2015年 · 第95卷第06期

Primary hepatocellular carcinoma (HCC) is one of the common malignant tumors, and its mortality rate is the third among common cancers worldwide, and the second highest in China. 85% of HCC in China is caused by chronic hepatitis B virus (HBV) infection. The annual incidence of HCC in patients with HBV-related cirrhosis is 3% ~5%, and about one third of the disease will eventually develop into HCC in the course of the disease. Surgical resection is the most important radical treatment for HCC, but the recurrence rate is as high as 70% within 5 years after surgery, which is a major obstacle to further improve the curative effect^[1]。 Up to now, there is still a lack of clinical adjuvant therapeutic drugs that can effectively control postoperative recurrence.

Venous thromboembolism (VTE) includes deep vein thrombosis (DVT) and acute pulmonary thromboembolism (acute pulmonary embolism, APE). APE is a kind of disease that seriously threatens human life and health. About 300,000 patients die of APE every year in the United States, of which about 1/3 are sudden deaths^[1]。 Anticoagulation therapy plays an important role in the treatment of APE. Some large-scale clinical trials in recent years have provided evidence-based medical evidence for the use of novel oral anticoagulants (NOACs) in pulmonary embolism^[2,3]。 NOACs are not only not inferior to warfarin in APE anticoagulant effectiveness, but also appear to be superior to warfarin in safety endpoint events such as major bleeding. To this end, the 2014 European Society of Cardiology (ESC) APE guidelines made the first comprehensive recommendation on the use of NOACs in APE (Level of Evidence: IB)^[4]。 At present, the NOACs that have been marketed in my country include dabigatran etexilate and rivaroxaban, and their indications are to prevent venous thrombosis after orthopedic surgery. A few doctors in China have started to use these NOACs to treat APE, but due to insufficient experience in their use, the treatment is still not standardized. This article focuses on the application of NOACs in the treatment of APE according to the 2014 ESCAPE diagnosis and treatment guidelines.

The 43-year-old female was admitted to the Department of Nephrology of Peking Union Medical College Hospital in June 2013 due to repeated purpura for more than 1 year, oliguria for 2 months, abdominal pain and bloody stool for 1 week. The patient developed purpura-like rash on both calves in March 2012. He went to the local hospital and was given dexamethasone and anti-allergic treatment. Later, due to hepatitis B, he was stopped and changed to entecavir antiviral therapy, and his platelets returned to normal. After recurrent rash, bone marrow puncture examination was negative. In April 2013, he developed oliguria with edema, multiple joint swelling and pain with numbness in the extremities. Routine urine check, red blood cells + +, urine protein + + +. In June 2013, daily upper abdominal colic began to occur, and blood stools were discharged 12 to 13 times, 50 to 100 ml each time. The local hospital checked the white blood cells 15.6×10⁹/L, neutrophils 0.718, platelets 69×10⁹/L, albumin 28 g/L. Gastroscopy showed an ulcer on the anterior wall of the duodenal bulb, which was relieved after fasting and water, fluid rehydration and anti-infection treatment. In June 2013, he came to the emergency department of our hospital and was transferred to the nephrology department for further treatment. Past history: Hepatitis B Xiaosanyang was found in physical examination in 2003, and he was treated with traditional Chinese medicine. In 2012, he started antiviral treatment. After admission, the relevant examinations were completed. Blood routine: white blood cells 7.8×10⁹/L, neutrophils 0.897, hemoglobin (Hb) 82 g/L, platelets 139×10⁹/L; Urinary routine: 200 red blood cells/μ L, urine protein 0.3-3.0 g/L; 24-h urine protein quantitation was 3.22-4.69 g; Fecal routine occult blood (+); Alanine aminotransferase (ALT) 17 U/L, albumin 26 g/L, creatinine 164 μ mol/L, urea 35.19 mmol/L, uric acid 1 060 μ mol/L; Coagulation function: Plasma prothrombin time assay (PT) 17.0 s, activated partial thromboplastin time (APTT) 25.6 s, D-Dimer (D-Dimer) 10.22 mg/L, fibrinogen (Fbg) 2.48 g/L; Complement C3 0.111 g/L, complement C4 0.001 g/L, IgG 2.14 g/L, IgA and IgM normal, rheumatoid factor (RF) 324.4 U/ml; anti-soluble antigen (ENA), anti-glomerular basement membrane antibody (anti-GBM) negative (-); Anticardiolipin antibody (ACL), anti-beta₂-Glycoprotein I antibody (anti-beta₂-gpI antibody), lupus anticoagulant (LA) (-); cytomegalovirus (CMV), Epstein-Barr virus (EBV) (-); Serum protein electrophoresis monoclonal immunoglobulin percentage (M protein %) 0.6%, M protein quantitation 0.30 g/L; Blood free light chain κ 27.1 mg/L increased (↑), λ 10.1 mg/L, κ/λ 2.68 ↑; Immunofixation electrophoresis: IgA kappa type M protein (+); Cryoglobulin (CG) (+). Hepatitis B surface antibody (HBsAg), hepatitis B core antibody (HBcAb), hepatitis B e antibody (HBeAb) (+), hepatitis B virus DNA (HBV DNA) 49 U/ml. Hepatitis C virus antibody (HCV Ab) (–). Three items of liver fibrosis: hyaluronic acid, type III procollagen peptide N-terminal, and type IV collagen (–). Renal vein, portal system, vein ultrasound of both upper limbs, lower limbs (–). Abdominopelvic CT: low-density shadow of the liver, considering the possibility of cyst, splenomegaly, increased peripancreatic fat density with multiple cord shadows, and multiple small lymph nodes retroperitoneal. Bone scan: roughly normal. Bone puncture + bone marrow biopsy: approximately normal. Admission diagnosis: acute kidney injury, cryoglobulinemia? Purpura nephritis? Multiple peripheral neuropathy, gastrointestinal hemorrhage, chronic HBV infection, duodenal ulcer.

In recent years, with the application of spiral CT technology and the publication of the results of low-dose CT early lung cancer screening research, the number of chest CT examinations in healthy physical examination population is increasing day by day, and the detection rate of pulmonary ground glass density nodules (GGN) is also increasing year by year^[1]。 GGN is a special type of small pulmonary nodule. It appears as a round or oval cloud-like thin density-increased shadow on the pulmonary window of high resolution CT (HRCT). The bronchial vascular texture in the lesion is still recognizable, and the solid components in the lesion are not visible or only visible on the mediastinal window. GGN can be divided into pure GGN (pGGN) and partially solid GGN according to whether solid components can be seen in the mediastinal window^[2]。 The retrospective data of physical examination in our hospital showed that the number of chest CT examinations increased from 1 019 cases/year to 26 108 cases/year from 2005 to 2013, among which the detection rate of GGN accounted for about 1.19%, especially single pGGN (86%). Different from the high malignant proportion of partially solid GGN (63%) requiring aggressive surgical resection^[3]The vast majority of pGGN need long-term follow-up to dynamically observe the changes of lesions to clarify the nature of lesions, but the follow-up time and follow-up interval of CT are still lacking standards. How to follow up the unknown single pGGN found by physical examination is a new problem faced by health management. The research results of pGGN at home and abroad in recent years are summarized as follows.

Antibiotic-associated diarrhea (AAD) is diarrhea that occurs after the application of antibiotics and cannot be explained by other causes^[1]。 With the widespread application of antibiotics, especially broad-spectrum antibiotics, the occurrence of AAD is very common, accounting for 5% to 25% of all antibiotic-treated patients^[2]。 Microecological preparations have significant curative effects on the prevention and treatment of AAD. In recent years, the research and development and clinical application of some new microecological preparations, as well as the development of microecological research technology, have made new progress in clinical and basic research of AAD.

particulate matter 2.5 (PM2.5) refers to particulate matter in the atmosphere having a diameter of ≤2.5 μ m, also known as pulmonary particulate matter. On average, the human body inhales about 10 000 L of air every day. PM2.5 can enter the human body through the respiratory system with the inhaled air and cause a series of pathophysiological changes^[1,2,3,4,5]。 The peripheral vascular system affected by PM2.5 has both systemic effects and special effects on blood vessels. From this perspective, this paper tries to review the mechanism of PM2.5 leading to peripheral vascular disease.

Chronic thromboembolic pulmonary hypertension (CTEPH) refers to an increase in pulmonary artery pressure due to one or repeated pulmonary embolism that blocks the pulmonary vascular bed, increasing blood flow resistance. Clinical studies have shown that the incidence of CTEPH is increasing year by year. CTEPH has become a public health problem of great concern because of its hidden onset, rapid progression and high mortality^[1,2]。 In recent years, research on the mechanism of CTEPH has increased day by day, but the lack of animal models and clinical specimens has hindered the research progress of the mechanism of occurrence and development of CTEPH. Therefore, it is particularly important to establish animal models that are simple to operate, high success rate, low price, objective and practical, and can transform basic research results into CTEPH diseases. Moreover, it has positive practical significance for deeply exploring the pathogenic mechanism of the disease, fully understanding the natural course of the disease, perfecting the diagnostic technology, establishing effective intervention measures, prolonging survival and reducing mortality. This paper briefly introduces and evaluates the methods of constructing CTEPH experimental animal models at home and abroad in recent years.

A 59-year-old female, farmer, with chest tightness, shortness of breath and dry cough for 3 months as the main complaints, went to the local health center on February 5, 2010. Chest X-ray showed a large amount of pleural effusion in the left chest. 300 ml was extracted by puncture, adenosine deaminase (ADA) 50 U/L, and white blood cells 400×10⁶/L, pleural effusion, serum alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), nerve-specific enolase (NSE), etc. were all normal, erythrocyte sedimentation rate (ESR) was 80 mm/1 h, pure protein derivative tuberculin (PPD) test was positive, and pleural effusion was tested at 50-80 U/L after multiple extractions. Considering the possibility of left tuberculous pleural effusion, the patient was given oral anti-tuberculosis treatment with isoniazid 0.3 g once/d, rifampicin 0.45 g once/d, pyrazinamide 0.5 g three times/d, and ethambutol 0.75 g once/d. Symptoms such as chest tightness and dry cough improved once, and continued anti-tuberculosis treatment for 3 months after discharge. During the treatment, the condition tended to worsen, and he could not lie down, and his weight gradually lost. He visited our hospital on June 9, 2010. The outpatient reexamination of chest X-ray showed that the trachea and mediastinum shifted to the right, and high-density shadows were seen in the left middle and lower lungs, considering left pleural effusion or occupying space (Figure 1), admitted to hospital with "left lung occupying space to be examined". Past history, personal history, and family history are not special.