2017年 · 第97卷第46期

Sepsis is an uncontrolled inflammatory response caused by infection, and the release of a large number of inflammatory mediators can cause acute circulatory failure and multiple organ failure (MODS). Since the first edition of the "Guidelines for the Treatment of Severe Sepsis and Septic Shock" was published in 2004, the "clustered" treatment strategies including fluid resuscitation, early anti-infection and circulatory support have been continuously advanced. More and more sepsis patients can survive the early stage of circulatory failure and MODS. 70% of sepsis patients die 3 days after the onset of the disease, and some patients even die after several weeks^[1]。 The rate of late death in patients with septic shock is as high as 62.7%, and the trend is increasing year by year^[2]。 The data showed that nearly half of the pathogens obtained from blood culture and tissue culture of patients with advanced sepsis were fungi and other opportunistic pathogens, suggesting the occurrence of secondary infection. More importantly, secondary infection increases the risk of death in sepsis patients by more than five times, and the absolute mortality rate also increases by nearly 20%^[2,3]。 In view of this, effective prevention and treatment of sepsis secondary infection will help to further reduce the mortality of sepsis patients.

With the progress of medicine, the pregnancy rate of women with chronic kidney disease (CKD) is higher than before, and the overall fetal live birth rate is significantly increased. However, there is still a great risk of pregnancy in patients with CKD: adverse outcomes for pregnant women include aggravation of original kidney damage, acute kidney injury and pregnancy-related kidney disease, increased proteinuria, increased blood pressure, and preeclampsia (PE), etc.; Adverse fetal outcomes include stillbirth, fetal growth restriction (FGR), and preterm birth. With the comprehensive liberalization of the two-child policy in China, the pregnancy problem of CKD patients has increasingly become a common challenge faced by nephrologists and obstetricians. Therefore, in order to reduce the damage of pregnancy to the maternal kidney and mitigate the adverse effects on pregnant women and fetal outcomes, nephrologists and obstetricians need to normally assess the risk of pregnancy in patients with CKD, determine the optimal timing of pregnancy, stabilize the patient's condition, and closely monitor during pregnancy to detect pregnant women and fetal complications early. Chinese experts in the field of nephrology and obstetrics have drawn on the recent clinical research literature on CKD pregnancy at home and abroad and combined with domestic clinical practice to formulate pregnancy guidelines for CKD patients, aiming at guiding pregnancy of CKD patients, strengthening pregnancy management, improving pregnancy success rate, reducing pregnancy complications, improving maternal and infant survival rate, and improving pregnancy outcomes of CKD patients in China.

Pulmonary hamartoma is the most common benign lung tumor, accounting for 75% of all benign lung tumors^[1]； According to the site of occurrence, they are divided into intrapulmonary type, intrabronchial type and intrapulmonary combined intrabronchial type. Among them, intrabronchial hamartoma accounts for about 1.4% ~10%^[2]。 The traditional treatment for pulmonary hamartoma is surgical resection, but it is more invasive. With the rapid development of respiratory interventional techniques, snare, argon plasma coagulation (APC), CO can be performed under bronchoscopy₂Many operations such as cryoablation, clamp removal and tumor removal^[3]。 Bronchoscopic treatment is minimally invasive, and is very suitable for the treatment of endobronchial hamartoma. The clinical data of 12 patients with endobronchial hamartoma diagnosed and treated under bronchoscopy since 2007 in the Department of Respiratory and Oncology of Coal General Hospital are summarized and analyzed as follows.

Acute aortic dissection (AAD) is a disease with high mortality and disability rate. Classical AAD mainly takes chest pain and back pain as the first manifestation, but there are many clinical findings that AAD takes neurological defect as the first manifestation. This study summarized the clinical, imaging, treatment and outcome characteristics of 6 patients with AAD with neurological symptoms as the first manifestation, and carried out relevant literature analysis to further improve the understanding of such cases and avoid clinical misdiagnosis and misdiagnosis.

The 27-year-old male was admitted to the 254th Hospital of the People's Liberation Army on February 8, 2017 due to "a tumor in the right adrenal area found in physical examination for 2 months". In late December 2016, the patient was found to have a tumor with a diameter of 3 cm in the right adrenal area during physical examination in the local hospital. During the illness, he had no discomfort such as dizziness, palpitations and hyperhidrosis, and had no symptoms such as purple lines on the skin, full moon face and buffalo back. On February 3, 2017, CT examination of both kidneys in our hospital further confirmed that it was a right adrenal mass and diagnosed as "adrenal mass". During the course of the disease, the patient's spirit, diet and sleep were good, and there was no discomfort such as fever, chest tightness and shortness of breath. The patient was previously in good health. No abnormalities were found in physical examination, and the indexes of adrenal-related laboratory examination were all within the normal reference range. Plasma renin activity: 2.09 μ g/L, angiotensin II: 96.4 ng/L, aldosterone (recumbent position): 33.7 μ g/24 h, blood cortisol: 145 μ g/L, corticotropic hormone: 20.3 ng/L. Enhanced CT showed an oval mass shadow in the medial branch of the right adrenal gland, with smooth outline and clear boundary, patchy high-density shadow and irregular low-density area (Figure 1), no enlarged lymph nodes were seen in the peritoneum and retroperitoneum, and cyst with calcification was considered. The patient's vital signs were stable, and he was given intravenous drip of hydroxyethyl starch and sodium chloride to expand the volume before operation. On February 24, 2017, he underwent laparoscopic adrenal tumor resection under general anesthesia.

Heparin-induced thrombocytopenia (HIT) is a side effect mediated by antibodies during the treatment of heparin drugs (including unfractionated heparin and low molecular weight heparin). It is mainly manifested by a significant reduction in platelet count, and in severe cases it can lead to venous and arterial thrombosis. The incidence of HIT is low, but the clinical consequences are serious. Among hospitalized patients, thrombocytopenia and heparin exposure due to various causes are prevalent, resulting in significantly more suspected HIT patients than confirmed patients. Therefore, how to accurately identify HIT, treat it in a timely and effective manner, and avoid overtreatment has become an important challenge for clinicians^[1,2,3]。 Based on recent evidence-based research evidence (systematic review, meta-study, clinical controlled trials and guidelines, etc.), this paper expounds the research progress of clinical diagnosis and treatment of HIT.

Hepatitis-cirrhosis-liver cancer is the "three steps" of liver disease evolution. Pathology, molecular biology and imaging studies confirmed^[1,2]In the process of malignant transformation of liver cirrhosis-liver cancer, a long process of precancerous lesions of liver cancer will be experienced. Precancerous lesions of liver cancer^[3]Including hepatocytic dysplasia, dysplasia foci, low-grade dysplasia nodules (LGDN), high-grade dysplasia nodules (HGDN), and hepatocellular adenoma (HCA). Precancerous lesions of liver cancer are the transitional stage from benign lesions to malignant lesions. It is a kind of proliferative lesions with atypical cells and abnormal differentiation, and it lasts for a long time. If the cause is removed in time or treated appropriately, this malignant process may be stopped or even recovered.

Hemophagocytic syndrome (HLH) is a macrophage proliferative disease with multiple organ and system involvement and progressive exacerbation with immune dysfunction. Diseases can be divided into primary HLH with abnormal cell function due to gene mutation and secondary HLH secondary to infection, autoimmune diseases, malignant tumors, etc^[1]。 Rivieve et al.^[2]A study of 162 patients with HLH showed that hematological malignancies, especially non-Hodgkin's lymphoma, were the main causes of HLH, accounting for 56% of the subjects studied. It can be seen that malignant tumors, especially lymphoma, are one of the most common causes of HLH. In this paper, the clinical manifestations, laboratory tests, pathogenesis, diagnosis and treatment of LAHS are introduced, which can provide clinical reference.

There are many ways to classify tumors. According to the location of occurrence, they can be divided into lung cancer, breast cancer, gastric cancer, colorectal cancer, pancreatic cancer, etc. According to the disease stage, they can be divided into stages 1, 2, 3 and 4. According to whether it metastasized or not, it is divided into in situ tumors and metastatic tumors. With the popularity of immunotherapy, especially immune checkpoint inhibitors, hot and cold tumors appear in the new classification of tumors. If there are many immune cells around cancer cells that can recognize cancer cells, then the tumor is a hot tumor, otherwise it is a cold tumor. Mechanistically speaking, tumor cells prevent immune cells from killing cancer cells by initiating immunosuppressive mechanisms during evolution. This situation mainly occurs in hot tumors. In response to this situation, emerging immune checkpoint inhibitor therapies or other immunotherapies can specifically activate immune cells (mainly T cells) around tumor cells, thereby inducing an immune response and killing hot tumors. However, in cold tumors, the above-mentioned immune checkpoint inhibitors or immunotherapy are not very effective. It is mainly due to the lack of effective mutant proteins on the cell surface of cold tumors to activate and attract immune cells. Therefore, how to regulate the mutant proteins on the surface of cold tumors, or to strengthen immunotherapy and apply immune checkpoint inhibitors is the key to enhance the sensitivity of tumor immunotherapy, and it is also an important means to transform cold tumors into hot tumors^[1]。