2017年 · 第40卷第05期

In early summer, the summer is gradually growing, accompanied by the gradually rising heat wave, the 5th issue of this magazine in 2017 met with you readers!

Time passes by like fine sand. Inadvertently, the Tuberculosis Branch of Chinese Medical Association has entered its old age. Recalling the past, the prosperous years are thick, and the romantic figures still look at the present. In order to overcome the "white plague", under the leadership of the party and the government, generations of tuberculosis people bravely challenged and saved countless patients from the disease. Today, on the basis of their predecessors, through unremitting efforts, Chinese tuberculosis people have significantly reduced the incidence, prevalence and mortality of tuberculosis in 20 years. On the cover of the 2011 Global Tuberculosis Control Report released by the World Health Organization, three graphs of the downward trend of tuberculosis epidemic with Chinese elements are displayed^[1]。 China's achievements in tuberculosis control have won recognition and praise from the international academic community.

In 2017, the Tuberculosis Branch of Chinese Medical Association will celebrate its 80th anniversary. As one of the earliest specialized branches established by the Chinese Medical Association, the Tuberculosis Branch adheres to the spirit of the Chinese Medical Association, and with the joint efforts of generations of members, it has played a huge role in the prevention and control of tuberculosis in China. On the occasion of the 80th anniversary of the founding of the Tuberculosis Society, let us revisit the history and role of the Tuberculosis Society and gather strength for the future development of the Society.

No disease is as harmful and compelling as tuberculosis. For thousands of years, the fight between human beings and tuberculosis has never stopped, which has a long history and is difficult and tortuous. The Tuberculosis Branch of Chinese Medical Association has gone through 80 years of ups and downs in the fight against tuberculosis. In the past 80 years, China has made one achievement and breakthrough in the field of clinical diagnosis and treatment of tuberculosis, and accumulated rich experience and valuable wealth. Reviewing the research achievements of clinical diagnosis and treatment of tuberculosis in China in the past 80 years is not only a remembrance of our predecessors, a combing and inheritance of past achievements, but also a basis for the development of clinical diagnosis and treatment of tuberculosis in the future.

connective tissue disease (CTD) is a rheumatic disease involving multiple organs and systems, and pathologically manifests as chronic inflammation of blood vessels and connective tissues. Connective tissue disease has been listed as one of the risk factors of pulmonary embolism^[1]However, it has not been paid attention to in clinical work, and it is easy to misdiagnose and misdiagnose the diagnosis of potential CTD. In this paper, the clinical data of 13 cases of CTD with pulmonary thromboembolism as the first episode admitted to the First Affiliated Hospital of Guangxi Medical University were retrospectively analyzed, and their clinical characteristics and treatment experience were summarized.

A 29-year-old male, an engineer, had the first episode of sleeping disorder around the age of 5, and the episode frequency was monthly<Once, the patient himself and his family were not injured, and the symptoms were alleviated after puberty, so no attention was paid to them. The patient has snored for more than 10 years. In recent years, the snoring has aggravated with weight gain. The patient has snoring at night, apnea with waking up, dry mouth in the morning, headache, daytime drowsiness, memory loss, and easy fatigue, but it has not been treated in a standardized manner. One year ago, sleeping disorder had a recurrent attack with uncertain frequency. Recently, sleeping disorder had frequent attacks,>3 times a week. The patient hit his nose, and then came to see a doctor after smoking at night and igniting the sheets. The patient has a history of smoking for more than 10 years, with a smoking index of about 20 pack years, intermittent drinking, not abstaining from drinking, and snoring symptoms aggravated after drinking. The patient has not received medication or other treatment for the past 6 months, and has no previous history of epilepsy, and has no special family history.

From July to September 2016, I had the privilege of participating in the 7th phase of the China-Austria Exchange Project, and went to study in the pulmonary department of Otto-Wagner-Spital (OWS) Hospital in Vienna, the capital of Austria, which specializes in thoracic and lung diseases.

In 1998, the Global Initiative for Chronic Obstructive Pulmonary Disease (COPD) (GOLD) was launched with the goal of developing management recommendations for COPD based on the best published scientific research. The first edition of the Global Strategy for the Diagnosis, Treatment and Prevention of COPD was published in 2001 and was fully revised in 2006 and 2011 based on published studies, respectively. Recently, GOLD 2017 was officially released on November 16, 2016^[1]。 This update is the fourth major update in the history of GOLD, including the latest research results from 2015 to 2016. The updated content covers the definition of COPD, disease assessment, drug and non-drug treatment, complication management and many other aspects. This paper explains the main updated parts and related documents.

Since the Global Initiative for the Prevention and Treatment of Chronic Obstructive Pulmonary Disease (GOLD) was proposed in 1998, 18 years ago, the proposed airflow restriction has been throughout the definition and diagnosis, while the grouping and grading of patients and the drug treatment in the stable phase have undergone three major changes. First edition GOLD was released in 2001^[1]In GOLD 2006^[2]Refined and revised, based on airflow restriction, i.e. FEV₁, to classify COPD patients into GOLD grades 1, 2, 3, and 4, and to guide drug therapy in the stable phase. GOLD 2011^[3]There was a second change, in GOLD 2013^[4]Perfect, the introduction of symptoms and acute attacks during group grading, that is, acute exacerbation of symptoms, weakens lung function FEV₁The patients with COPD were divided into groups A, B, C and D. GOLD 2017 released in advance on November 16, 2016^[5], a third change occurred, the first complete abandonment of pulmonary function FEV at the time of group grading₁, using symptoms and acute exacerbations of symptoms alone, dividing patients into groups A, B, C, D, guiding medication in stable phase alone, and introducing respiratory symptoms into the definition for the first time, pulmonary function only guiding airflow restriction assessment, no longer guiding medication in stable phase. Here are a few of the author's thoughts on GOLD 2017 in terms of definition, evaluation, and stable-phase medication.

Tuberculosis is one of the major infectious diseases that threatens human health seriously, and rapid and accurate diagnosis methods are of great significance for effectively controlling tuberculosis. At present, proteomics technology has been widely used in the serological study of tuberculosis patients, and some important protein molecules have been discovered, which provides an important theoretical basis for the diagnosis and differential diagnosis of tuberculosis. This article reviews the application of serum proteomics in the diagnosis of tuberculosis patients.

idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic interstitial lung disease with unclear etiology and localized in the lungs. Its histology and/or chest high-resolution computed tomography (HRCT) is characterized by usual interstitial pneumonia (UIP)^[1,2]。 The clinical course of IPF is manifest as diverse, in which a significant proportion of patients can suddenly develop unpredictable acute exacerbations during a relatively stable period, resulting in acute respiratory failure and even death of the patient^[3,4]。 the Idiopathic Pulmonary Fibrosis Clinical Research Network (IPFnet), initiated by the National Heart, Lung, and Blood Institute (NHLBI) in 2007 The definition and diagnostic criteria of acute exacerbation of IPF were presented^[5]。 Since then, this definition and diagnostic criteria have been widely used in clinical practice and trials, deepening people's understanding of acute exacerbation of IPF and promoting the clinical and treatment research of acute exacerbation of IPF. However, many years of clinical practice and research have also found that there are some problems in the definition and diagnostic criteria of acute exacerbation of IPF in basic and clinical research^[6]。 2016 by Collard et al.^[7]An international special working group composed of many experts once again reviewed the literature related to acute exacerbation of IPF published in the past 10 years, and put forward important suggestions for modification of the definition and diagnostic criteria of acute exacerbation of IPF according to the existing research evidence.

Chronic obstructive pulmonary disease (COPD) is a kind of disease characterized by persistent airway inflammation and incomplete reversible airflow restriction, which develops progressively. During its pathophysiological process, due to the action of inflammatory factors, mediators and adhesion factors, the trachea and blood vessels are gradually remodeled, resulting in emphysema and pulmonary hypertension^[1]。 Nitric oxide is one of the biological active substances in the body, which can be used as messenger and regulator to participate in many physiological and pathological processes of the body, and has a good correlation with the degree of airway inflammation. The results showed that nitric oxide was involved in the regulation of pulmonary vascular tension and pulmonary vascular remodeling, and played an important role in the development of COPD to pulmonary heart disease^[2]。 fractional exhaled nitric oxide (FeNO) can reflect the level of nitric oxide in the airway. The results of the study show that the use of FeNO to monitor airway inflammation has high specificity and sensitivity, and can help to differentiate the phenotype of patients with COPD, guide treatment and evaluate the prognosis. The application of FeNO measurement in COPD is summarized as follows.

acute respiratory distress syndrome (ARDS) is a rapidly progressing clinical syndrome of dyspnea, hypoxemia, diffuse pulmonary infiltration and respiratory failure caused by many etiologies. Under the existing treatment methods, ARDS still has an extremely high mortality rate. Therefore, it is urgent to find new methods for treating ARDS. mesenchymal stem cell (MSC) is a kind of pluripotent stem cell with high self-renewal ability and multidirectional differentiation potential. It can differentiate into a series of mesenchymal cells, such as adipose tissue or cartilage tissue. MSCs can be isolated from a variety of tissues, such as bone marrow, umbilical cord, adipose tissue, and the like. MSC can regulate the host immune response to injury and infection, and promote tissue repair after injury, so MSC may be a good method for the treatment of ARDS. The research progress of MSC in the treatment of ARDS is summarized as follows.

The patient was a 66-year-old female. The main cause was "cough for 10 years and hemoptysis for 3 months", and he was seen in the outpatient clinic of our hospital on December 17, 2015. The patient developed dry cough without obvious trigger 10 years ago, and chest CT in the local hospital showed multiple small nodules and bronchiectasis in both lungs (Figure 1、Figure 2、Figure 3), diagnosed as "chronic bronchitis, bronchiectasis". Thereafter, the cough intermittently worsened, and levofloxacin anti-infective treatment was effective (details unknown). Hemoptysis occurred 3 months ago, a small amount of bright red bloody sputum daily, no fever, chest pain, shortness of breath. Chest CT showed that nodules and bronchiectasis in both lungs were more and more aggravated than before, and multiple new thin-walled cavities in the right upper lung (Figure 4、Figure 5、Figure 6), sputum smear acid-fast staining positive, diagnosed as "tuberculosis", given quadruple anti-tuberculosis treatment for 2 months, still intermittent hemoptysis, so came to our hospital. The patient had a history of spontaneous pneumothorax on the right side 15 years ago, and subsequently underwent right pleurodesis. Deny infection history of juvenile measles, whooping cough, pneumonia, etc. Denial of smoking history. Physical examination: emaciated body type, mild anemic appearance, unpalpable swelling of superficial lymph nodes, a little inspiratory damp rales can be heard in both lower lungs, no abnormalities in the heart and abdomen, and no pestle-shaped fingers/toes. Preliminary diagnosis: The cause of pulmonary cavity is to be investigated, bronchiectasis.

A 68-year-old male was admitted to the hospital on December 22, 2014 due to "chest pain, cough, asthma with fever for 10 days". The patient developed dull pain in the left chest without trigger 10 days ago, which was aggravated when coughing and deep breathing, coughing a small amount of white phlegm, accompanied by sustaining asthma, aggravated after activity, accompanied by fever, without night sweats and hemoptysis. Previous history of diabetes 1 year. Physical examination: temperature 37.6 ℃, blood pressure 120/80 mmHg (1 mmHg =0.133 kPa), superficial lymph nodes were not palpable for enlargement. Percussion of the left lower lung showed void sound, auscultation breathing sound was weakened, and pleural friction sound was not heard. The abdomen is soft, and the liver and spleen are untouched under the costs. No pestle fingers. Auxiliary examination: Blood routine showed that white blood cells were 12.8×10⁹/L, neutrophils were 0.68, CRP was 101.4 mg/L, ESR was 73 mm/1 h, and fasting blood glucose was 7.7 mmol/L. Serum ferritin was 1563.86 μ g/L (normal reference value: 21.81-274.66 μ g/L), lactate dehydrogenase (LDH) was 337 U/L (normal reference value: 114-240 U/L), β₂-Microglobulin was 2.47 mg/L. The liver, kidney and thyroid function were normal, and Epstein-Barr virus antibody and HIV antibody were negative. The serum tumor markers carcinoembryonic antigen (CEA), soluble cytokeratin 19 fragment (CYFRA211), neuron-specific enolase (NSE) and alpha-fetoprotein were not abnormal. PPD test (+). Bone marrow cytology: granular and giant hyperplasia, and erythroid hyperplasia decreased. Abdominal color Doppler ultrasound showed hyperechoic area of the right lobe of the liver, thick and rough gallbladder wall and hyperechoic inside (except polyps). Enhanced CT of thoracic abdomen and pelvic cavity showed left pleural nodule, pleural mesothelioma? Left pleural effusion, partial consolidation of left lung; Fatty liver (Figure 1，Figure 2)。 Pleural effusion was drawn by thoracentesis and submitted for examination. Pleural effusion routinely showed: orange-red, turbid and clot in appearance, positive protein, and white blood cells of 1 050×10⁹/L, 90% for unilobar nuclei and 10% for multilobar nuclei. Pleural effusion had LDH of 1 030 U/L, adenosine deaminase (ADA)>200 U/L, positive chyle test, normal CEA and CYFRA211, and NSE of 21.3 μ g/L. Pleural effusion smear was negative for acid-fast bacilli and culture, and lymphocytes and mesothelial cells were found in multiple exfoliative cytology, but no cancer cells were found. CT-guided percutaneous biopsy pathologically revealed malignant tumor, and immunohistochemical detection diagnosed non-Hodgkin's lymphoma, tending to non-specific peripheral T-cell lymphoma (Figure 3、Figure 4、Figure 5、Figure 6)。 The patient was transferred to the oncology department for 3 cycles of CHOP regimen chemotherapy (cyclophosphamide 1 g d₁, epirubicin 60 mg d₁, 50 mg d₂, vincristine 2 mg d₁, prednisone 100 mg d_1－5, 21 d 1 cycle). The patient's body temperature dropped to normal, but he still had chest pain and wheezing. Re-examination of chest CT showed uneven thickening of left pleura, increased and enlarged nodules in both lungs, pericardial effusion, low-density areas in thoracic vertebrae and ribs, and metastasis could not be ruled out. The patient refused further chemotherapy and died 10.5 months after diagnosis.

November 10-12, 2016, 2nd International Cough Conference (2^ndInternational Cough Conference) Held in Shenzhen. Academician Zhong Nanshan, director of the State Key Laboratory of Respiratory Diseases, served as the chairman of this conference, Professor Kian Fan Chung, chairman of the British Cough Forum, Professor Peter Dicpinigaitis, chairman of the American Cough Conference, and Professor Lai Kefang, the drafter of the first cough diagnosis and treatment guidelines in China, served as the co-chairmen of the conference. The conference set up 8 special sessions and 27 special topics. Top experts in cough and related fields from China, some European countries, the United States, Canada, Australia, Japan, South Korea and other domestic and foreign countries gave wonderful reports to the participants. This conference called for papers worldwide, set up oral speeches and poster exchange sessions, and displayed the publicity poster of "Chronic Cough in China", which reflected China's achievements in Chronic Cough research and Cough guidelines promotion, increased the understanding of domestic and foreign peers about each other, and greatly promoted the exchanges between domestic and foreign peers. Professor Alyn Morice, President of the European Respiratory Association (ERS) Cough Guidelines, described the meeting as the best cough conference he has attended. This article captures the highlights of related topics of the conference for readers.

Recently, I had the honor to read "Physiological Basis and Strategy of Mechanical Ventilation for Bronchial Asthma" published in the 7th Issue of Chinese Journal of Tuberculosis and Respiration in 2014^[1]One article, benefited a lot. From the pathophysiological characteristics of bronchial asthma (asthma) during acute attack and the application strategy of mechanical ventilation, this paper introduces the timing and methods of mechanical ventilation support treatment for severe asthma patients, and provides a reference for respiratory and critical care doctors to use mechanical ventilation reasonably and correctly, so as to reduce complications and improve the prognosis of asthma patients.

Most of our initial understanding of inspiratory dyspnea came from the textbook of Diagnostics. Later, when we saw the "three concave signs" in clinic, we naturally first thought of "stenosis and obstruction of the larynx, trachea and big bronchus". In fact, for respiratory physicians, the three concave signs are common, as well as severe chronic airflow obstructive diseases such as chronic obstructive pulmonary disease (COPD) and bronchial asthma (asthma). In patients with severe COPD, assistive respiratory muscle activity and three concave signs can appear even at ordinary times, and it is more obvious in acute exacerbation. While for asthma, assisting respiratory muscle activity and the triple concave sign are important signs of severe attacks and are meaningful for assessing the severity of acute attacks^[1]。

hyper-IgE syndrome (HIES), also known as Job syndrome, is a rare and complex primary immunodeficiency syndrome. Characteristic clinical manifestations are repeated skin abscess formation (mostly caused by staphylococcal infection), eczema, and pulmonary infection with significantly elevated serum IgE levels and increased blood eosinophilia. According to different inheritance patterns, HIES can be divided into autosomal dominant HIES (AD-HIES) and autosomal recessive HIES (AR-HIES). The majority of clinical cases are AD-HIES, accounting for more than 60% ~70%, mainly caused by STAT3 gene mutation.

Reverse halo sign is a special chest CT sign, which is characterized by annular high-density shadow surrounding the central low-density lung shadow. It was first reported by Voloudaki et al. in 1996 and was seen in 2 cases of cryptogenic organizing pneumonia. This CT sign is described as the lung shadow surrounded by annular high-density shadow. In 2003, Kim et al. named it "reversed halo sign (RHS)", and compared the CT images of 31 cases of cryptogenic organizing pneumonia with 30 cases of other lung diseases, and found that the reversed halo sign was only seen in cryptogenic organizing pneumonia, thus considering the reversed halo sign as a characteristic sign of cryptogenic organizing pneumonia; However, the reverse halo sign has since been reported in a variety of other diseases, such as pulmonary paracoccidioidomycosis, pulmonary lymphomatoid granulomatosis, pulmonary sarcoidosis, invasive pulmonary mycosis, active pulmonary tuberculosis, and granulomatous polyangiitis (formerly Wegener's granuloma), as well as in organizing pneumonia secondary to infection or collagen angiopathy. In 2008, the Fleischner Society's thoracic imaging glossary officially included the "reversed halo sign (RHS)".

Pulmonary hypertension (PAH) is a chronic fatal disease characterized mainly by an increase in pulmonary vascular resistance and ultimately right heart failure. Progressive pulmonary vascular wall thickening and remodeling is the pathological basis of increased vascular resistance in PAH. Sodium tanshinone IIA sulfonate (STS), one of the active ingredients of Salvia miltiorrhiza, a water-soluble product of tanshinone IIA sulfonation, has been shown to improve right ventricular hypertrophy and pulmonary vascular remodeling in a rat model of chronic hypoxic pulmonary hypertension. The mechanism of this process involves the protective effect of STS on calcium homeostasis in pulmonary artery smooth muscle cells (PASMCs). Our previous study showed that STS can inhibit calcium pool manipulative calcium ion influx (SOCE), i.e., calcium ion influx through calcium pool manipulative calcium ion channels (SOCC), mainly by inhibiting the expression of the main component of SOCC, the classical transient receptor potential channel protein (TRPC). However, its specific molecular mechanism remains unclear. Previous studies have demonstrated that inhibition of protein kinase G (PKG) and peroxisome proliferator-activated receptor gamma (PPAR gamma) signaling pathways can upregulate the expression of TRPC, suggesting that the restoration of the function of this signaling pathway may be an effective therapeutic strategy for pulmonary hypertension. This study aims to demonstrate that STS treatment can prevent the inhibition of PKG-PPAR γ signaling pathway by hypoxia, thus playing a benign role in the hypoxia-induced increase of calcium influx and cell proliferation in rat distal pulmonary artery and pulmonary artery smooth muscle cells (PASMCs).