2016年 · 第36卷第10期

There are many causes of acute pancreatitis (AP). Mild cases are characterized by local inflammatory reaction of the pancreas, and severe cases can occur systemic inflammatory response syndrome (SIRS), which can be accompanied by organ dysfunction and even life-threatening. Therefore, the etiology of AP plays an important role in evaluating the disease and prognosis, and formulating the treatment plan. At present, clinical attention is paid to common causes such as biliary and alcohol consumption, but the development of disease induced by rare and special causes is no less harmful to AP patients than common causes, and it is easy to induce severe acute pancreatitis (SAP).

acute pancreatitis (AP) refers to a disease characterized by local and systemic inflammatory reactions of the pancreas due to the activation of pancreatic enzymes due to various causes. According to the severity of the disease, it can be divided into mild acute pancreatitis (MAP), moderately severe acute pancreatitis (MSAP) and severe acute pancreatitis (SAP). AP patients are in a state of stress, their energy consumption is increased by about 50% compared with the basic value, their protein metabolism is increased by about 80%, and they are prone to hypoalbuminemia, negative nitrogen balance, and digestion and absorption dysfunction. The nutritional status of patients directly determines the immune level, the incidence of infection and the maintenance of organ function of patients with pancreatitis, thus affecting the mortality rate of patients. Therefore, stabilizing the nutritional metabolism of patients is of great significance to the prognosis of AP, and nutritional support therapy is a very important link in the treatment strategy of AP.

The incidence of acute pancreatitis (AP) is increasing year by year, and the overall mortality rate is 5% ~10%. 2012 New Revised Atlanta Classification Criteria for Acute Pancreatitis^[1]AP was classified into 2 types, i.e., interstitial edematous pancreatitis and necrotizing pancreatitis. Necrotizing pancreatitis accounts for about 20% of AP, and the overall mortality rate exceeds 30%; One third of necrotizing pancreatitis has secondary infection in the pancreas or peripancreatic necrosis, that is, infected pancreatic necrosis (IPN)^[2]。 With the improvement of intensive care and organ function maintenance, as well as the emphasis on early fluid resuscitation, the threat of early complications of severe acute pancreatitis (SAP) to patients' life gradually decreased, but the overall mortality rate of SAP patients remained high, mainly due to IPN in the later stage of the disease. The diagnosis and treatment of IPN is the most difficult problem in the field of AP at present, and it is a comprehensive diagnosis and treatment process that requires multi-disciplinary participation.

acute pancreatitis (AP) is a disease characterized by pancreatic enzyme activation caused by various etiologies, followed by local or systemic inflammatory reaction of the pancreas, with or without changes in other organ function. Clinically, the course of disease in most patients is self-limiting, and 20% to 30% of critically ill patients have a dangerous clinical experience. The overall mortality rate was 5% to 10%. According to the severity of the disease, it is divided into mild acute pancreatitis (MAP), moderately severe acute pancreatitis (MSAP) and severe acute pancreatitis (SAP). The differentiation is based on the presence or absence of multiple organ dysfunction syndrome (MODS) and whether MODS can recover within 48 h. The pathophysiological basis of MODS is systemic inflammatory response syndrome (SIRS)^[1,2]。

In recent years, the incidence of acute pancreatitis (AP) has been increasing, and it has become one of the common diseases in hospitalized patients of digestive system. Because the pathogenesis of systemic inflammatory response caused by AP is still unclear, the current clinical treatment is still aimed at the support of important organs and the management of complications, and the efficacy is limited^[1]。 As one of the important digestive organs, intestinal dysfunction occurs in the early stage of AP, and the translocation of bacterial microorganisms, toxins and inflammatory mediators in the intestinal tract is the main source of systemic inflammatory response syndrome (SIRS), secondary infection of distant organs and multiple organ dysfunction syndrome (MODS)^[2]。 Protecting and maintaining intestinal function has important clinical significance in reducing the mortality and complication rate of severe acute pancreatitis (SAP).

Fatty liver is one of the diseases that clinicians pay widespread attention to at present. In contrast, fatty pancreas is rarely known by clinicians and has not been written into classic textbooks. As early as 1933, Ogilvie first proposed the concept of "fat pancreas" during autopsy. However, many scholars only regard pancreatic steatosis as a complication caused by type 2 diabetes, pancreatitis, pancreatic cancer, etc., and do not pay enough attention to it as an independent disease. Fatty pancreas is a clinicopathological syndrome mainly caused by acinar cell steatosis and pancreatic interstitial fat deposition caused by multiple factors related to genetic-environmental-metabolic stress. It is a pathological change of aging and systemic diseases in pancreas. At present, the etiology, pathogenesis, clinical manifestations, diagnostic methods and prevention and treatment of adipose pancreas are insufficient, which leads to the inability to obtain timely and correct diagnosis and treatment of these patients.

The advent of capsule endoscopy ushered in a new era for the diagnosis of small intestine diseases^[1]。 Because the traditional capsule endoscope has a blind spot in the upper gastrointestinal tract examination, especially the fundus and upper part of the stomach body, capsule endoscope is generally not used for the diagnosis of upper gastrointestinal tract diseases^[2]。 The magnetic-controlled capsule endoscope controls the movement of the capsule in the stomach through an external magnetic field, and realizes the movement of the capsule in all directions in the stomach, which makes it possible for the capsule endoscope to be used for upper gastrointestinal tract examination. This study analyzed the diagnostic value of this new non-invasive upper gastrointestinal tract examination by observing 40 patients undergoing magnetically controlled capsule endoscopy.

With the aging of society, the incidence of gallbladder stones increases year by year, and the incidence of gallbladder stones in adult population is 7% ~10%^[1]。 The commonly used treatment is open or laparoscopic cholecystectomy. Because the anatomical structure of the gallbladder triangle varies greatly and the operator's experience is different, no matter which method is used to remove the gallbladder, the postoperative residual cystic duct is too long or residual cystic duct stones still occur from time to time, with an incidence rate of 0.6% ~3.0%^[2]And rediagnosis of residual cystic duct stones is difficult, often diagnosed as post-cholecystectomy syndrome^[3]Even if it can be diagnosed, it is difficult to operate again, and it is easy to damage the surrounding blood vessels and biliary tract. The clinical data of 8 patients with common cholangiolithiasis combined with residual cystic cholangiolithiasis were retrospectively analyzed, and the diagnosis, treatment and safety of endoscopic retrograde cholangiao pancreatography (ERCP) were discussed in combination with the literature.

IBD is a chronic non-specific intestinal inflammatory disease, mainly including UC and CD. Clinically, it is mainly characterized by abdominal pain, diarrhea, mucus, pus and bloody stool, and tenesmus, and is characterized by an alternating process of recurrence and remission. The etiology and pathogenesis of IBD are still unclear, but the results of existing studies suggest that it is caused by the interaction of genetic, immune, environmental factors and intestinal infection^[1,2,3]。 Clinically, oral aminosalicylic acid drugs such as mesalazine are often used for treatment, which can significantly improve the intestinal inflammatory reaction, but the disease is prone to recurrence. In recent years, clinical studies have shown varying degrees of dysbiosis in the intestine of patients with UC^[4], suggesting that intestinal dysbiosis is closely related to the occurrence and development of UC. Supplementation of probiotics in UC patients can improve their intestinal flora imbalance and alleviate their disease, so the application of probiotics in UC treatment has been paid more and more attention. This study investigated the clinical efficacy and safety of Lactobacillus casei combined with mesalazine in patients with mild and moderate active UC, and compared the changes of various laboratory indexes before and after treatment.

Abnormal defecation is a common disease in the elderly, which seriously affects their quality of life. Anorectal motility and paresthesia are present in patients with functional defecation abnormalities, but their specific pathogenesis has not been fully elucidated. In this study, we retrospectively analyzed the difference of rectal and anal canal dynamics between elderly patients with functional constipation, functional fecal incontinence, constipation type IBS and diarrhea type IBS and healthy controls, and aimed to explore their pathogenesis.

In recent years, with the endless clinical research results of IBS, the treatment guidelines for IBS have been further updated. The American Gastroenterological Association (AGA) and the American College of Gastroenterology (ACG) issued guidelines on drug treatment of IBS and chronic constipation in 2014, which evaluated the effectiveness of clinically commonly used drugs in the treatment of IBS and chronic constipation, and provided a new basis for rational choice of drug treatment. The purpose is to interpret the relevant features in the above guidelines, hoping to provide guidance for clinicians in the rational application of drugs to treat IBS.

Globally, the incidence of gastric cancer ranks fifth among malignant tumors, and the incidence rate in East Asia is much higher than that in other parts of the world. The ranking of gastric cancer mortality among different cancers of gender showed that men were 3rd and women were 5th^[1]。 The occurrence and development of gastric cancer are affected by many factors, among whichH.pyloriIt is classified as a class I carcinogen by WHO. Studies confirm that,H.pyloriInfection can increase the risk of gastric cancer. Lauren classification is divided into intestinal type, diffuse type and mixed type according to the histomorphology and cellular characteristics of gastric cancer. The multi-step hypothesis of Correa's intestinal gastric carcinogenesis suggests that,H.pyloriInfection causes the gastric mucosa to undergo chronic inflammatory reaction, atrophy, intestinal metaplasia and even dysplasia, and eventually develops into intestinal gastric cancer. The theory has been widely accepted.H.pyloriInfection can also promote the occurrence of diffuse gastric cancer, which does not experience the above changes, suggestingH.pyloriA variety of carcinogenic pathways exist. chronicH.pyloriThe mechanism of gastric cancer caused by infection is quite complex. In recent years, related research has been continuously improved, which is helpful to predict the risk of gastric cancer and prevention and treatment of gastric cancer.

CD is a chronic, non-specific and transmural intestinal inflammatory disease. With the progression of the disease, it is easy to cause intestinal wall thickening and ulcer, accompanied by intestinal stenosis, intestinal perforation and fistula formation. More than 50% of patients with CD develop various complications within 20 years of initial diagnosis^[1]These patients undergo at least one surgical treatment during the course of their disease, and the cause of surgery in most patients is intestinal stenosis^[2]。

The gastric mucosa has a series of self-defense and repair mechanisms, and the secretory function of gastric parietal cells and the defensive function of gastric mucosa maintain a balanced state. Once the two are out of balance, gastric ulcer will be caused^[1]。 Drugs for the treatment of gastritis and gastric ulcer are mainly divided into two categories: acid inhibitors and gastric mucosal protectants, which play a role in relieving symptoms and promoting ulcer healing. With the widespread application of H2 receptor antagonists and PPI, the cure rate of peptic ulcer is significantly improved^[2]。 But one study found that the maximum diameter<After single acid suppression treatment, the cure rate of 10 mm ulcer can reach 90%; However, the cure rate of ulcers with maximum diameter>10 mm or larger is only 50%^[3]。 This indicates that acid suppressant treatment can only reduce the invasiveness of pathogenic factors to mucosa, but cannot enhance the self-defense function of mucosa, so it cannot comprehensively treat gastric ulcer. The acid secretion function of gastric body wall cells in Asian populations is weakened, and the incidence of gland atrophy is significantly higher than that in Western populations. Patients with gastric ulcer are mostly accompanied by atrophic gastritis, and the incidence of gastric ulcer with low gastric acid secretion is high, so reasonable protection of gastric mucosa is more important. Tarnawski et al.^[4]Studies have found that gastric ulcers are subjected to acid suppression andH.pyloriAfter eradication treatment, although gastroscopy showed healing of the ulcer, there were significant histological and ultrastructural abnormalities, which were manifested as thinning of mucosal layer, non-functional connective tissue filling, gland reduction, gastric gland dilation and disorder. Abnormal tissue structure reduces the defense of mucosa against invasive agents, and acid suppressants do not change the natural course of ulcer.