2014年 · 第37卷第04期

Chronic obstructive pulmonary disease (COPD) is a common and frequently occurring disease that seriously endangers human health. Acute exacerbation of COPD is an important part of the disease process. The average acute exacerbation of COPD patients occurs 0.5~3.5 times per year, which has a serious negative impact on the quality of life, lung function status, disease progression and socioeconomic burden of patients^[1,2]。 Currently, acute exacerbation of COPD is defined as "an acute onset process characterized by a patient's respiratory symptoms worsening beyond daily variation and requiring a change in pharmacological treatment regimen". COPD is a heterogeneous disease with multiple phenotypes^[3,4]This heterogeneity is also reflected in the etiology, pathogenesis, clinical characteristics and severity of acute exacerbation in patients with COPD. Because of this heterogeneity, patients also respond differently to existing treatment options. At present, a large number of clinical phenotypes of patients with stable COPD have been studied at home and abroad. Some of the phenotypes with clinical application prospects are helpful to distinguish the therapeutic response of patients, and the corresponding diagnosis and treatment strategies are formulated^[3]。 There are few heterogeneous studies on acute exacerbation of COPD, and strengthening this research has important clinical significance for individualized diagnosis and treatment of patients with acute exacerbation.

The 2011 edition of the Global Strategy for the Diagnosis, Management and Prevention of COPD (referred to as the Global Strategy for COPD) and China's Guidelines for the Diagnosis and Treatment of COPD (revised in 2013) have been revised in content, which has brought new ideas and new challenges to the diagnosis and treatment of COPD (referred to as COPD). One of the important aspects is that we should pay attention to the acute exacerbation of COPD, including adding the content of acute exacerbation to the definition of COPD and revising the definition of acute exacerbation. Add an assessment of the risk of acute exacerbation to the assessment of the condition; Add long-term goals to treatment goals related to reducing the risk of future acute exacerbations in patients^[1,2]。 By definition, acute COPD exacerbations are clinical events in which a patient is characterized by an exacerbation of respiratory symptoms, with symptomatic changes exceeding the range of daily variation and leading to a change in the pharmacological regimen^[1,2]。 However, COPD is a heterogeneous disease, and this heterogeneity is also manifested in acute exacerbation, which is reflected in the heterogeneity of symptoms, etiology and pathogenesis, severity of the disease, frequency of exacerbation, and treatment^[3,4]。 Here, the author expounds the heterogeneity of clinical manifestations of acute exacerbation of COPD.

Acute exacerbation of chronic obstructive pulmonary disease (COPD) has been the focus of attention in recent years. Patients with COPD have about 0.5~3.5 acute exacerbations every year^[1]Acute exacerbation of COPD has a serious negative impact on the quality of life, lung function, disease progress and socioeconomic burden of patients. It is an important factor in the death of COPD patients and the main reason for the high medical expenses of COPD patients^[2]。 The 2013 revision of the Global Strategy for the Diagnosis, Management, and Prevention of COPD emphasizes in the COPD definition that acute exacerbations and comorbidities affect the overall severity of the patient's disease and uses acute exacerbations as the primary measure for future risk assessment for COPD grouping^[3,4]。 The essence of COPD is a chronic airway inflammatory disease. In the acute exacerbation period, under the action of microorganisms, pollution and other predisposing factors, airway inflammation is aggravated, causing bronchial mucosal congestion and edema, increased mucus secretion, smooth muscle spasm, aggravated airway stenosis, resulting in expiratory airflow restriction, dynamic lung hyperinflation, and acute exacerbation symptoms. On the other hand, inflammation in the lungs overflows, leading to a systemic inflammatory response^[5]。 At present, the diagnosis of acute exacerbation of COPD completely depends on clinical manifestations and lacks quantitative indexes. As a quantitative index, inflammatory biomarkers are worth looking forward to in the auxiliary quantitative diagnosis, severity assessment and judgment of the etiology and prognosis of acute exacerbation of COPD. At present, the following kinds of inflammatory biomarkers are commonly used.

exercise-induced bronchoconstriction (EIB) refers to increased airway resistance during exercise, accompanied by symptoms such as cough, wheezing or dyspnea in patients with no prior history of bronchial asthma. The incidence of this disease in endurance athletes is significantly higher than that in healthy people, especially those engaged in high-intensity athletics, such as long-distance running and swimming, which suggests that exercise intensity may be related to the onset of EIB. Due to the lack of adrenergic innervation, the diastolic regulation of airway smooth muscle mainly depends on the binding of circulating adrenergic to β 2-adrenergic receptors on airway smooth muscle. Findings from previous studies have shown that circulating epinephrine levels in EIB patients are lower compared to healthy individuals, suggesting that epinephrine may be associated with the pathogenesis of EIB. Epinephrine in the circulatory system is mainly synthesized and secreted by adrenal medulla chromaffin cells (AMCC), and the elevated level of nerve growth factor (NGF) can cause neural transdifferentiation of AMCC, thus affecting its neuroendocrine function and leading to insufficient adrenaline level.

Bone morphogenetic protein (BMP) signaling pathway plays a very important role in the pathogenesis of pulmonary hypertension. Our previous study found that BMP4 can increase the expression of calcium channel protein classical transient receptor potential protein (TRPC) 1,4,6 in pulmonary artery smooth muscle cells, and then increase the basal calcium concentration and calcium pool manipulative calcium influx (SOCE), and promote cell proliferation and migration. However, how BMP4 affects TRPC expression remains unclear. Studies have shown that p38MAPK and ERK1/2 are related to vascular remodeling in the downstream pathway of BMP4. In this study, we explored whether BMP4 affects TRPC expression through this pathway.

Enhanced palliative care and end-of-life care for end-stage patients with chronic obstructive pulmonary disease (COPD) is a global strategy for the diagnosis, management and prevention of COPD "(Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease, New ideas presented in the 2013 revised edition of the Global Strategy for COPD (abbreviated as the Global Strategy for COPD^[1]。 With the progression of COPD, the patient's physical condition declines, cough, expectoration, dyspnea and other symptoms gradually aggravate, and complications such as cardiopulmonary insufficiency appear. Every acute exacerbation may be life-threatening. Palliative care and hospice care are very important for end-stage COPD patients, which are conducive to relieving the physical and mental pain of patients and their families and making rational use of medical resources. However, there has been no guideline to mention this problem for a long time, and in the process of diagnosis and treatment, most clinicians also avoid communicating with patients. Therefore, we review the research progress and implementation status of palliative care and hospice care for end-stage COPD patients at home and abroad in recent years, hoping to help understand the palliative concepts and methods proposed in the global strategy for COPD.

At present, lung cancer is the most common malignant tumor in the world, ranking first among malignant tumor death causes in both men and women, which is a serious threat to human health^[1]。 Smoking has been proven to be the most important environmental risk factor for lung cancer. Tobacco produces polycyclic aromatic hydrocarbons, arsenic, benzene and other carcinogenic substances during combustion, which damages bronchial epithelial cells and leads to cancer. Inflammation also plays an important role in the occurrence and development of lung cancer^[2]。 Chronic obstructive pulmonary disease (COPD) is the most common chronic inflammatory disease of respiratory system, and patients with lung cancer combined with COPD are also commonly seen in clinical work. Therefore, it is speculated that lung cancer and COPD may have a complicated relationship. Pay attention to the coexistence of lung cancer and COPD, and explore the same risk factors and potential related pathogenesis of both, which is expected to further promote the comprehensive prevention and treatment of lung cancer and COPD.

Stents have been used for the treatment of airway stenosis for more than 100 years, but the damage to airway mucosa and the stimulation of stents as foreign bodies during implantation can lead to granulation tissue proliferation and luminal restenosis, which seriously affects the clinical efficacy after implantation. Topical application of antiproliferative drugs can inhibit the proliferation of granulation tissue, but the action time of the drugs is short, which cannot inhibit the recurrence of stenosis. drug eluting stent (DES) has emerged in recent years to solve this problem. DES is composed of bare metal stent, drug and carrier. The drug and carrier are prepared into a coating solution according to a certain proportion, and coated on the stent. The purpose of restenosis is inhibited by continuous and slow release of drug. However, the research of airway DES is still in its infancy. Restenosis also exists after coronary stenting, and the emergence of coronary drug-coated stents has made an exceptional contribution to the cardiovascular field. The design ideas and recent research progress of airway DES are summarized as follows.

Bordley and Carey in 1949^[1]It was reported for the first time that intramuscular injection of adrenocorticotropic hormone can quickly improve the symptoms of some patients with bronchial asthma (asthma for short). Later, glucocorticoids (hormones for short) gradually became the most effective drug for the treatment of asthma and other inflammatory diseases. At present, inhaled glucocorticoids (ICS) are still the first-line drugs for the treatment of asthma, and play an important role in asthma control and relief treatment. Although most asthma patients currently have symptoms that can be treated by ICS in combination with long-acting beta₂Receptor agonist (LABA) treatment regimens are well controlled, but some patients have a poor response to hormone therapy, which is difficult to control even with high-dose hormone therapy, and repeated acute exacerbations of the condition, which is called steroid resistant (SR). There are about 3 million asthma patients worldwide, although this proportion of hormone-resistant asthma patients is small (about 5%)^[2]However, there are still quite a few patients who are deeply troubled by the disease, which not only decreases the quality of life, but also increases the economic burden of individuals and society. Therefore, the awareness and prevention of these patients should attract the attention of medical workers. In this paper, the clinical characteristics, risk factors, molecular mechanism, prevention and treatment of hormone resistance (insensitive) asthma patients are expounded.

Air pollution is closely related to the incidence of chronic obstructive pulmonary disease (COPD), and it is also one of the important influencing factors besides smoking. The results show that fine particles in the atmosphere (fine particular matter diameter ≤2.5 μ m, PM_2.5) exposure was associated with total population mortality and cardiopulmonary disease mortality, PM_2.5Every 10 μ g/m increase in concentration³After 14 days, the total mortality rate of the population increased by 2.6%, and the mortality rate of COPD increased by 9%^[1]。 PM_2.5It can also reduce the internalization and killing effect of mouse alveolar macrophages (AM) on Streptococcus pneumoniae, resulting in a decrease in the ability of AM to phagocyte and remove bacteria^[2]。 The purpose of this study was to explore the PM in Lanzhou urban area_2.5Effects of monocyte-derived macrophages (MDM) on cell activity and phagocytic ability of Escherichia coli in patients with COPD and their relationship with oxidative damage.

In recent years, nontuberculous mycobacteria (NTM) pulmonary disease has received more and more attention at home and abroad, and bronchiectasis (abbreviated as bronchiectasis) is a common predisposition factor of NTM pulmonary disease^[1,2]。 In China, bronchial expansion is a common disease and frequently occurring disease, which has shown an obvious increasing trend in recent years. Bronchiectasis and NTM pulmonary disease are mutually causal and cannot be clarified. This study retrospectively analyzed the clinical data of patients with bronchiectasis and NTM pulmonary disease admitted to Shanghai Pulmonary Hospital in recent years, in order to guide the diagnosis and treatment of bronchiectasis and NTM pulmonary disease.

The central link of hypoxic pulmonary hypertension (HPH) is the increase of pulmonary vascular resistance, which is dominated by pulmonary vasoconstriction and pulmonary vascular remodeling in the early stage of hypoxia. As the disease progresses, it can lead to right ventricular hypertrophy, heart failure and even death^[1,2]。 Abnormal proliferation of pulmonary artery smooth muscle cells is the basic pathological change of pulmonary vascular remodeling^[3]。 Signal transduction pathways related to division and proliferation of pulmonary artery smooth muscle cells in the formation mechanism of hypoxic pulmonary vascular remodeling have been a hot research topic in recent years^[4]。 The results of digoxin intervention on hypoxia-induced HPH in rats showed that digoxin could significantly reduce pulmonary arterial pressure, inhibit right ventricular hypertrophy, alleviate the thickening of pulmonary arteriole wall, and improve hypoxia-induced pulmonary vascular remodeling^[5]。 Based on the results of animal experiments, the effect of digoxin on the proliferation mechanism of human pulmonary artery smooth muscle cells was observed in this study, which provided further preclinical evidence for digoxin in the treatment of HPH.

The patient, female, 70 years old, was admitted to the respiratory department of Huai' an First Hospital affiliated to Nanjing Medical University on April 22, 2013 due to "repeated chest tightness and asthma after right chest trauma for more than 1 month". The patient fell at home 1 month ago and felt right chest pain, chest tightness and asthma. An emergency chest CT showed "right 8th posterior rib fracture with right hydropneumothorax" (Figure 1), performed right thoracic closed drainage in the thoracic surgery department of the local hospital, draining about 700 ml of hemorrhagic fluid, re-examination of chest CT, right lung recruitment was good, and a small amount of right pleural effusion (Figure 2), chest tightness and asthma are relieved. Two weeks later, chest tightness and asthma were aggravated again, and chest CT showed that the right pleural effusion was significantly increased than before (Figure 3), so admitted to hospital. The patient had no history of special medication in the past, no history of travel and exposure to epidemic water, epidemic area or asbestos. Physical examination on admission: body temperature 37 ℃, blood pressure 120/70 mmHg (1 mmHg =0.133 kPa), no thoracic deformity, localized tenderness at the right 8th posterior rib, void sound at right lung percussion, significantly reduced breathing sound, no dry and wet rales, no abnormalities in left lung, and no positive signs in heart and abdomen. Laboratory test: white blood cells 4.49×10⁹/L, the neutrophil ratio was 0.51, the lymphocyte ratio was 0.37, and the eosinophil ratio was 0.03. No parasites and eggs were found in the feces. Blood biochemical examination showed no hypoalbuminemia, no abnormalities in C-reactive protein and ESR, no abnormalities in blood tumor markers, anti-neutrophil cytoplasmic antibody, anti-cyclic citrulline peptide antibody, extractable nuclear antigen polypeptide antibody spectrum and anti-nuclear antibody were all normal, blood immunoglobulin E was 82 IU/ml, blood complement C₃is 0.9 g/L, C₄It was 0.25 g/L and the gamma-interferon release test was negative. On the 5th day after hospitalization, a closed right thoracic drainage was performed again. A total of 1 500 ml of pleural effusion was drained, which was yellow in appearance and slightly mixed, with a specific gravity of 1.019 and leukocytes of 1 100×10⁶/L, mononuclear cells accounted for 0.65, lobulated nuclei accounted for 0.35, and eosinophils accounted for 31.5% of the total number of white blood cells (Figure 4), lactate dehydrogenase was 173.9 U/L, protein was 41.2 g/L, sugar was 7.30 mmol/L, adenosine deaminase was 6.4 U/L, complement C₃is 0.4 g/L, C₄0.1 g/L, negative for chyle test, negative for bacterial and fungal cultures, negative for tumor markers and exfoliated cells. The final diagnosis was "post-traumatic eosinophilic pleural effusion (EPE)". After admission, 300~400 ml of pleural effusion was drained daily. On May 7 (37 days of hospitalization), 20 mg of dexamethasone was injected into the pleural cavity at one time. By May 10, the daily drainage volume was less than 50 ml. After removing the thoracic drainage tube, he was discharged from the hospital. No pleural effusion has occurred since follow-up.

Professor Zhang Deping, Department of Respiratory Affairs, Gulou Hospital affiliated to Nanjing University School of Medicine, died at 13: 31 on March 11, 2014 at the age of 52 due to ineffective treatment.

subglottic tracheal benign stenosis (STBS) is a very difficult clinical problem. This area is in the interdisciplinary field of laryngeal surgery, interventional respiratory medicine and thoracic surgery, and there is no consensus on treatment methods. Bronchoscopic interventional treatment of STBS should be cautious. Excessive energy therapy or metal stents can easily move the lesions upward, causing irreversible respiratory and vocal dysfunction in patients. Surgical resection and reconstruction can cure some patients. Montgomery T-tube is a silicone artificial airway stent, which has little irritation to the airway mucosa and will not be displaced. While restoring normal ventilation, it can ensure the normal vocal function of patients. For patients who are not suitable for surgical resection, T-tube is another treatment option. Below we introduce an interventional treatment method for STBS by placing T-tubes under rigid bronchoscope.

With the miniaturization of equipment, the improvement of optics and the innovation of engineering design, new respiratory interventional equipment is constantly presented, which makes interventional pulmonology develop rapidly, and changes the traditional diagnosis and treatment methods of many respiratory diseases. However, due to the lack of prospective, large-sample, randomized differential comparative studies, there are many controversies in the clinical application of new technologies and therapies. This article reviews the controversial interventional diagnosis and treatment techniques in order to improve the understanding and understanding of the problems.

Mechanical ventilation is the most common and effective respiratory support for patients with respiratory failure in modern medicine. Mechanical ventilation technology is becoming more and more mature after nearly a hundred years of development. The use of appropriate mechanical ventilation techniques can maintain the ventilation function and oxygenation state of patients, improve the symptoms of dyspnea, relieve respiratory muscle fatigue, and provide the opportunity for further treatment of clinical diseases.

Pulmonary function examination is an important auxiliary examination method in the diagnosis and treatment of respiratory diseases. It plays an important role in the management of chronic respiratory diseases, such as chronic obstructive pulmonary disease (COPD) and bronchial asthma. Its follow-up and monitoring not only contribute to the early diagnosis, follow-up and efficacy evaluation of diseases, but also reduce the disease burden of patients and society. However, due to the limitation of current medical mode, environment and resources in China, the application of pulmonary function test in the follow-up and monitoring of chronic respiratory diseases still faces many difficulties, such as uneven distribution of resources in various places, lack of uniform standards for operation, and timeliness of test results.

The 5th event of Beijing Young Respiratory Scholars Salon 2013 was held in Chinese Medical Association on December 26, 2013. The purpose of this salon activity is to summarize the experience of the content and form of the salon in the past year, and to determine the theme of the salon activity in 2014. It is presided over by Professor Sun Yongchang, Department of Respiratory Affairs, Beijing Tongren Hospital affiliated to Capital Medical University.

There are common characteristics in the population and individual differences between different patients in the manifestation of any disease. Group law and individual differences are the contradictions that need to be dealt with in clinical medicine. Chronic obstructive pulmonary disease (COPD) is also a heterogeneous disease, and patients have obvious differences in clinical manifestations, disease progression and response to treatment. This issue contains special written talks on "Attaching importance to the heterogeneity of acute exacerbation of chronic obstructive pulmonary disease and its individualized diagnosis and treatment" and "Heterogeneity of clinical manifestations of acute exacerbation of chronic obstructive pulmonary disease". From the perspective of unity of opposites between universality and particularity, inevitability and contingency of objective laws of things, the author tries to explain the relationship between group laws and individual differences in clinical manifestations of chronic obstructive pulmonary disease and individualized diagnosis and treatment, so as to improve the clinical thinking level of clinicians. So far, the clinical diagnosis of acute exacerbation of COPD belongs to qualitative diagnosis, which is far from reaching the level of accurate quantitative diagnosis, and there is a lack of single biomarker for quantitative diagnosis of acute exacerbation of COPD. The article "Biomarkers for Diagnosis of Acute Exacerbation of COPD" discusses the exploration of quantitative diagnosis of acute exacerbation of COPD in recent years. With the deepening of research, it is believed that one or one group of biomarkers may be used for accurate etiology and quantitative diagnosis of COPD in the future.