2015年 · 第35卷第05期

Esophageal disease is a common disease of the digestive system. The esophagus is located at the beginning of the digestive tract, and various examination methods are easy to access. Therefore, the diagnosis and treatment of esophageal disease are abundant. In recent years, with the progress of imaging technology, digestive endoscopy technology, esophageal function examination technology and molecular biology, the clinical diagnosis and treatment of esophageal diseases has made great progress, and many hot clinical research issues have emerged in the field of esophageal diseases, which are worthy of further discussion by colleagues in future work.

The occurrence of esophageal adenocarcinoma is associated with a long-term chronic inflammatory response, and Barrett's esophagus is a major risk factor for this disease. In the past 40 years, the incidence of esophageal adenocarcinoma has increased year by year, and epidemiological data show that the incidence of esophageal adenocarcinoma has increased seven times compared with 1970. Previous studies have confirmed that most of the occurrence of esophageal adenocarcinoma is caused by Barrett's esophagus, and the occurrence of Barrett's esophagus is directly related to gastroesophageal reflux. However, clinically, 40% of patients with esophageal adenocarcinoma do not have a definite history of reflux disease^[1]And less than 50% of patients with esophageal adenocarcinoma revealed specialized Barrett's esophageal mucosal lesions on biopsy. Therefore, the idea that Barrett's esophagus and gastroesophageal reflux are the main causes of increased incidence of esophageal adenocarcinoma needs to be rethought. To understand a disease from multiple angles, the most critical entry point is the origin of the disease. The origin of esophageal adenocarcinoma has been controversial in academic circles. In recent years, with the continuous deepening of research, new viewpoints have emerged in this field. Therefore, it is necessary to re-understand the origin of esophageal adenocarcinoma, provide new ideas for exploring the pathogenesis of esophageal adenocarcinoma, and finally provide new strategies for the prevention and clinical diagnosis and treatment of this disease.

China is one of the countries with high incidence of esophageal cancer, with more than 220,000 new cases and about 200,000 deaths every year. More than 90% of patients with esophageal cancer have progressed to the middle and late stage at the time of diagnosis, and the 5-year survival rate is less than 20%. Early esophageal cancer can usually be cured by endoscopic treatment, the curative effect is equivalent to that of surgery, and it has the advantages of less trauma and fast recovery, and the 5-year survival rate can exceed 95%. Therefore, endoscopic treatment on the basis of improving the detection rate of early esophageal cancer is an effective way to improve the prognosis of patients and save national medical resources.

Functional esophageal disease is a disease that is characterized by typical esophageal symptoms, but cannot be explained by definite pathological esophageal dysmotility or organic lesions such as gastroesophageal reflux^[1,2,3]。 Clinically, functional esophageal diseases are common, with an incidence rate of 42% in European and American populations^[4]The incidence rate in China is also showing an increasing trend. However, at present, people's understanding of the pathogenesis of functional esophageal diseases is not deep, and symptoms are still used as the basis of exclusion diagnosis in clinic, so differential diagnosis is very difficult. In recent years, the advent of high-resolution manometry (HRM) technology has greatly improved people's understanding of esophageal motility disorders. In this study, 74 patients with highly suspected functional esophageal disease were analyzed by HRM to explore its diagnostic value for this disease.

GERD is a common multiple disease, including Barrett's esophagus, reflux esophagitis (RE), and non-erosive reflux disease (NERD)^[1]。 In recent years, great progress has been made in basic research, epidemiological investigation, prevention, diagnosis and treatment of GERD, but its pathogenesis is still not completely clear, and the endoscopic manifestations, pathological changes, pathogenesis and drug response of different types of GERD are different. At the same time, more and more patients are becoming resistant to PPI. protease-activated receptors 2 (PAR-2) are receptors with 7 transmembrane units coupled to G protein, which are involved in the release and regulation of various inflammatory factors in vivo, and thus are widely involved in the occurrence and development of various inflammatory diseases^[2]。 In this study, the expression of PAR-2 in different types of GERD patients was detected by immunohistochemistry, and its correlation with serum IL-1 β and IL-8 was analyzed. The role and clinical significance of PAR-2 in the pathogenesis of GERD were discussed.

Abnormal expression or mutation of ubiquitin proteasome pathway members can lead to the development of a variety of diseases, including malignant tumors^[1]。 As one of the important recognition factors of the ubiquitin proteasome pathway, many substrates of F-box and WD-40 domain protein 7 (FBXW7) are oncogenes, such as c-myc, cyclin E, c-jun and Notch, which are degraded through the ubiquitin proteasome pathway mediated by FBXW7^[2,3,4,5,6]。 Recent studies have found that the expression of FBXW7 in various tumors is deleted to varying degrees. In this study, the expression of FBXW7 and c-myc protein in esophageal squamous cell carcinoma and adjacent normal tissues was detected by tissue microarray, and the relationship between FBXW7 and c-myc protein and clinicopathological features and prognosis of esophageal cancer patients was analyzed.

The occurrence and development of gastric cancer is a multi-gene, multi-factor and multi-stage dynamic sequential evolution process, which involves the activation of many kinds of oncogenes, the inactivation of tumor suppressor genes and the change of cell biological behavior caused by this. Among many oncogenes and tumor suppressor genes, P53 is the most closely related tumor suppressor gene in humans, and the change of its gene structure can lead to malignant cell transformation. caudal type homeobox transcription factor (CDX) 2 is an important index in the process from intestinal metaplasia to cancer development, and is closely related to the occurrence of intestinal gastric cancer. Ki67 is a positive marker of nuclear proliferation and an important indicator of cell proliferation activity. The positive expression of CDX2, P53 and Ki67 in gastric cancer respectively has a clear effect on the biological behavior of gastric cancer. In this study, the expression of the above three factors in gastric cancer tissues was jointly detected in order to understand their significance in the diagnosis of gastric cancer.

adenoma detection rate (ADR) is an important criterion to evaluate the quality of colonoscopy^[1,2]。 However, ADR requires a combination of colonoscopy results and histological findings, which is usually difficult to obtain directly.

Chronic abdominal pain refers to recurrent or prolonged abdominal pain (the course of the disease exceeds 3 months). Its etiology includes organic disease and functional abdominal pain syndrome (functional abdominal pain syndrome, FAPS)^[1]。 Difficult diagnosis of the etiology of chronic abdominal pain. multi-slice computed tomography (MSCT) can not only observe the abdominal parenchymal organs, but also show the lesions of the cavity organs. This study intends to use this technique to prospectively screen and diagnose the etiology of patients with chronic abdominal pain, and explore its diagnostic value.

The patient was a 45-year-old male. Due to retrosternal burning sensation accompanied by swallowing pain and acid reflux for more than 1 month, I went to the doctor on May 20, 2014. The patient began to experience retrosternal burning sensation more than 1 month ago, accompanied by acid reflux, swallowing pain, no obvious dysphagia, nausea, vomiting and other symptoms, and the local hospital gave omeprazole and other treatments were ineffective. The patient had a history of chronic gastritis, no history of allergic diseases, no history of ingestion or inhalation of special substances, and her mother suffered from esophageal cancer. Physical examination: The spirit is slightly poor, the superficial lymph nodes are not swollen, and no abnormalities are found in cardiopulmonary examination. There was no tenderness in the abdomen and no mass was palpable. Blood routine: WBC count 7.1×10⁹/L, neutrophils were 0.62, lymphocytes were 0.31, eosinophils were 0.03, eosinophil counts, RBC counts, Hb, PLT counts were all within the normal values. The urine and fecal routine were normal, and the fecal occult blood test was negative. Liver and kidney function was normal. Serum IgA, IgG and IgM were in the normal range, and hypersensitivity CRP was 3.1 mg/L. The serum tumor markers CEA, CA19-9 and AFP were in the normal range. Ultrasound examination of hepatobiliary and pancreatic did not show space occupation. Chest X-ray: No abnormalities were found in both lungs and mediastinum. Gastroscopy: The esophageal wall is scattered with more mucus and white plaques attached, the esophageal mucosa is gray-white, the blood vessels are not clear, and a large flushing area is seen on the right wall of the esophagus 35 cm away from the orifice, the size is 3 cm ×3 cm, the surface is slightly depressed, and there is a large area of erosion, brittle, and the boundary is still clear, seeFigure 1There is no stenosis in the esophageal lumen, and peristalsis is acceptable; No abnormalities were found in the cardia, fundus, body, antrum and duodenum. Suspected of early esophageal cancer, biopsy of esophageal lesion showed chronic inflammatory reaction with erosion, more eosinophil infiltration in inflammatory granulation tissue, the densest area reached 200/low magnification field,>50/high magnification field, and lymphoid follicular formation, seeFigure 2。 Based on clinical manifestations, gastroscopic findings and pathological findings, the diagnosis of eosinophilic esophagitis was made. The patient was given oral prednisone 20 mg/d and rabeprazole 20 mg/d, and instructed to avoid eating dairy products, seafood and other drugs. Symptoms were relieved 1 week after treatment, and the treatment was continued until 1 month, and the symptoms disappeared. After reexamination of blood routine, WBC and its classification were normal, and the prednisone dose was reduced to 15 mg/d. Treatment was continued for 2 weeks without recurrence of symptoms. The reexamination of gastroscopy did not repeat, and the white plaque on the esophageal wall disappeared, and the original flushing and erosion lesions also disappeared, leaving only mild edema. Pathological biopsy showed squamous epithelial hyperplasia and no eosinophil infiltration. The dose of prednisone continued to be reduced to 10 mg/d, changed to 5 mg/d 2 weeks after treatment, maintained for 2 weeks and then discontinued, and observed for another month without recurrence of symptoms.

A 58-year-old male was admitted to the hospital on August 28, 2012 after suffering from repeated diarrhea for more than 3 years, difficulty in defecation for more than 2 months and worsening for 1 day. The patient developed diarrhea after drinking more than 3 years ago, up to 5 times/d, with yellow stool, shape-free, mucous stool, no melena and bloody stool, no abdominal pain, no nausea, vomiting, and no fever. The diarrhea improved after UC treatment with mesalazine in the other hospital, and no formal diagnosis and treatment had been made. Two months ago, the patient had repeated difficulties in defecation, which occurred once a week, each time lasting for about 2 days, accompanied by lower abdominal distension and pain, no radiating pain, suspicious mass in the left lower abdomen, no fever, no nausea and vomiting. After taking phenolphthalein tablets, he defecated yellow watery stool, and abdominal pain, abdominal distension and mass could be relieved after defecation. The patient experienced abdominal pain and distension after meals 1 d before admission, accompanied by nausea, vomiting and cessation of anal exhaustion and defecation, without fever, and was considered for emergency admission for intestinal obstruction. Previous long-term drinking for 30 years, ethanol intake was 45 g/d. Admission blood routine: white blood cells 12.8×10⁹/L, hemoglobin 132 g/L, neutrophils 0.887, platelet count 199×10⁹/L; CRP 11.4 mg/L; Total abdominal CT enhancement (Figure 1) shows multiple calcifications of the ascending and transverse mesocolic veins and colon wall, thickening of the colon wall, narrowing of the lumen, and dilatation of the upper part of the small intestine, showing multiple gas-liquid levels. Colonoscopy (Figure 2) suggest that the mucosa from the ileocecal region to the ascending colon is congested and edema, and diffuse ulcers of varying sizes can be seen with filthy coating; The transverse colon mucosa is congested and edema, which is dark brown; The mucosa of descending colon, sigmoid colon and rectum was dark-brown, congested and edema, and the vascular texture disappeared. Colonoscopic pathology (Figure 3) showed that the intestinal mucosa showed ischemic enteritis changes, the wall of small vessels under the intestinal mucosa was thickened, hyalinized, and some lumens were stiff and twisted, and the intestinal submucosa was marked by fibroid degeneration, resulting in green Masson staining. He was considered to be phlebosclerotic colitis (PC), and was discharged after fasting, parenteral nutrition, anti-infection, low molecular weight heparin anticoagulation, mosapride, lactulose, gastrointestinal pacing and laxative treatment. The patients were followed up by telephone until the deadline without abdominal pain and intestinal obstruction, defecation 1~2 times/d, and basically formed.

A 41-year-old male patient had dull periumbilical pain with intermittent bloody stool for more than 20 days and purpura in both lower limbs for 10 days. The patient took the drug under the trade name "Qiangguli Capsule" on October 23, 2013 due to joint pain. On October 28, he developed periumbilical paroxysmal pain with bloody stools and stopped taking the drug. At that time, CT of the upper abdomen showed liver and kidney cyst, thickened intestinal wall at the end of ileum, and gastroscopy showed chronic gastritis with erosion. After anti-infective treatment, the symptoms did not improve. On November 3, the patient developed symmetrical red rash on both lower limbs, and was admitted to hospital on November 13 due to aggravation of abdominal pain. The patient had a previous history of rheumatoid arthritis for 3 years and had been treated with methotrexate (10 mg once weekly) and prednisone (5 mg once daily) for 1 year. The above drugs were stopped 6 months before the onset of this disease. The patient denied a history of drug allergy. Physical examination at admission: clear, dark red maculopapular rash on both lower limbs, partially fused into pieces, not fading when pressed, soft abdomen, mild tenderness around the umbilicus, mild rebound pain, no mass, unpalpable liver and spleen under the costs, negative Murphy's sign, no tenderness at McBurney point, and mild swelling of both finger joints. Hb 134 g/L, WBC count 11.9×10⁹/L, neutrophils 0.81, PLT count 304×10⁹/L, ESR 67 mm/1 h, CRP 64 mg/L, immunoglobulin A was significantly increased. Tumor indexes, liver and kidney function, blood amylase, hemagglutination routine, anti-streptolysin O test, rheumatoid factor and autoantibodies were all normal. Chest CT showed no abnormalities. Abdominal ultrasound showing cholesterol polyps of the gallbladder. Abdominal CT angiography showed no abnormalities. Colonoscopy the next day of admission (Figure 1) showed no abnormalities in the terminal ileal mucosa, congestion, edema and erosion in the ileocecal valve mucosa, normal diastolic and contractive, diffuse congestion, edema and erosion in the whole colon mucosa and rectal mucosa, multiple punctate ulcers, congestion around the ulcer, flushing-like manifestations, poor vascular texture, and more dark red bloody fluid in the intestinal lumen. Pathological examination showed edema and hemorrhage of mucosal membrane propria, infiltration of lymphocytes and eosinophils in mucosa and submucosa, erosion in some areas, sparse glands, disappearance of goblet cells, and focal necrosis of small vessel walls. Abdominal allergic purpura was diagnosed. Methylprednisolone (40 mg, twice a day) was given intravenously, and the dose was reduced to 40 mg once a day after 3 days. The symptoms of abdominal pain and bloody stool disappeared, and oral prednisone (20 mg, once a day) was changed after 3 days, and the drug was discontinued after 6 days. After 1 week of treatment, colonoscopy revealed scattered congestion of rectal mucosa, and no abnormalities were found in the mucosa of other intestinal segments.

achalasia of cardic (AC) is a disease due to neuromuscular dysfunction of the esophagogastric junction (EGJ), characterized by lack of esophageal peristalsis and poor relaxation of the lower esophageal sphincter (LES). Clinical symptoms include dysphagia, reflux, chest pain and weight loss. Esophageal barium angiography and gastroscopy are common methods for diagnosing AC, and esophageal manometry is the gold standard for diagnosing this disease.

A century ago, radiologist Demetrius Chilaiditi reported three cases with abnormal localization of special thoracic and abdominal structures^[1]。 In these three patients, the colon was inserted between the liver and the diaphragm, and thoracic and abdominal radiographs showed a clear inflated intestinal tube under the right diaphragm, a sign named metacolonic syndrome.

Colorectal cancer is one of the most common malignant tumors in the world, and its mortality rate ranks fourth among tumor diseases. According to statistics, there were about 694,000 deaths from colorectal cancer worldwide in 2012^[1]。 Analyzing the reasons, the main reason is that most patients have colorectal cancer in the middle and advanced stage when they see the doctor, and miss the best opportunity for treatment. At present, there are limited methods for early screening of colorectal cancer. Colonoscopy is not widely used because of its invasive characteristics and inconvenient sampling. Fecal occult blood test is not widely used because of its low specificity. Therefore, searching for a simple, quick, sensitive and specific marker has become a hot topic in this field. In recent years, many studies have shown that the occurrence and development of colorectal cancer are closely related to DNA methylation, and there may be methylation changes of many genes in tumor tissue and peripheral blood of colorectal cancer patients^[2,3,4]。 Detect methylation in plasma nowseptin9 genes, and their research progress as a marker of colorectal cancer is reviewed.