäcklund A Rönmark E Larsson LG Lundbäck B 《Respiratory medicine》2006,100(2):264-272
BACKGROUND: There is a lack of epidemiological data on COPD by disease severity. We have estimated the prevalence and underdiagnosis of COPD by disease severity defined by the British Thoracic Society (BTS) and Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. The impact of smoking was evaluated by the population attributable fraction of smoking in COPD. METHODS: A random sample of 1500 responders of the third postal survey performed in 1996 of the Obstructive Lung Disease in Northern Sweden (OLIN) Studies' first cohort (6610 subjects recruited in 1985) were invited to structured interview and spirometry. One thousand two hundred and thirty-seven subjects (82%) performed spirometry. RESULTS: The prevalence of mild BTS-COPD was 5.3%, moderate 2.2%, and severe 0.6% (GOLD-COPD: mild 8.2%, moderate 5.3%, severe 0.7%, and very severe 0.1%). All subjects with severe COPD were symptomatic, corresponding figures among mild COPD were 88% and 70% (BTS and GOLD), Subjects with severe BTS-COPD reported a physician-diagnosis consistent with COPD in 50% of cases, in mild BTS-COPD 19%, while in mild GOLD-COPD only 5% of cases. The major risk factors, age and smoking, had a synergistic effect on the COPD-prevalence. The Odds Ratio (OR) for having COPD among smokers aged 76-77 years was 59 and 34 (BTS and GOLD) when non-smokers aged 46-47 was used as reference population. CONCLUSIONS: Most subjects with COPD have a mild disease. The underdiagnosis is related to disease-severity. Though being symptomatic, only a half of the subjects with severe COPD are properly labelled. Smoking and increasing age were the major risk factors and acted synergistic. 相似文献
14.
Chronic obstructive pulmonary disease (COPD) is a major cause of chronic morbidity and mortality and represents a substantial economic and social burden throughout the world. It is the fifth leading cause of death worldwide and further increases in its prevalence and mortality are expected in the coming decades. The substantial morbidity associated with COPD is often underestimated by health-care providers and patients; likewise, COPD is frequently underdiagnosed and undertreated. COPD develops earlier in life than is usually believed. Tobacco smoking is by far the major risk for COPD and the prevalence of the disease in different countries is related to rates of smoking and time of introduction of cigarette smoking. Contribution of occupational risk factors is quite small, but may vary depending on a country's level of economic development. Severe deficiency for alpha-1-antitrypsin is rare and the impact of other genetic factors on the prevalence of COPD has not been established. COPD should be considered in any patient presenting with cough, sputum production, or dyspnoea, especially if an exposure to risk factors for the disease has been present. Clinical diagnosis needs to be confirmed by standardised spirometric tests in the presence of not-fully-reversible airflow limitation. COPD is generally a progressive disease. Continued exposure to noxious agents promotes a more rapid decline in lung function and increases the risk for repeated exacerbations. Smoking cessation is the only intervention shown to slow the decline. If exposure is stopped, the disease may still progress due to the decline in lung function that normally occurs with aging, and some persistence of the inflammatory response. 相似文献
15.
This review critically evaluates the recent scientific literature relevant to occupational risk factors for chronic obstructive pulmonary disease (COPD) and chronic bronchitis. The 2003 American Thoracic Society statement on the occupational contribution to the burden of airway disease synthesized relevant data on this topic through 1999. Since 2000, 14 separate studies have published values or provide data that allow estimation of the population attributable risk per cent (PAR%) for the proportion of chronic bronchitis or COPD due to work-related factors. Based on data since 2000, the median PAR% value for both chronic bronchitis and COPD is 15%. A number of additional studies have been published that underscore the association between specific occupational exposures and airflow obstruction. In addition, data are emerging that indicate the extent to which COPD is a cause of work disability; limited data raise the possibility that among those with occupational COPD, disability may be even more prominent. This review supports previous analyses concluding that there is a causal association between work-related exposures and COPD. 相似文献
16.
COPD is characterized by a poorly reversible airflow limitation resulting from chronic inflammation, mainly due to tobacco exposure. Over the past few years, the understanding of COPD has evolved from it being a disease affecting the lungs to it being a complex, heterogeneous, and generalized disorder in an aging population. Extrapulmonary comorbidities significantly complicate the management and influence the prognosis of patients with COPD. Although certain comorbidities like cardiovascular diseases share some risk factors with COPD, such as cigarette smoking, other frequently observed comorbidities, including musculoskeletal wasting, metabolic syndrome, and depression, cannot be easily attributed to smoking. There is increasing evidence that chronic inflammation is a key factor in COPD and that inflammation might be the common pathway linking these comorbidities and explaining why they typically develop together. Physicians treating patients with COPD need to become aware of these extrapulmonary aspects. Any patient with COPD should be carefully evaluated for comorbidities and the systemic consequences of COPD since they not only influence the prognosis but also have an impact on disease management. The treatment of COPD is no longer focused exclusively on inhaled therapy but is taking on a multidimensional approach, especially because the treatment of the comorbidities might positively affect the course of COPD itself. 相似文献
17.
The Norwegian Multicenter Group Study noted the effect of smoking habits before and after myocardial infarction and their relation to mortality and reinfarction rate after treatment with timolol in patients surviving acute myocardial infarction. The mean follow up period was 17.3 (range 12-33) months. No relation was found between initial smoking habits and risk category after infarction or between initial smoking habits and later outcome. At the time of their first infarct smokers were seven years younger than non-smokers. One moth after infarction nearly 60% of the smokers had stopped smoking completely. A significantly lower incidence of early cardiac death and lower total mortality was found in patients treated with timolol in both those who continued smoking and in the combined non-smoking groups and a significantly lower reinfarction rate among non-smokers. Cessation of smoking alone was associated with a reduced reinfarction rate by 45% but a non-significant reduction in mortality by 26%. It is concluded that treatment with timolol and cessation of smoking have an additive effect in reducing mortality and reinfarction rate after myocardial infarction. 相似文献
18.
Cardiovascular disease (CVD) contributes significantly to morbidity and mortality in COPD. There is a high prevalence of traditional risk factors in this patient group including smoking, sedentary behaviour and low socio-economic class. However, large studies have shown that airflow limitation is an independent risk factor for CVD. Therefore there may be a 'COPD effect' that contributes to CVD in this condition, adding to the body of evidence that COPD has important systemic consequences, as well as being a lung disease. In this article, we review the evidence for CVD in COPD. Next, we examine systemic factors present in COPD, and link these to the pathogenesis of atherosclerosis, including inflammation, oxidative stress and hypoxia. Finally, we review those studies that have investigated therapeutic interventions in COPD that may modify cardiovascular risk. 相似文献
19.
Effect of smoking habits and timolol treatment on mortality and reinfarction in patients surviving acute myocardial infarction.
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The Norwegian Multicenter Group Study noted the effect of smoking habits before and after myocardial infarction and their relation to mortality and reinfarction rate after treatment with timolol in patients surviving acute myocardial infarction. The mean follow up period was 17.3 (range 12-33) months. No relation was found between initial smoking habits and risk category after infarction or between initial smoking habits and later outcome. At the time of their first infarct smokers were seven years younger than non-smokers. One moth after infarction nearly 60% of the smokers had stopped smoking completely. A significantly lower incidence of early cardiac death and lower total mortality was found in patients treated with timolol in both those who continued smoking and in the combined non-smoking groups and a significantly lower reinfarction rate among non-smokers. Cessation of smoking alone was associated with a reduced reinfarction rate by 45% but a non-significant reduction in mortality by 26%. It is concluded that treatment with timolol and cessation of smoking have an additive effect in reducing mortality and reinfarction rate after myocardial infarction. 相似文献
20.
Hunninghake DB 《Proceedings of the American Thoracic Society》2005,2(1):44-49
Smoking is a major cause of chronic obstructive pulmonary disease (COPD) and cardiovascular disorders, including coronary heart disease (CHD) and peripheral arterial disease. Smoking-induced inflammation and other risk factors like dyslipidemia cause vascular endothelial damage via oxidative stress, and a vicious cycle with the characteristics of atherosclerosis ensues. Inflammatory cytokines stimulate hepatic acute-phase protein production, and C-reactive protein is now used widely to assess inflammation in the arterial wall. Smoking is associated with many alterations in lipids and lipoproteins, and is also prothrombotic. Global risk assessment, which determines the absolute risk for developing CHD in 10 years, is used widely to determine who should receive lipid-lowering therapy. Major CHD risk factors include age, sex, smoking, blood pressure, lipoproteins, and cholesterol, but COPD is not among them. Future studies should determine the absolute risk for developing CHD in patients with COPD. The 3-hydroxy-3-methylglutaryl coenzyme-A reductase inhibitors (statins) are used widely to treat and prevent cardiovascular disease. The statins may also produce other beneficial pleiotropic effects, including increased nitric oxide and prostacyclin, antithrombosis, and decreased inflammation, perhaps indicating utility in the therapy for COPD. Efforts are currently underway to determine if such antiinflammatory effects are independent of or in addition to simply lowering low-density lipoprotein cholesterol. 相似文献