Osteoporosis in chronic obstructive pulmonary disease patients

PURPOSE OF REVIEW: The purpose of this review is to examine the state of knowledge and clinical practice in the association of chronic obstructive pulmonary disease to osteoporosis and fracture incidence. RECENT FINDINGS: There is a clear association between chronic obstructive pulmonary disease and excessive bone loss/risk of fractures. Little is known about the pathophysiological processes involved in the bone loss, but recent reports point to a continuous systemic inflammatory state in patients with chronic obstructive pulmonary disease. This inflammation involves the release of inflammatory cytokines such as tumour necrosis factor-alpha and interleukin-1. During the course of chronic obstructive pulmonary disease, a protein catabolic process takes place, including increased production of catalytic enzymes (matrix metalloproteinases etc.), which together with the inflammatory cytokines induces bone resorption. SUMMARY: Patients with chronic obstructive pulmonary disease are at increased risk of osteoporosis and fractures. Risk factors such as smoking, advanced age, physical inactivity, malnutrition, and low weight may be responsible, but a number of pathophysiological explanations including the presence of a chronic inflammatory state with increased levels of proinflammatory cytokines and protein catalytic enzymes may also be involved. The use of oral glucocorticoids is also a significant risk factor. Increased awareness is highly warranted to diagnose osteoporosis at an early stage, and professionals should be aware of the risk of osteoporosis in this patient population.     

Cardiovascular disease in chronic obstructive pulmonary disease

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.     

Cardiac disease in chronic obstructive pulmonary disease

The cardiac manifestations of chronic obstructive pulmonary disease (COPD) are numerous. Impairments of right ventricular dysfunction and pulmonary vascular disease are well known to complicate the clinical course of COPD and correlate inversely with survival. The pathogenesis of pulmonary vascular disease in COPD is likely multifactorial and related to alterations in gas exchange and vascular biology, as well as structural changes of the pulmonary vasculature and mechanical factors. Several modalities currently exist for the assessment of pulmonary vascular disease in COPD, but right heart catheterization remains the gold standard. Although no specific therapy other than oxygen has been generally accepted for the treatment of pulmonary hypertension in this population, there has been renewed interest in specific pulmonary vasodilators. The coexistence of COPD and coronary artery disease occurs frequently. This association is likely related to shared risk factors as well as similar pathogenic mechanisms, such as systemic inflammation. Management strategies for the care of patients with COPD and coronary artery disease are similar to those without COPD, but care must be given to address their respiratory limitations. Arrhythmias occur frequently in patients with COPD, but are rarely fatal and can generally be treated medically. Use of beta-blockers in the management of cardiac disease, while a theoretical concern in patients with increased airway resistance, is generally safe with the use of cardioselective agents.     

Nutrition in chronic obstructive pulmonary disease

Weight loss is a frequently occurring complication in patients with chronic obstructive pulmonary disease (COPD) and is a determining factor of functional capacity, health status, and mortality. Weight loss in COPD is a consequence of increased energy requirements unbalanced by dietary intake. Both metabolic and mechanical inefficiency contribute to the elevated energy expenditure. A disbalance between protein synthesis and protein breakdown may cause a disproportionate depletion of fat-free mass in some patients. Nutritional support is indicated for depleted patients with COPD because it provides not only supportive care, but direct intervention through improvement in respiratory and peripheral skeletal muscle function and in exercise performance. A combination of oral nutritional supplements and exercise or anabolic stimulus appears to be the best treatment approach to obtaining significant functional improvement. Patients responding to this treatment even demonstrated a decreased mortality. Poor response was related to the effects of systemic inflammation on dietary intake and catabolism. The effectiveness of anticatabolic modulation requires further investigation.     

Prognosis in chronic obstructive pulmonary disease

We recruited 985 patients with COPD but without hypoxemia or other serious disease, treated them in a standard fashion, and followed them closely for nearly 3 yr. At the time of recruitment the patients were carefully characterized as to symptom severity, lung function, exercise tolerance, and quality of life, and studies of lung function were repeated during follow-up. Overall mortality was 23% in 3 yr of follow-up. Patient age and the initial value of the FEV1 were the most accurate predictors of death; when FEV1 before bronchodilator was used, the response to bronchodilators was directly related to survival, but this relationship became nonsignificant when postbronchodilator FEV1 was used as a primary predictor. After adjustment for age and FEV1, mortality was related positively to TLC, resting heart rate, and perceived physical disability, and related negatively to exercise tolerance. These relationships, though significant, were relatively weak. When standardized for age and FEV1, mortality in the present series was less than that of a previous series (4), and the same as that of hypoxemic patients with COPD who received continuous home O2 therapy. Changes in FEV1 with time averaged -44 ml/yr, but the standard deviation was large. Patients with low initial values of FEV1 showed relatively little further decline, probably indicating a survivor effect. In patients with well-preserved initial FEV1, rate of decline correlated negatively with bronchodilator response, symptomatic wheezing, and psychological disturbances.     

Senescence in chronic obstructive pulmonary disease

There is a growing realization that chronic obstructive pulmonary disease involves several processes present in aging and cellular senescence. The impact of these processes in the pathogenesis of the main manifestations is multiple, particularly in the propagation of a proinflammatory phenotype, loss of reparative potential, and amplification of oxidative stress, all ultimately leading to tissue damage. This review highlights salient aspects related to senescence discussed in the 2011 Aspen Lung Conference.     

Exercise in chronic obstructive pulmonary disease

Several important differences exist between the training responses in normal patients and those in patients with chronic obstructive pulmonary disease (COPD). Chief among these is the lack of cardiovascular and metabolic changes in patients with COPD. Despite this, important and significant improvements do occur in exercise endurance after exercise training programs. Experience has shown that simple forms of exercise training and testing are effective and safe.     

自噬与慢性阻塞性肺疾病

自噬现象是一个广泛存在于真核细胞中的生命过程,最早于1962年由Ashford和Porter发现的.近年来,随着对自噬作用研究的深入,发现自噬在多种疾病中都扮演着十分重要的角色.慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)逐渐成为一个不容忽视的公共健康问题,据世界卫生组织/世界银行研究推测,截至2020年该病将成为全球经济负担的第五大疾病.但是,COPD的发病机制尚不明确,随着自噬现象及其与COPD的关系研究进一步深入,为COPD的防治寻找新的治疗策略.因此,该文着重讨论自噬在COPD发病机制中的作用及其在COPD中的临床运用价值.     

Advances in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is characterised by progressive airflow limitation in the presence of identifiable risk factors. Inflammation is the central pathological feature in the pathogenesis of COPD. In addition to its pulmonary effects, COPD is associated with significant extrapulmonary manifestations, including ischaemic heart disease, osteoporosis, stroke and diabetes. Anxiety and depression are also common. Spirometry remains the gold standard diagnostic tool. Pharmacologic and non‐pharmacologic therapy can improve symptoms, quality of life and exercise capacity and, through their effects on reducing exacerbations, have the potential to modify disease progression. Bronchodilators are the mainstay of pharmacotherapy, with guidelines recommending a stepwise escalating approach. Smoking cessation is paramount in managing COPD, with promotion of physical activity and pulmonary rehabilitation being other key factors in management. Comorbidities should be actively sought and managed in their own right. Given the chronicity and progressive nature of COPD, ongoing monitoring and support with timely discussion of advanced‐care planning and end‐of‐life issues are recommended.     

Imaging in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is divided into pulmonary emphysema and chronic bronchitis (CB). Emphysema is defined patho-anatomically as "permanent enlargement of airspaces distal to the terminal bronchiole, accompanied by the destruction of their walls, and without obvious fibrosis" (1). These lesions are readily identified and quantitated using computed tomography (CT), whereas the accompanying hyperinflation is best detected on plain chest X-ray, especially in advanced disease. The diagnosis of CB is clinical and relies on the presence of productive cough for 3 months in 2 or more successive years. The pathological changes of mucosal inflammation and bronchial wall thickening have been more difficult to identify with available imaging techniques. However, recent studies using Multi-detector row CT (MDCT) reported more reproducible assessment of air wall thickening.     

Cough in chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease (COPD) most commonly complain of cough, production of phlegm and breathlessness. The cough reflex sensitivity is heightened compared with that in healthy volunteers and is similar to that in subjects with asthma. The degree of airflow obstruction does not predict cough reflex sensitivity or objective cough counts, implying an independent process. Objective cough rates seem to be relatively low in COPD, despite frequent reporting of the symptom by patients. The relative contribution of cough to disability in COPD seems to be small, if assessed by subjective reporting. Effective treatments for cough in COPD have not yet been identified. Improved outcome measures of cough, a better understanding of the mechanisms underlying cough, and the importance of cough to patients is required to progress in this field.     

Comorbidities in chronic obstructive pulmonary disease

Comorbidities such as cardiac disease, diabetes mellitus, hypertension, osteoporosis, and psychological disorders are commonly reported in patients with chronic obstructive pulmonary disease (COPD) but with great variability in reported prevalence. Tobacco smoking is a risk factor for many of these comorbidities as well as for COPD, making it difficult to draw conclusions about the relationship between COPD and these comorbidities. However, recent large epidemiologic studies have confirmed the independent detrimental effects of these comorbidities on patients with COPD. On the other hand, many of these comorbidities are now considered to be part of the commonly prevalent nonpulmonary sequelae of COPD that are relevant not only to the understanding of the real burden of COPD but also to the development of effective management strategies.     

Prognosis in chronic obstructive pulmonary disease

Although many factors have been shown to relate to survival in patients with COPD, the patient's age and baseline postbronchodilator FEV1 are the best predictors of mortality. The presence of mild obstructive airway disease is not indicative of a progressive downhill course and shortened survival. Mortality in patients with a baseline postbronchodilator FEV1 greater than or equal to 50% of predicted was only slightly greater than that of a group of healthy smokers. Investigators attempting to compare survival in patients with COPD should attempt to exclude patients with asthma or asthmatic bronchitis, because these individuals have a much better prognosis than those with typical COPD (emphysema and chronic bronchitis). Patients should be matched closely for age and severity of impairment, because younger individuals and those with milder impairment are likely to live longer. Other factors besides age and baseline FEV1 have been shown to affect survival. Patients who stop smoking are likely to survive longer than those who continue to smoke. The presence of malnutrition has clearly been shown to worsen survival. Further studies will be necessary to determine if corticosteroid therapy can slow down progression of disease in patients with typical COPD. Oxygen therapy improves survival in COPD patients with significant hypoxemia, many of whom also have CO2 retention, polycythemia, and cor pulmonale. There are now multiple studies in the literature suggesting that the type of comprehensive respiratory care provided by pulmonary rehabilitation programs can not only improve the quality of life but also survival in patients with chronic obstructive pulmonary disease.     

Malnutrition in chronic obstructive pulmonary disease

Malnutrition in patients with COPD is associated with an impaired pulmonary status, reduced diaphragmatic mass, lower exercise capacity, and higher mortality rate when compared with adequately nourished individuals with COPD. Deterioration in patients with COPD may be the result of malnutrition. In addition, malnutrition could be a sign of other factors directly altered by the disease.     

Transplantation in chronic obstructive pulmonary disease

Lung transplantation is a surgical option for patients who fail optimization of medical treatment for the severe symptoms that result from COPD. This review will discuss patient selection, transplant listing, and the surgical technique for transplantation in COPD. Furthermore, it will describe transplant outcomes and its effects on recipient survival, pulmonary function, exercise capacity, respiratory muscle function, and quality of life. The respective roles of transplantation and lung volume reduction surgery as therapies for advanced disease will be outlined.     

Definitions in chronic obstructive pulmonary disease

States of airflow obstruction are common disorders which span the spectrum from asthmatic-chronic bronchitis to emphysema. Asthmatic and chronic bronchitic states are at least potentially reversible by systematic, pharmacologically oriented therapy focusing on bronchodilators and corticosteroids. Both asthmatic bronchitis, particularly when it is not adequately treated, and emphysema result in the final common pathway of COPD. These are generally progressive states, unless smoking cessation can be achieved in early or mild stages of disease. The future focuses on the great challenge of early identification, classification, and intervention. Thus, all patients with cough, dyspnea, and wheeze should be carefully evaluated by health workers who understand the history, physical examination, and simple pulmonary function tests in the context of chest radiology. These clinical methods together can help define the disease states characterized by airflow obstruction. Often, a final definition of disease cannot be made until aggressive attempts at the treatment of the airflow obstruction and its attendant symptoms complex have been vigorously pursued by experienced clinicians.     

慢性阻塞性肺疾病的呼吸困难

呼吸困难是慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)的首要症状,也是COPD患者最痛苦的症状.COPD诊断、处理和预防全球策略2011年报告推荐采用修订版呼吸困难分级(the modified Medical Research Council Dyspnea Scale,mMRC)评估COPD患者的呼吸困难,对mMRC达到和(或)超过2分的患者积极进行药物干预,以缓解呼吸困难.指南建议转化到临床实践的过程中,医师需要认识COPD呼吸困难的发生机制;理解呼吸困难测量工具的测定原理,包括信度、效度、对呼吸困难变化的敏感度;各种新老药物缓解呼吸困难的疗效.这篇文章从呼吸困难发生机制、呼吸困难测量、呼吸困难治疗三方面,综述COPD呼吸困难的最新进展.     

Sleep in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death, affecting 14 million adults in the United States. Symptoms related to sleep disturbances are common in moderate to severe COPD, particularly in elderly patients, in the form of morning tiredness and early awakenings. One major cause of morbidity in this population is abnormalities in gas exchange and resultant hypoxemia. Sleep has profound adverse effects on respiration and gas exchange in patients with COPD. There are several mechanisms underlying nonapneic oxygen desaturation during sleep. They include decreased functional residual capacity, diminished ventilatory responses to hypoxia and hypercapnia, impaired respiratory mechanical effectiveness, diminished arousal responses, respiratory muscle fatigue, diminished nonchemical respiratory drive, increased upper airway resistance, and the position of baseline saturation values on the oxyhemoglobin dissociation curve. Smoking cessation, bronchodilation, and pulmonary rehabilitation are cornerstones of treatment of COPD. Improvement in lung mechanics and gas exchange should lead to better sleep quality and health status.     

慢性阻塞性肺疾病合并侵袭性肺曲霉病的研究进展

侵袭性肺曲霉病(invasive pulmonary aspergillosis,IPA)常常继发于免疫受损和器官移植患者,病死率较高.近年来,COPD患者继发IPA国内外均有报道,其病死率在80%以上[1],亦有文献报道[2]COPD是IPA的危险凶素.临床上治疗时机的延误是主要的死亡原因,呼吸道标本中发现其他致病微牛物是延误治疗的原因之一.COPD患者IPA的发生率较高,长时间肺部浸润影和临床病情的短时间恶化需警惕IPA发生的可能性[3].现将COPD合并IPA的进展综述如下.