2015年 · 第35卷第06期

IBD is a group of idiopathic, chronic, and inflammatory reactive intestinal diseases. Its course is prolonged and recurrent, which consumes a lot of medical resources and affects the quality of life of patients. Ng et al.^[1]Prospective studies on the incidence and prevalence of IBD in different regions of the Asia-Pacific have found that the incidence of IBD in Asia is growing at the same or even faster rate than in Western countries. There are 51 ethnic minorities in Yunnan Province, accounting for 33.41% of its total population. Among them, 26 ethnic minorities have a population of more than 5,000 and have their fixed distribution ranges. The distribution of each ethnic group is characterized by large mixed living and small settlement. This study conducted a preliminary analysis of IBD patients in 15 cities of Yunnan Province, and intended to provide data for the epidemiological study of IBD in Yunnan Province and ethnic minorities in China.

Colorectal cancer is the third most common cancer in the world and ranks fourth in cancer mortality^[1]。 The incidence of colorectal cancer in China is second only to gastric cancer in digestive tract tumors^[2]。 Colorectal cancer mostly evolves from adenoma, which usually takes 5 to 10 years or more. Precancerous lesions are accompanied by mutations in acquired genes, and mutations in tumor suppressor genes, oncogenes and other genes can progress to invasive cancer^[3,4]。 At present, colonoscopy is the most accurate examination method for diagnosing colorectal cancer, but its examination cost is high, and complications may occur^[5]。 Therefore, a non-invasive, highly sensitive and highly specific marker is urgently needed for the early diagnosis and screening of colorectal cancer. This study investigated the diagnostic significance of serum colon cancer specific-antigen (CCSA) -3 and CCSA-4 in colorectal cancer.

Colorectal cancer is one of the common malignant tumors of digestive system, and its mortality rate is second only to lung cancer and breast cancer^[1]。 In recent years, tumor associated macrophage (TAM) has become a research hotspot, but few studies in colorectal cancer have been reported. Studies have proved that the higher the expression of matrix metalloproteinase-2 (MMP-2) and cell proliferation-related protein Ki-67 in malignant tumors, the stronger the cell infiltration, metastasis and proliferation ability, and the worse the prognosis^[2,3]。 In this study, the expression of TAM count, MMP-2 and Ki-67 in colorectal cancer was examined to investigate the influence of these indexes on the invasion, metastasis, proliferation and prognosis of colorectal cancer.

Pelvic floor achalasia syndrome is a group of syndromes, and constipation caused by it is a hot spot in clinical research. dyssynergic defecation (DD) caused by pelvic floor achalasia belongs to the category of functional defecation disorders in the diagnostic criteria of functional gastrointestinal diseases in Rome III. The main symptoms are laborious defecation, incomplete defecation, and anal obstruction. Anorectal manometry is widely used in clinical practice because of its characteristics of less trauma, non-radiation and non-invasiveness. Functional defecation disorders were classified into three types based on the pressure gradient changes in the rectum and anal canal in the diagnostic criteria of Rome III, Rao^[1]On this basis, the constipation caused by pelvic floor achalasia is divided into four types. The clinical characteristics of each type of constipation are reported as follows.

Visceral hypersensitivity refers to the phenomenon that visceral tissues enhance their sensitivity to stimuli, including enhanced response to various peripheral nociceptive stimuli and normal physiological stimuli. It is one of the main pathophysiological mechanisms of IBS. transient receptor potential ankyrin 1 (TRPA1) is a non-selective calcium channel mainly distributed in the dorsal root ganglia of the vagus nerve and spinal afferent nerves, and its expression is elevated in inflammatory visceral hypersensitivity^[1]。 In this study, a non-inflammatory visceral hypersensitivity model was established after maternal-infant separation, and the relationship between TRPA1 and visceral hypersensitivity was investigated.

non-alcoholic fatty liver disease (NAFLD) refers to fat deposition in liver cells caused by excessive drinking and other liver damaging factors. Its pathogenesis is closely related to insulin resistance and genetic susceptibility. It is the main cause of liver damage in recent years, and it is also related to atherosclerotic diseases^[1]。 The NAFLD disease spectrum includes nonalcoholic simple fatty liver (NAFL), non-alcoholic steatohepatitis (NASH), and their associated cirrhosis and hepatocellular carcinoma. NAFLD has no typical symptoms in the early stage, and is mostly found by routine physical examination. Early treatment can slow down the degree of liver damage and the process of fibrosis, and reduce the occurrence of diabetes, metabolic syndrome and cardiovascular and cerebrovascular diseases. In this study, polyene phosphatidylcholine combined with diammonium glycyrrhizinate was used to treat patients with NAFLD. The changes of serum ALT, AST and GGT were detected, and the changes of liver ultrasound images were compared, so as to explore an effective method for the treatment of NAFLD.

asparaginyl endopeptidase (AEP) gene is localized on human chromosome 14q32.1, and encodes a polypeptide chain consisting of 433 amino acid residues. Its structure is quite conserved^[1]。 AEP is highly expressed in colon, breast, prostate and other solid tumors, including neovascular endothelial cells and related macrophages in tumor stroma^[2,3]。 Studies have found that AEP is closely related to behaviors such as tumor metastasis, spread and invasion^[4,5]。 At present, there are few reports on AEP in gastric cancer. This study investigates the expression of AEP in gastric cancer and its influence on the prognosis of gastric cancer patients, and provides a valuable molecular biological index for clinical targeted therapy and prognosis evaluation.

acute pancreatitis (AP) refers to a disease in which pancreatic enzyme activation is caused by various causes, followed by pancreatic self-digestion, resulting in local inflammatory reaction, which may or may not be accompanied by other organ function changes. The vast majority of AP patients have mild and self-limiting symptoms, but some patients will develop systemic inflammatory response syndrome (SIRS), sepsis, and even multiple organ failure^[1]。 20% ~25% of AP patients were critically ill, and the mortality rate was 30% ~50%^[2,3]。 In 1952, Klatskin and Gordon^[4]A case of recurrent episodes of AP caused by primary hyperlipidemia is reported for the first time. 1% to 12% of AP is caused by hyperlipidemia, that is, hyperlipidemic acute pancreatitis (HLAP). Because hyperTGemia is an important cause of AP, and hypercholesterolemia alone does not cause its onset, HLAP is also called hyperTGemia AP. In AP, SIRS is induced by inflammatory mediators, cytokines and tissue factors, which initiates endogenous and exogenous coagulation pathways, resulting in imbalance of coagulation and anticoagulation systems. This study retrospectively analyzed the changes of blood coagulation, protein C and D-dimer in patients with HLAP and explored their value in early prediction of HLAP severity.

A 42-year-old female was admitted to the hospital in March 2014 due to abdominal distension for 8 years and melena for 1 d. The patient developed abdominal distension and increased abdominal circumference 8 years ago. Abdominal Doppler ultrasound in the First Hospital of Jilin University showed cavernous degeneration of portal vein, thrombosis of portal vein and splenic vein, splenomegaly, and massive effusion of abdominal cavity. Liver MRI + three-phase enhancement showed main portal vein and left and right embolus, portal vein cavernous degeneration, splenomegaly and ascites; Gastroscopy showed severe esophagogastric varices; The liver function, blood routine and coagulation routine were normal, and hepatitis B markers, hepatitis C antibodies and antinuclear antibodies were all negative. The diagnosis was "cavernous transformation of portal vein (CTPV) and portal hypertension", and oral anticoagulation treatment with warfarin 2.5 mg/d was given. The patient's abdominal CT 4 years ago showed CTPV, splenomegaly and massive peritoneal effusion; Gastroscopy showed severe esophagogastric varices; Blood routine and liver function were normal. The white blood cell count was 40.25×10 after re-examination 3 months ago⁹/L, neutrophils were 37.51×10⁹/L, with a red blood cell count of 4.0×10¹²/L, Hb 102 g/L, PLT 412×10⁹/L; Bone marrow smear showed bone marrow dry extraction, increased proportion of granulocytes, mainly in mature stage, PLT piles were more common, bone marrow biopsy showed bone marrow fibrosis, and the diagnosis was primary bone marrow fibrosis. Physical examination: blood pressure 100/60 mmHg (1 mmHg =0.133 kPa), consciousness, anemic appearance, no yellowing stain on the skin and sclera, no abnormalities in the heart and lungs, several varicose veins on the abdominal wall, slightly swollen abdomen, soft abdomen without tenderness, and positive mobile voicing. The subcostal of the liver is unpalpable, and the subcostal of the spleen is 6 cm, hard in texture, with clear margins. There was no edema in both lower limbs. Abdominal CT plain scan + three-phase enhancement (Figure 1) showed cirrhosis, splenomegaly, ascites, unclear display of the main portal vein, abnormal enhanced shadow around the running area of the portal vein and the extrahepatic biliary tract, and cavernous degeneration of the portal vein was considered. Gastroscopy showed severe esophagogastric varices. Hb 95 g/L, PLT 426×10⁹/L; PT 18.7 s, international normalized ratio 1.45, prothrombin time ratio 1.56, PTA 49%, plasma fibrinogen 1.5 g/L; Albumin 16 g/L, acetylcholinesterase 903 U/L; Anti-HBs positive, hepatitis C antibody, anti-nuclear antibody, anti-mitochondrial antibody M2 negative. After admission, esophageal varices were ligated, gastric varices were embolized, and upper gastrointestinal bleeding stopped. After 3 months follow-up, the patient developed superficial vein thrombosis of the left upper limb.

The 43-year-old male was admitted to the hospital in June 2011 due to upper abdominal pain for more than March. Gastroscopy revealed a bulge of the mucosa on the large curved side of the gastric antrum, and a bridge-shaped mucosal fold was visible. Endoscopic ultrasound revealed very hypoechoic lesions in the submucosa of the gastric antrum, and underwent subtotal gastrectomy in the gastrointestinal surgery department. Postoperative pathology revealed deep cystic gastritis (gastric antrum).

severe acute pancreatitis (SAP) is often associated with intra-abdominal hypertension (intra-abdominal hypertension) or abdominal compartment syndrome (ACS), which leads to organ failure. It is an important cause of death in SAP patients, with a mortality rate of 36% ~50%^[1]。 It was previously believed that early surgical treatment should be performed when SAP was combined with ACS, but there were more complications after operation. In recent years, early non-surgical treatment tends to be adopted, but its efficacy and safety are still lacking high-quality evidence-based medical evidence. The non-surgical therapy of SAP combined with intraabdominal hypertension or ACS is reviewed.

autoimmune pancreatitis (AIP) is a kind of pancreatic disease with painless obstructive jaundice and mild abdominal pain as the main clinical manifestations, benign fibroinflammatory reaction characterized by pancreatic enlargement with or without pancreatic mass, pancreatic duct stenosis, lymphoplasma cell infiltration and fibrosis, and sensitivity to glucocorticoid treatment^[1,2]。 In recent years, it has been found that some idiopathic ductal central pancreatitis with a large number of neutrophil infiltration in pancreatic duct epithelial tissue, whose characteristics are not exactly the same as the aforementioned, is called type 2 AIP. Due to the late discovery of type 2 AIP, the understanding of this disease is insufficient. Now, by reviewing the relevant literature in recent years, we hope to improve the understanding of this disease by the majority of doctors.

portal hypertension refers to the obstruction of blood flow and/or increase of blood flow in the portal vein system, resulting in continuous increase of hydrostatic pressure in the portal vein and its branch vessels. It is mostly caused by chronic liver disease, and can lead to complications such as ascites, esophagogastric varices and hypersplenism. Its early diagnosis and evaluation are of important clinical significance. In recent years, with the development of science and technology and the in-depth exploration of scholars, the diagnosis of portal hypertension has made great progress. Now, the commonly used diagnostic methods and application status of portal hypertension are reviewed and analyzed.

Mr. Edit:

Dear Dr. Gong Jun: