2016年 · 第36卷第09期

Aspirin has been confirmed by a large amount of evidence-based medical evidence to have anti-platelet aggregation effect, and it has been widely used in the primary and secondary prevention of cardiovascular and cerebrovascular diseases^[1,2]There are also increasing reports on gastric mucosal injury caused by it^[3]And even life-threatening, seriously affecting the quality of life of patients. The relationship between pepsinogen (PG) and gastrin in gastrointestinal diseases has been widely concerned^[4,5]。 This study investigated the diagnostic value of PG and gastrin in aspirin-related gastric mucosal injury by detecting the changes of serum PGⅠ, PGⅡ and gastrin-17 in patients taking oral aspirin.

CD is an unexplained chronic inflammatory disease of the intestine that can develop at all ages, with a long course and diverse clinical manifestations. Studies have shown that the clinical manifestations and disease progression of CD are closely related to the initial onset age of patients^[1]。 With the rising incidence of CD in children in China, the research on CD in children in China is increasing in recent years, but the clinical diagnosis and treatment of CD in children still stems from the accumulation of experience in diagnosis and treatment of CD in adults. This study aims to provide a reference for clinical diagnosis and treatment by comparing the similarities and differences between children and adults in CD in clinical characteristics, treatment response and recurrence.

IBD, which includes CD and UC, is a group of diseases characterized by chronic, recurrent, abnormal intestinal inflammatory responses with genetic predisposition. At present, the etiology and pathogenesis of IBD are not completely clear, and the research of its susceptibility genes has attracted much attention. In 2001, European and American research teams simultaneously discovered the first CD susceptibility gene, namely nucleotide-binding oligomerization domain 2,NOD2)^[1,2]。 Later, autophagy-related 16-like proteins were discovered 1 (autophagy related 16-like protein 1,ATG16L1), signal transduction and transcriptional activators 4 (signal transduction and activator of transcription 4,STAT4) Isogenes are associated with IBD^[3,4]。 At present, 163 gene susceptibility loci related to IBD have been identified by genome-wide association (GWA) analysis^[5]。 This study is intended to testATG16L1 andSTAT4 loci of two genes to explore their relationship with IBD susceptibility in China.

UC is a kind of chronic, non-specific colitis of unknown cause. Most scholars believe that this disease is caused by the interaction of many factors, which leads to the imbalance of the immune system in the body and the destruction of the cytokine network balance, causing the inflammatory reaction of intestinal tissue^[1,2]。 In addition to aminosalicylic acids and adrenocortical hormones, "Consensus Opinion on the Diagnosis and Treatment of Inflammatory Bowel Disease (Guangzhou, 2012)"^[3]Immunosuppressants such as azathioprine are also recommended, but azathioprine has adverse reactions such as bone marrow suppression, which limits its clinical application. Tripterygium wilfordii polyglycoside tablet is an oral preparation extracted from the peeled root of Tripterygium wilfordii of Euonymus family. It has been clinically found that it has immune regulation and anti-inflammatory effects, and can be used for treating some autoimmune diseases^[4]And the incidence of adverse reactions such as myelosuppression is also low^[5]。 At present, there are few studies on the treatment of UC with tripterygium glycosides, and the pathogenesis of UC is related to immune abnormalities. Literature review suggests that the rat model of trinitro-benzene-sulfonic acid (TNBS) /ethanol UC is an excellent model for studying the pathogenesis of UC^[6]。 Therefore, in this study, a rat model of UC was established by TNBS/ethanol method, and azathioprine was used as a control to observe the controlling effect of Tripterygium wilfordii polyglycosides on inflammatory response, which provided a theoretical basis for its further application in the clinical treatment of UC.

Hepatic hydatidosis is a parasitic disease with high incidence in pastoral areas, which is divided into hepatocystic hydatidosis and hepatic alveolar hydatidosis. The incidence of hepatic alveolar hydatidosis is lower than that of hepatic cystic hydatidosis, accounting for about 3% ~5% of hepatic hydatidosis^[1]。 Qinghai Province, Xinjiang Uygur Autonomous Region, Gansu Province and Ningxia Hui Autonomous Region are the high incidence areas of hepatic hydatidosis in China, with an incidence rate of about 5%. In addition, the lack of medical resources in pastoral areas seriously threatens the health of local people^[2]。 In the early stage of alveolar hydatid infection, patients often have no obvious symptoms and signs due to the compensatory function of the liver, so they are ignored. When they are discovered, they are already in the middle and late stages, and some patients have lost the opportunity of surgery. In the late stage, they often die due to liver failure and portal hypertension complicated by gastrointestinal bleeding. Therefore, it is necessary to improve the diagnosis level of hydatidosis and strive for early detection, early diagnosis and early treatment.

non-alcoholic fatty liver disease (NAFLD) refers to a clinicopathological syndrome characterized by excessive intracellular fat deposition caused by alcohol and other definite liver damaging factors, including simple fatty liver, non-alcoholic steatohepatitis and its associated cirrhosis. long noncoding RNA (lncRNA) is a newly discovered class of RNA with length greater than 200 base pairs and no long reading frame, but often has the structural features of mRNA (cap structure and polyadenine tail). In this study, lncRNA/mRNA microarray analysis was performed on human liver tissue specimens with NAFLD, so as to understand the characteristics of lncRNA expression profiles in NAFLD liver tissues, and to explore the pathogenesis related to NAFLD from a new perspective, so as to provide new ideas and clues for the treatment of NAFLD.

A 45-year-old male saw a doctor in February 2015 because he swallowed a bottle cap for half a day while drinking. The patient had clear consciousness, painful face, no subcutaneous emphysema, no abnormalities in the heart and lungs, flat and soft abdomen, no tenderness, rebound pain, no liver and spleen under the costs, and no palpable mass. The X-ray film of the mouth opening position of the neck showed a metal density shadow at the height of the 7th cervical vertebra in the esophageal area (Figure 1), diagnosed as a foreign body at the esophageal entrance. After adequate communication with the family, the patient took the left lateral position and underwent gastroscopy under propofol anesthesia. Under the gastroscopy, a round metal foreign body was seen at the esophageal entrance (18 cm from the incisors) (Figure 2), which cannot be clamped by mouse tooth forceps or net baskets. External pull method with double lumen catheter^[1]Through a guide wire along the edge of the foreign body, a urinary catheter was placed 25 cm along the guide wire, and after 12 mL of air was injected into the balloon, the foreign body was slowly pulled out under direct vision of the gastroscope. The balloon suddenly popped out in the middle, and no foreign body was found in the oral cavity under the gastroscope, and no foreign body was touched when the finger explored the oral cavity. The gastroscopic exploration of the esophageal entrance passed smoothly, no foreign body was found in the esophagus and gastric cavity, and no foreign body was found at the tracheal opening. Then, a bedside X-ray examination was performed, and the foreign body was located at the posterior end of the oral cavity and was vertical (Figure 3)。 No foreign body was found in the oral cavity again. Considering the possibility of being located in the posterior nasal passage, an ultra-fine gastroscopy biopsy forceps was given to enter along the nares, and the foreign body was found to be located in the posterior nasal passage (Figure 4)。 The foreign body was pushed into the oral cavity with an ultra-fine biopsy forceps, and then clamped out with a rat tooth forceps. The posterior nasal passage and upper esophagus were explored again, and no obvious damage was found. The patient recovered well after surgery.

A 57-year-old female was admitted to hospital in September 2015 due to liver damage for more than ten years and skin itching for more than 10 days. The patient underwent cholecystectomy due to gallbladder stones in 2004. Postoperatively, he developed unknown jaundice with pancreatic enlargement. In 2005, he underwent surgical cholangioenterostomy. Intraoperatively, the bile duct was removed for pathological examination, and was diagnosed as primary sclerosing cholangitis. In the past 10 years, the liver function indexes ALP and GGT fluctuated at 300 U/L, ALT and AST were normal, and no special treatment was given. About 10 days ago, the patient developed mild yellowing and itching of the whole body skin, accompanied by deepening urine color. The liver function indicators were ALT 244 U/L, AST 603 U/L, ALP 603 U/L, GGT 635.6 U/L, LDH 222 U/L, TBil 39.8 μ mol/L and DBil 27.8 μ mol/L, so he was admitted to hospital for treatment. He had a history of hypertension for 10 years, diabetes for 7 years, and denied a history of drinking alcohol, special drug treatment, hepatitis and tuberculosis. Immunological indexes: antinuclear antibody 1:100 positive cytoplasmic granular type, anti-smooth muscle antibody, anti-liver and kidney microsomal-1 antibody, anti-mitochondrial antibody, anti-mitochondrial antibody type M2, anti-nuclear membrane glycoprotein 210 and anti-soluble acid phosphorylated protein 100 antibody were all negative; IgG 13.40 g/L ( Normal value<15.60 g/L), IgG4 3.69 g/L (normal 0.03-2.01 g/L), IgE 339 kU/L (normal<165 kU/L); Five indicators of hepatitis B and hepatitis C antibodies were all negative. CA19-9 was 73.63 kU/L (normal value<37.00 kU/L) and 27.68 kU/L (normal value) for cancer antigen 242<20.00 kU/L). Magnetic resonance cholangiopancreatography and MRI of the upper abdomen revealed irregular liver morphology, considering cholestatic cirrhosis, seeFigure 1。 The patient's surgical pathological section 10 years ago was stained again, which showed that a few small bile ducts were scattered in the dense fibrous connective tissue in the hilar of the liver, a large number of lymphocytes and plasma cells infiltrated in the interstitium, and no obvious fibrosis was found around the small bile ducts (because the patient refused to provide the pathological section pictures, only the written consultation report of the pathologist was seen). Immunohistochemical staining showed that plasma cells were positive for CD38 and CD138, IgG4 positive plasma cells>1/high power field, and the ratio of IgG4 positive cells to IgG positive cells>40%. IgG4-related diseases could not be excluded. Thus, the patient met the diagnostic criteria for immunoglobulin G4-related sclerosing cholangitis (IgG4-SC)^[1], re-diagnosed as IgG4-SC. After admission, the patient was treated with reduced glutathione and magnesium isoglycyrrhizinate. The symptoms and liver function of the patient were significantly improved. The liver function indexes of ALT 27 U/L, AST 22 U/L, ALP 303 U/L, GGT 146 U/L, LDH 320 U/L, TBil 21.9 μ mol/L, DBil 17.9 μ mol/L were re-examined. After continued administration, ALP and GGT No sustained decline was observed, so oral prednisone 40 mg/dose (1 dose/d) was given maintenance therapy, and the dose was reduced by 5 mg every week after 4 weeks, and glucocorticoids (hereinafter referred to as hormones) were withdrawn after the 11-week course of treatment. The patient's liver function returned to normal after 3 months of follow-up.

With the development of China's economy and the change of dietary structure, the incidence of nonalcoholic fatty liver disease (NAFLD) is increasing year by year, and it has become the first major liver disease. The pathogenesis of NAFLD has not been fully elucidated, and it may be closely related to insulin resistance (IR) and genetic susceptibility. With the development of microbial metagenomic sequencing platform and metagenomics technology, more and more studies have confirmed that gastrointestinal microecological imbalance can participate in the occurrence of NAFLD through the intestinal-hepatic axis^[1,2]。 It is of great significance to review the progress of occurrence and development of NAFLD from the perspective of microecology for the use of microecological intervention to prevent and control NAFLD. The role of intestinal flora in the pathogenic mechanism of NAFLD and the application of microecological agents are reviewed.

submucosal tumor (SMT) generally refers to a class of gastrointestinal lesions in the tissues below the mucosal layer (non-mucosal tissues), which are divided into benign, potentially malignant and malignant. Common SMTs include gastrointestinal stromal tumor (GIST), leiomyoma, ectopic pancreas, carcinoid tumors, lipoma, cystic lesions, lymphangioma, etc. Among them, GIST and leiomyoma are collectively referred to as mesenchymal cell-derived tumors, which are the most common types of SMTs. The majority of SMTs usually have no obvious clinical signs and are only detected when gastroscopy is performed on an occasional basis. The distribution of SMT in the digestive tract is not uniform. For example, mesenchymal cell-derived tumors are mainly distributed in the upper digestive tract, among which GIST is mainly distributed in the stomach and duodenum, and leiomyoma is mainly distributed in the esophagus. Carcinoid tumors are the most common SMT in the colorectum, while the distribution of other SMTs is rarely reported.