2017年 · 第40卷第07期

In the middle of summer, the sun is like fire. In this enthusiastic season, the 7th issue of this magazine in 2017 met with you readers.

In recent years, non-invasive ventilation technology has made great progress, new ventilation modes have emerged constantly, its indications are more and more broad, and its efficacy is supported by more and more evidence-based medical evidence^[1,2,3,4]。 With the understanding of sleep respiratory diseases and the development of diagnosis and treatment technology, noninvasive ventilation is gradually moving from hospital to family and playing a great role, which has become an important guarantee to improve patients' quality of life and long-term prognosis. At present, due to the lack of respiratory therapists in China, most sleep centers lack a professional sleep technician team, and the discipline construction is relatively lagging behind. In addition, the purchase of home noninvasive ventilation has not yet been included in prescription management. It is necessary to further standardize the following aspects from the application technical level: clarify the indications, select the appropriate ventilation mode, perform pressure titration and set parameters, deal with adverse reactions, improve treatment compliance and long-term follow-up management, etc. Therefore, the Sleep Apnea Group of the Respiratory Branch of Chinese Medical Association organized experts to refer to the existing guidelines and clinical research literature at home and abroad, and combined with the experience of domestic experts, in the 2012 edition of "Expert Consensus on Clinical Application of Continuous Positive Airway Pressure in Patients with Obstructive Sleep Apnea Hypopnea Syndrome (Draft)"^[5]Taking the clinical application technology of home noninvasive positive pressure ventilation for sleep respiratory diseases as the starting point, an expert consensus on clinical application technology of home noninvasive positive pressure ventilation was formulated.

Chronic obstructive pulmonary disease (COPD) complicated with pulmonary hypertension has high morbidity and mortality^[1]。 Right cardiac catheterization is still the gold standard in the diagnosis of pulmonary hypertension, but it is often difficult to achieve in practical clinical work^[2]Right ventricular function was assessed by transthoracic echocardiography^[3]。 In recent years, it has been reported that the expression of myostatin is increased in the model of heart failure induced by volume load^[4,5]Similar reports have been made in patients with chronic pulmonary heart disease^[6]。 In this study, the levels of muscle growth inhibitory protein in the blood of patients with COPD complicated with pulmonary arterial hypertension were investigated to explore the relationship between it and COPD complicated with pulmonary arterial hypertension.

pulmonary alveolar proteinosis (PAP) is a diffuse pulmonary disease characterized by the accumulation of a large amount of periodate Schiff-stained lipid-rich protein-like substances in the alveolar cavity and terminal bronchioles. Its pathogenesis is related to the impairment of granulocyte-macrophage colony stimulating factor signaling pathway or abnormal alveolar macrophages. It is difficult to diagnose early, monitor the disease and cure it^[1,2]。 Proteomics can identify and identify the whole proteins of cells, tissues, organs and organisms, obtain their functions and information, and make a holistic and comprehensive understanding of disease occurrence and cell metabolism at the protein level. Therefore, relying on proteomics to find specific proteins related to PAP is an important way to further elucidate the pathogenesis. However, there are no proteomics reports in adult patients with PAP at home and abroad^[3]。 For this purpose, multidimensional liquid chromatography combined with mass spectrometry was used in this study (high performance liquid chromatography tandem mass spectrometric, HPLC-MS/MS)^[4]The protein in PAP bronchoalveolar lavage fluid (BALF) was isolated and identified, and the complete expression profile of the protein deposited in the alveoli of PAP patients was established, which laid the experimental foundation for further identification of proteins and signaling pathways related to PAP pathology.

ARDS is an acute, diffuse, inflammatory lung injury^[2]。 The results of an international multicenter epidemiological study showed that ARDS accounted for 10.4% of ICU patients, and the mortality rate was high^[1]。 Identifying patients at high risk for ARDS can contribute to early intervention. However, there remain challenges in ARDS diagnosis^[3]Severe pneumonia overlaps with pulmonary ARDS (ARDSp); ARDS heterogeneity and definition limitations may contribute to the failure of many interventions^[4,5]。 Thus, there is a need for biomarkers capable of differentiating severe pneumonia from ARDSp and capable of predicting the occurrence of ARDSp. In this paper, the dynamic changes of serum decoy receptor 3 (DcR3), IL-8 and pulmonary surfactant-associated protein D (SP-D) were investigated in assessing and predicting ARDSp. The study was approved by the Ethics Committee of Newbridge Hospital with informed consent of all subjects.

Allergic rhinitis (AR) is a common Allergic disease of upper respiratory tract, which is closely related to bronchial asthma^[1]。 Airway inflammation, airway hyperresponsiveness and reversible airflow restriction are the main characteristics of asthma. In previous studies, the effects of AR on asthma were mainly evaluated from lung function, symptom score and small airway function^[2,3]However, there are few studies on the effects of AR on airway inflammation, airway reactivity and allergy grade in asthma patients. In this study, we used serum total immunoglobulin (IgE) to reflect allergy grade, exhaled nitric oxide (FeNO) to reflect airway inflammation, and challenge test to reflect airway reactivity, to explore the effect of AR on asthma patients.

Nocardiosis is a local or disseminated infection caused by gram-positive Nocardia bacteria, commonly found in the lungs, skin, and central nervous system. Nocardia pulmonary infections were more common in Nocardia stellata and Nocardia brasiliensis^[1,2,3,4]。 In clinical work, it is difficult to accurately identify Nocardia species by traditional methods alone, such as Nocardia gelsenkirchen and Nocardia astroformis^[5]。 The clinical characteristics, diagnosis and treatment process of 7 patients with Nocardia pulmonary infection (including Nocardia gelsenkirchen, Nocardia guinea pig otitis, Nocardia asiatica and Nocardia mallei) diagnosed in our hospital are reported as follows, and the clinical characteristics of non-Brazilian and Nocardia astreata pulmonary infection are discussed.

The patient, a 52-year-old female, went to the local hospital on March 18, 2016 because of "coughing and expectoration for more than 2 months after catching a cold and hemoptysis for 10 days". The patient developed cough and expectoration after catching cold 2 months before seeing the doctor. The cough is paroxysmal cough with low and dull voice; The sputum is white foamy sputum, the amount is about 50 ml/d; Intermittent fever, body temperature up to 39.0 ℃; With fatigue and night sweats. There were no symptoms such as hemoptysis, chills, chest tightness and shortness of breath. Previous history of tuberculosis without standardized treatment. Symptomatic treatment such as anti-infection, phlegm resolution and cough relief (details unknown) was given, and the above symptoms were improved and discharged. The patient developed cough and hemoptysis without obvious trigger 10 days ago. The cough is paroxysmal cough with low and dull sound, no barking cough, no metallic cough; The amount of hemoptysis was about 100 ml/time, 2 to 3 times/d, and the color was bright red, so I went to the local hospital again. Chest enhanced CT showed: (1) bilateral hilar lymph nodes were enlarged and calcified, and mediastinal lymph nodes were enlarged and tended to calcify; (2) Bronchiectasis and infection of the middle lobe of the right lung, and suspected nodules in the bronchial opening of the middle lobe of the right lung; (3) Left upper lobe anterior segment cord, left lower lobe lateral basal segment induration focus (Figure 1，Figure 2)。 Bronchoscopy showed bilateral inflammatory changes of bronchial mucosa, endocarbonosis and bronchial stenosis. The above symptoms were not significantly relieved after quadruple anti-tuberculosis treatment, so he was transferred to our hospital on April 25, 2016. After admission, blood routine showed that hemoglobin was 85 g/L and red blood cells were 2.88×10¹²/L, platelets were 303×10⁹/L; ESR was 85 mm/1 h; Sputum bacterial culture: Streptococcus viridis, Orococcus viscosus, Candida albicans growth. On the second day of admission, massive hemoptysis occurred suddenly after coughing, about 1 500 ml, dark red in color, with blood clots. The respiratory rate was 26 beats/min, the pulse rate was 146 beats/min, the blood oxygen saturation was 92%, and the blood pressure was 66/42 mmHg (1 mmHg =0.133 kPa). Dopamine was administered to maintain blood pressure and tracheal intubation was performed. No abnormal blood vessels were found in emergency bronchial arteriography, during which non-coagulation was gushed out multiple times through tracheal intubation. Double pulmonary angiography with a 5 F pigtail catheter showed reduced branching of the right lower pulmonary artery and light staining in the parenchymal phase. Then, a 5 F vertebral artery catheter was placed into the right lower pulmonary artery and re-angiography showed that the contrast agent directly entered the right bronchus through the right lower pulmonary artery, which was diagnosed as pulmonary bronchial fistula. Then, two cook coils (one 10-80 mm and one 6-80 mm) were filled, and angiography confirmed that the pulmonary arteriobronchial fistula disappeared (Figure 3、Figure 4、Figure 5)。 After operation, he was closely observed in the intensive care unit for 48 hours without repeated hemoptysis, and was transferred to the respiratory department. He was discharged after no hemoptysis occurred within 2 weeks. At discharge, the respiratory rate was 22 beats/min, the pulse rate was 89 beats/min, the blood oxygen saturation was 97%, the blood pressure was 117/69 mmHg, and the physical fitness (eastern cooperative oncology group, ECOG) score was 1. Six months after discharge: respiratory rate was 19 beats/min, pulse rate was 87 beats/min, blood oxygen saturation was 99%, blood pressure was 107/72 mmHg, pulmonary artery systolic pressure and mean pressure were 23 and 15 mmHg, respectively, and there were no symptoms such as hemoptysis and shortness of breath.

tracheobronchial tuberculosis (TBTB) refers to tuberculosis that occurs in the tracheobronchial mucosa, submucosa, smooth muscle, cartilage and adventitia^[1]。 TBTB is prone to tissue structure destruction, permanent stenosis or occlusion of the airway, leading to serious complications such as atelectasis or lung damage, and some may be secondary to tracheal and bronchiectasis. Three cases of cavity-like changes in the affected lung caused by bronchial tuberculosis lesions admitted to the Tuberculosis Department of Nanjing Chest Hospital from January 2013 to April 1, 2015 are reported below.

In recent years, as an important public health issue, obesity has attracted more and more attention. Obesity is not only a disease state, but also an important risk factor for many other diseases. obesity hypoventilation syndrome (OHS) refers to chronic hypoventilation caused by obesity. This concept was first developed by Bickelmann et al.^[1]Proposed in 1956 and defined as obese patients (body mass index ≥30 kg/m²), CO is present in the awake state₂Retention (PaCO₂≥45 mmHg, 1 mmHg =0.133 kPa), At the same time, hypercapnia caused by other causes, such as obstructive airway disease and neuromuscular disease, are excluded. The incidence rate is about 0.3% ~0.4%^[2]About 90% of the patients had simultaneous obstructive sleep apnea (obstructive sleep apnea, OSA)^[3]。 The pathogenesis is still unclear, but it may be caused by a variety of factors, such as changes in respiratory mechanics, muscle insufficiency caused by obesity, dysfunction of respiratory drive center, changes in hormone levels and OSA, etc^[4]。 The prognosis of untreated patients is poor. The 18-month mortality rate is as high as 23%. The causes of death are mostly heart failure, myocardial infarction and other cardiovascular and cerebrovascular diseases (48%), tumors (15%), respiratory failure (11%) and infection (11%), etc. After treatment, the mortality rate can be reduced to 3%^[5]。 Currently, the main treatment modalities are weight loss and non-invasive positive pressure ventilation support, which refers to the provision of single or bi-level positive pressure ventilation to patients through a ventilator at night to eliminate apnea and hypopnea events and improve PaCO₂Level. This article mainly describes the types of noninvasive ventilation widely used at present and the related research progress, aiming at providing some guidance for the treatment of such patients.

interstitial lung disease (ILD) is a common pulmonary manifestation in patients with systemic sclerosis (SSc), and it is also the leading cause of death in SSc patients in recent years. So far, although there are no diagnosis and treatment guidelines at home and abroad, in recent years, great progress has been made in the treatment strategies and related drugs of SSC-associated ILD (systemic sclerosis associated interstitial lung disease, SSc-ILD). In order to improve the understanding of SSc-ILD, the relevant literature in the past three years is reviewed as follows.

The patient was a 64-year-old female. The main reason is "shortness of breath, fatigue, and weight loss for 6 months", and I saw the doctor on September 13, 2016. Six months ago, the patient had shortness of breath, fatigue, and weight loss without obvious trigger, which gradually worsened. Chest CT examination was performed on 7 Sep 2016, showing enlargement of right hilar lymph nodes (Figure 1，Figure 2)。 Previous lacunar infarction, long-term aspirin. Physical examination: The superficial lymph nodes were not palpable and swollen, and no abnormalities were found in the heart, lungs and abdomen. Preliminary diagnosis: The cause of right hilar space occupation is to be investigated. Auxiliary examination: blood routine, biochemistry, tumor markers, angiotensin converting enzyme (ACE) were normal. Lung function was normal. Bronchoscopy: infiltrating mucosal changes at the opening of the right lower lobe, mild stenosis of the opening of the basal segment of the right lower lobe, and enlarged N7 lymph nodes. Pathological report of N7 lymph node EBUS-TBNA: A few epithelioid cells and individual multinucleated giant cells were seen under microscope, and granulomatous lesions were considered, but sarcoidosis was not excluded. The results of rapid culture of Mycobacterium histiocytogenes by lymph node puncture, acid-resistant staining by fluorescence, and DNA of tuberculous and non-tuberculous mycobacterium complexes were negative. After more than 1 month of inhalation treatment with salmeterol and ticasone powder on September 29, 2016, the patient felt shortness of breath, aggravated chest tightness, and chest pain. On November 17, 2016, a reexamination of the chest CT showed that the right hilar lymph nodes were significantly enlarged, the left hilar and mediastinal lymph nodes were enlarged, multiple small nodules in both lungs, and bilateral pleural effusion (Figure 3，Figure 4)。 Thoracocentesis and catheter drainage were performed. Pleural effusion routine, biochemistry, carcinoembryonic antigen (CEA) and lymphocyte culture + interferon (A + B) were all normal. Reexamination of bronchoscopy showed multiple small nodules in the trachea and bronchial mucosa, with the right side. Right middle lobe mucosal biopsy, pathological report of epithelioid cell granuloma nodules in bronchial mucosa, no caseous necrosis, sarcoidosis not excluded (Figure 5)； Acid-TB and hexamine silver staining were negative. On 7 December 2016, prednisone tablets were given 9 tablets/d in consecutive doses; Reduce 1 tablet every 10 days to 6 tablets/d, and take it continuously for 8 days, and the symptoms are relieved. On January 13, 2017, the chest CT chest lymph nodes and intrapulmonary lesions were significantly improved compared with before, and the pleural effusion absorption (Figure 6，Figure 7)。 Final diagnosis: pulmonary sarcoidosis.

A 56-year-old female was admitted to the hospital on August 24, 2016 due to "dry cough, fatigue, weight loss for more than 1 year, and right chest pain for 1 week". The patient had intermittent irritating dry cough more than 1 year before admission, which was obvious when catching cold and inhaling peculiar smell, accompanied by fatigue and loss of appetite. No obvious abnormalities were found in the routine blood examination and X-ray chest X-ray in the local hospital. Considering "allergic pharyngitis", symptomatic treatment such as cough relief was not effective, and the symptoms recurred later, which was not paid attention to. One week before admission, the patient developed right chest pain without obvious trigger, which was persistent dull pain, independent of body position and breathing, without radiant pain, fever, night sweats, chest tightness, shortness of breath and other symptoms. X-ray chest radiographs in the local hospital showed multiple radiographs in both lungs. Considering the possibility of "pneumonia", piperacillin/tazobactam 4.5 g was given once/12 h for intravenous drip for 1 week, but the symptoms were not relieved. Re-examination of chest radiographs showed that the shadows in the lungs were not absorbed. Since the onset of the disease, the patient had poor spirit, appetite and sleep, and lost 8 kg of weight. Past physical health, no history of infectious diseases and genetic diseases, no history of tobacco and alcohol addiction and allergies, no history of exposure to special occupations and environments. Admission physical examination: body temperature 36.5 ℃, pulse 76 beats/min, respiratory rate 18 beats/min, blood pressure 130/80 mmHg (1 mmHg =0.133 kPa), no swelling of superficial lymph nodes, no erythema, rash and nodules on the skin, coarse respiratory sounds in both lungs, and no dry and wet rales. The heart rate was 76 beats/min, and the rhythm was homogeneous without murmur. The abdomen was flat and soft, and no abnormalities were found in the rest of the palpation.

It is well known that BCG has formed substrains with different biological, genetic and protective properties during long-term passage^[1,2]Although BCG vaccine has been used for a hundred years, there is a lack of systematic research data on the protective power of different strains of BCG vaccine on human body. In the absence of relevant data on the effect of human use, the protection against animals is the main evaluation criterion. However, the same animal model may obtain different results due to the difference of immunization dose and cycle, virulence and challenge amount of infected bacteria and evaluation index^[3,4]。 February 2016Molecular TherapyPublished the results of the lateral comparison of safety and protection effects conducted by the State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University using 13 BCG vaccines that are currently widely used worldwide^[4]。 This study involved BCG strains currently in use in China, but the results showed that the protective power of BCG production strains in China was not significantly different from that of buffer control group at 4 weeks or 9 weeks, among which the number of spleen bacteria isolated at 4 weeks and the number of lung bacteria isolated at 9 weeks were higher than those of control group. The results of this study are completely inconsistent with the results we have collected from other investigators on the protective power of BCG strains in China and our long-term monitoring of the protective power of BCG strains^{[5,6,7,8,9,10,11,12,13,14]}。 The information about the BCG production strains in China and the public and unpublished results of animal protection are summarized as follows. I hope that researchers can understand whether the BCG production strains in China are effective, and I also hope that everyone will discuss and put forward different opinions.

In recent years, the results of studies have shown that pulse pressure variability (Δ PP) can accurately predict fluid responsiveness in mechanically ventilated patients. The main mechanism is that the periodic change of intrathoracic pressure (Δ PPL) caused by mechanical ventilation can trigger the periodic change of cardiac preload, thus triggering the periodic change of stroke volume (SV). The periodic change of SV with respiration in patients in the steep section of Frank-Starling curve (those who respond to fluid resuscitation) is larger than that in patients in the flat section (those who do not respond to fluid resuscitation), so it can be used as an important predictor of fluid responsiveness. This periodic change in SV is closely related to arterial pulse pressure and can be replaced by Δ PP. However, ARDS patients generally adopt the pulmonary protective ventilation strategy with low tidal volume as the core. The results of the study show that Δ PP cannot predict fluid reactivity in ARDS patients with mechanical ventilation; Many scholars believe that this is mainly due to the smaller Δ PPL due to the lower small tidal volume, and Δ PPL is the main driving force for Δ PP production, so Δ PP is smaller even in liquid reactors (false negative). However, using low tidal volume to correct Δ PP (Δ PP/Vt) does not improve the predictive ability of this parameter. This study attempts to observe whether using Δ PPL to correct Δ PP can improve the ability of this parameter to predict fluid responsiveness in ARDS patients, and at the same time to explore which respiratory mechanical parameters [airway driving pressure (Δ PAW), low tidal volume, total respiratory elastic resistance (Ers), respiratory compliance (Crs), chest wall elastic resistance (Ecw), etc.] are the key factors affecting the ability of Δ PP to predict fluid responsiveness in ARDS patients.

Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death worldwide, and tobacco smoke is the main risk factor. Adenovirus is a common cause of acute exacerbation of COPD and promoting COPD progression. The occurrence and development of COPD is closely related to chronic repeated injury and abnormal repair of lung epithelial cells, while lung epithelial stem/progenitor cells are directly involved in the maintenance and repair of epithelium after injury, including lung CD₃₁^-CD₄₅^-SCA-1^＋Cells. Shh signaling pathway is one of the important pathways to regulate the self-renewal and maintenance of stem cells, and is involved in the regeneration and repair of lung injury. This study investigated the intrapulmonary CD induced by cigarette smoke extract (CSE) in emphysema mice₃₁^-CD₄₅^-SCA-1^＋Cell number and expression level of Shh signaling pathway, and the influence of acute adenovirus infection on it.