2017年 · 第40卷第04期

In this editor's essay column, Liu Youning, the editor-in-chief of this journal, wrote the article "Low-dose CT screening for lung cancer is indispensable". He believes that in the article "The right and wrong of low-dose chest CT screening for lung cancer" written by Zhang Guozhen and Bai Chunxue published in the fourth issue of 2015, the author very incisively demonstrated the advantages and disadvantages of low-dose chest CT screening for lung cancer, and fully affirmed this method on the basis of citing a large number of irrefutable facts. CT screening for lung cancer began in Japan. At the beginning, there was indeed controversy about whether it could reduce mortality and whether patients could really benefit, but a large number of convincing evidence in the later stage basically proved that it was both effective and beneficial. Subsequently, Professor Liu discussed this issue in depth, believing that lung cancer is different from some surface tumors, and CT screening can significantly reduce the mortality rate of lung cancer, which can obviously benefit the subjects. He also explained the role of CT screening on lung nodules, whether screening will lead to excessive surgical treatment and medical expenses, etc., with clear views and strong readability.

In the fourth issue of 2015, this journal published an article signed by Zhang Guozhen and Bai Chunxue^[1]This article demonstrates the advantages and disadvantages of low-dose chest CT screening for lung cancer (referred to as CT screening) very incisively, and fully affirms this method on the basis of citing a large number of irrefutable facts. The controversy could have been settled, but recently the scheme has faced unprecedented challenges in China, and it is even in danger of being completely subverted. The reason for this is that the expert who raised the objection is too high and too authoritative.

Although medical science and technology have made "leaps and bounds" in recent years, most diseases faced by doctors until today, such as tumors, metabolic diseases, autoimmune diseases, etc., cannot be completely cured. Even the most common bronchial asthma and COPD often require lifelong uninterrupted treatment. Infectious diseases are quite different from the above diseases, and most of them are expected to be completely cured in a relatively short time as long as they are accurately diagnosed and treated appropriately. Infection can occur in all clinical departments and any part of the human body. Therefore, the diagnostic techniques and treatment methods related to infection are one of the basic skills that all clinicians should master.

Tuberculosis is a chronic infectious disease caused by MTB infection. Its pathogenesis is complicated, and some mechanisms are not very clear. Nuclear factor-kappa B plays a key role in the transcriptional regulation of genes involved in a variety of animal immune and inflammatory responses. When the body is infected with MTB, the activated CD₄^＋Th1 cells can secrete a large number of pre-inflammatory factors such as IL-2 and gamma-interferon (INF-γ), and induce the activation of nuclear factor-κ B. Coactivator-associated arginine methyltransferase 1 (CARM-1) induction is required for nuclear factor-κ B-dependent gene subsets. CARM-1 can enhance the recruitment of nuclear factor-κ B to relevant sites, activate the nuclear factor-κ B signal transduction pathway, and initiate the transcription of various pro-inflammatory genes, thus causing inflammatory response. This study was approved by the Ethics Committee of Affiliated Hospital of Zunyi Medical College. The expression of CARM-1 and nuclear factor-κ B in lung tissues of patients with pulmonary tuberculosis was detected by immunohistochemistry, and their role in the pathogenesis of pulmonary tuberculosis was observed.

Tuberculous pleurisy (TP) is one of the most common types of tuberculosis in China. The key to improving the prognosis of TP is early diagnosis and early treatment. Early drainage of pleural effusion and systemic anti-tuberculosis therapy can effectively control the growth of pleural effusion and prevent pleural thickening and pleural adhesion^[1,2,3]。 In recent years, it has been found that more and more patients have pleural tuberculoma in the treatment^[4]。 How to predict the occurrence of pleural tuberculoma in the early stage of TP treatment is of great significance to prevent the occurrence of pleural tuberculoma and improve the prognosis of patients. It has been reported that the level of plasminogen activator inhibitor-1 (PAI-1) in tuberculous pleural effusion is higher than that in cancerous pleural effusion, the level of tissue-type plasminogen activator (t-PA) is lower, and the level of PAI-1 and t-PA in TP patients with pleural thickening is higher than that in patients without pleural thickening^[5]。

Example 1Male, 52 years old, was admitted to the Department of Respiratory Medicine, the First Affiliated Hospital of Guangxi Medical University on March 27, 2012 due to "repeated cough, expectoration with hemoptysis for more than 3 years and recurrence for 6 days". In February 2010, the patient developed cough, expectoration and hemoptysis after drinking a lot of alcohol. The hemoptysis was bright red, 3~5 ml, accompanied by chest tightness and palpitations. He did not pay attention to it and consulted a doctor. The symptoms appeared repeatedly, and the daily hemoptysis volume varied, with a maximum of 25~50 ml. Chest CT performed at the local hospital showed multiple miliary nodules in both lungs and enlarged mediastinal lymph nodes, chronic inflammation of the tongue lobe of the left lung and the middle lobe of the right lung. Symptomatic treatment according to "pneumonia and bronchiectasis" was given many times, but hemoptysis still repeated, and the symptoms reappeared after catching cold 6 days ago. Weight loss of about 7 kg since illness. Admission physical examination: scattered folliculitis-like and acne-like rashes on the chest and back, painful ulcers on the skin and mucosa around the coronal sulcus of the mouth and penis, and no abnormalities were found on cardiopulmonary and abdominal examination. Blood routine: white blood cell count 5.60×10⁹/L, hemoglobin 142 g/L, platelet count 142×10⁹/L, lymphocyte ratio 0.226, neutrophil ratio 0.630. ESR 27 mm/1 h. High sensitivity C-reactive protein (whole course) 15.50 mg/L. Immunoglobulin G: 16.24 g/L, Immunoglobulin M: 1.37 g/L, Immunoglobulin A: 1.22 g/L. Autoantibodies: Anti-RO-52 antibody was weakly positive, and all other autoantibodies were negative. D-dimer 227 ng/ml. Blood gas analysis: pH 7.37, PaO₂was 75 mmHg (1 mmHg =0.133 kPa), PaCO₂46 mmHg. There were no abnormalities in liver and kidney function, electrolytes, myocardial enzymes, serum troponin, anti-streptococcal hemolysin O, rheumatoid factor, tumor markers, complement C3, C4 and HIV antibody. The electrocardiogram showed complete right bundle branch block. B-ultrasound of deep and superficial veins of both lower limbs showed no thrombosis. Color Doppler ultrasound showed a decrease in left ventricular compliance and no abnormalities in heart morphology and valve function. Chest CT showed inflammation of both lungs and enlarged mediastinal lymph nodes. CT pulmonary angiography (CTPA) showed dilatation and stenosis of the anterior branch of the left upper lobe pulmonary artery, and mural thrombosis (Figure 1)。 The acupuncture reaction at the cubital vein puncture site was positive. Behcet's disease with pulmonary embolism was clinically diagnosed. On April 24, 2012, he was given methylprednisolone 40 mg/d and cyclophosphamide (CTX) 0.2 g orally once/d. Hemoptysis disappeared. After discharge, he continued to take oral prednisone and dipyridamole, and returned to hospital regularly for CTX pulse therapy. In 2015, his condition was stable, and he was lost to follow-up after discontinuing the drug voluntarily.

Aspergillus is widely present in nature and leads to different types of disease states due to different host immune status. The lung is the most common site of aspergillosis. Compared with the lung parenchyma, airway-associated aspergillosis has been reported and studied less. Aspergillus-associated airway lesions come in many forms, including airway invasive pulmonary aspergillosis, allergic bronchopulmonary aspergillosis, and aspergillus globuli, reflecting the infectious, allergic, and parasitic states caused by Aspergillus in the airways^[1,2]。 "aspergilloma or aspergilloma" refers to fungal spheres composed of Aspergillus filaments and extracellular matrix, and the previous concept is more general^[3]； New guidelines for the diagnosis and treatment of chronic pulmonary aspergillosis (CPA)^[4]The concept of "single aspergilloma" is proposed in, which specifically refers to an aspergilloma that does not progress for a long time in a cavitary lesion. However, the broad sense of "aspergilloma" appears as an imaging feature in many types of CPA, and it is necessary to distinguish specific disease types according to clinical manifestations. A case of endo-bronchial aspergilloma (EBA) was reported, and its clinical characteristics, diagnosis and treatment were discussed.

Bronchial stump thoracic fistula (BPF) is a rare complication after lobectomy. With the development of medical devices and interventional diagnosis and treatment technology, there are more and more methods to occlude BPF. The authors have previously mainly used L-shaped or Y-shaped stents to treat BPF^[1]However, for patients with large fistulas, the efficacy is poor, and there are more complications after stent placement. Recently, the author used atrial septal occluder to block 2 cases of BPF, and achieved very good results, which are reported as follows.

The patient, a 66-year-old female, was admitted to the hospital on September 8, 2015 due to "intermittent cough and sputum for more than 9 months". The patient coughed 9 months ago and coughed a large amount of white foamy sputum without fever or dyspnea. She underwent chest CT in another hospital (Figure 1) showed a large consolidation shadow in the lower lobe of the right lung and diffuse ground glass shadow around it. Blood examination routine, blood carcinoembryonic antigen was normal, and the effect of anti-infective treatment for 9 days was not good. He went to the thoracic surgery department of our hospital and was considered to be lung cancer. On February 9, 2015, he underwent right lower lobe resection and mediastinal lymph node dissection. Postoperative pathology: central invasive mucinous adenocarcinoma, the tumor size is about 6 cm ×6 cm ×4.5 cm, the bronchi and blood vessels are clean, the mediastinum and hilar lymph nodes are not metastasized, but the tissue cells in the alveolar cavity are aggregated, and the postoperative stage is ⅡA (T_2bN₀M₀)。 The patient still had cough and sputum, but it was better than before. The patient was concerned about chemotherapy-related adverse reactions and did not consent to adjuvant chemotherapy. Four months ago, the patient was followed up in the thoracic surgery clinic, and the blood carcinoembryonic antigen was normal, and the chest CT (Figure 2，Figure 3) showed multiple cystic lesions in the right lung, which were not taken seriously. Chest CT was re-examined 2 months ago (Figure 4，Figure 5), the patient's lung cystic lesions and solid nodule lesions were significantly increased compared with before, and lung function: FEV₁% of estimates is 116.4%, FEV₁/FVC was 70.95%, TLC as % of the projected value was 99.4%, D_LCO accounted for 72.8% of the estimated value, and no obvious abnormalities were found under bronchoscopy. The left B3 BALF leukocyte classification: macrophages 51%, neutrophils 7%, lymphocytes 40%, eosinophils 2%, Aspergillus galactomannose antigen detection 0.168, smear was negative for acid-fast bacilli, bacterial and fungal cultures were negative, and cytomegalovirus DNA was negative. The right B4 bronchial TBLB pathology showed alveolar septum widening, fibrous tissue proliferation, chronic inflammatory cell infiltration, part of alveolar cavity dilatation, and more histiocyte aggregation could be seen in it. Past history: Disorder of lipid metabolism was found for 5 years, did not smoke, and underwent hysterectomy and double adnexal for ovarian cyst 30 years ago.

obstructive sleep apnea (OSA) is a common and frequently occurring disease caused by repeated collapse of the upper airway during sleep, which causes apnea and intermittent hypoxia, which leads to a series of clinical manifestations such as dry mouth in the morning, fatigue and drowsiness during the day, etc. Current clinical studies have shown that OSA can affect the prevalence and prognosis of cardiovascular disease (CVD)^[1,2,3,4]。 continuous positive airway pressure (CPAP), the preferred treatment for OSA, reduces the sympathetic nerve activity, reduces the production of inflammatory factors and reduces the risk of cardiovascular diseases in OSA patients by eliminating intermittent hypoxia at night^[5]。 However, the direct correlation between CPAP and CVD is not very clear. Therefore, Professor Doug McEvoy from the sleep Health Research Center in Adelaide, Australia initiated the sleep apnea cardiovascular endpoints study (SAVE) in 2008. This is a large-scale, multicenter, prospective, open-label, parallel randomized controlled study. The main purpose is to test whether long-term CPAP use in OSA patients can reduce cardiovascular endpoint events such as stroke, heart attack, heart failure and death. The study ended in December 2015 and was subsequently published onN Engl J Med。 The results of the study showed that for CVD patients with OSA, CPAP ventilation treatment did not reduce the risk of cardiovascular disease, but improved the quality of life of patients, including daytime sleepiness symptoms, depressive symptoms, and also increased attendance.

Although the guidelines for the diagnosis and treatment of community acquired pneumonia (CAP) are updated every year in various countries, there are still many new problems to be solved due to the aging of the population, pathogen changes and increasing antibiotic resistance rates. pneumonia recurrence and death from infection are still common^[1,2]。 Hospital discharge is important as a part of CAP diagnosis and treatment. Early discharge can shorten the hospital stay and reduce the hospitalization cost^[3]； However, the wrong timing of discharge may lead to adverse consequences, such as patient readmission or even death^[4,5,6,7]。 From the early days of CAP diagnosis and treatment guidelines to the present, the discharge criteria have been changing, and the criteria pay more and more attention to evidence-based medical evidence. However, in recent years, the discharge criteria have become increasingly stable, and the differences are not great.

Influenza A virus is an important pathogen of respiratory tract infection, which has caused many pandemics worldwide and seriously threatened human health. The novel outbreak of influenza A (H1N1) that swept 214 countries worldwide in 2009 killed at least 18,449 patients worldwide^[1]Since 1997, the highly pathogenic A (H5N1) virus was reported to infect and kill people, it has infected 848 people in 15 countries and killed 449 cases, with a case fatality rate of nearly 53%^[2]In 2013, the new type of influenza A (H7N9) was prevalent in China^[3]There are still new cases. Virus superinfection will also cause antigenic shift and antigenic drift between the main antigen hemagglutinin (HA) and neuraminidas (NA) genes, resulting in more virulent pathogens^[4]。 In recent years, scientists have discovered a novel anti-influenza virus factor-interferon-induced transmembrane (IFITM), which brings hope for the development of anti-influenza virus drugs.

community acquired pneumonia (CAP) is an important cause of death from infectious diseases. Even with the improvement of diagnosis and treatment, the mortality rate of hospitalized CAP patients is still high^[1]。 The percentage of CAP patients in the United States requiring ICU admission is as high as 21%^[2]And up to 10% to 20% of patients with severe CAP fail treatment^[3,4]。 Diffuse lung injury is the root cause of ARDS and respiratory failure in severe pneumonia. Neutrophils as an important factor in acute lung injury associated with severe pneumonia^[5]C5a is involved in this process in many ways as a chemokine and activator of neutrophils. At present, there is no effective drug for immune-mediated lung injury in clinical practice. If C5a can be used as an intervention target to reduce lung injury related to severe pneumonia and improve the prognosis of patients with severe pneumonia, it will be of great significance. In view of this, the mechanism of C5A-induced acute lung injury and the corresponding potential therapeutic links are reviewed below.