2015年 · 第35卷第08期

Portal hypertension is a syndrome of hemodynamic abnormalities that causes serious complications such as ascites, hepatic encephalopathy and variceal bleeding. Variceal bleeding is a clinical critical condition. Although the treatment has progressed in recent years, the 6-week mortality rate is still as high as 10% ~20%. Expert consensus meetings (Baveno I to V) have been held every five years since 1990 to discuss relevant issues. The most recent BAVENO VI consensus was held in April 2015, with the theme "Risk Stratification and Individualized Treatment of Portal Hypertension", which included the use of invasive and non-invasive methods to screen and monitor esophagogastric varices and portal hypertension, the role of etiological treatment on liver cirrhosis, primary prevention of decompensation, management of acute variceal bleeding, prevention of rebleeding and other decompensated events, cirrhotic and non-cirrhotic liver vascular diseases, etc. The full text of the BAVENO VI consensus was published in the Journal of the European Society of Hepatology in 2015^[1]。

The symptoms of patients with refractory IBS are prolonged and difficult to heal, and most of them are accompanied by anxiety and depression^[1,2]Seriously affects the quality of life and increases medical expenses, which has become the focus of attention of gastroenterologists. Amitriptyline, a tricyclic antidepressant (TCA), is limited in application because of the large adverse reactions caused by high-dose use. However, in recent years, foreign scholars have found that low-dose amitriptyline (10~75 mg/d) is effective in the treatment of IBS, and the adverse reactions are small^[3]。 This study aimed to investigate the combined efficacy and adverse effects of low-dose amitriptyline in patients with refractory diarrheal IBS.

From 18 to 20 June 2015, the 3rd meeting of the Asian Organization for Crohn's and Colitis (AOCC) was held in Beijing. This conference was hosted by AOCC and China Health Promotion Foundation, and hosted by IBD Group of Digestive Diseases Branch of Chinese Medical Association and Peking Union Medical College Hospital. Professor Qian Jiaming of Peking Union Medical College Hospital, head of IBD Group of Digestive Diseases Branch of Chinese Medical Association, served as the chairman of this conference. The AOCC was established on January 1, 2013 to develop and support relevant research and medical education in the field of IBD in Asia. Professor Hu Pinjin, the rotating chairman of AOCC 2015 and the Sixth Affiliated Hospital of Sun Yat-sen University in Guangzhou, put forward the theme of the conference "Development of AOCC: Facing Opportunities and Challenges". The conference was held in China for the first time, with more than 900 participants from 17 countries. It surpassed the 1st conference held in Tokyo, Japan and the 2nd conference held in Seoul, South Korea in terms of number of participants, conference scale and academic content. It was an academic event in the field of IBD in Asia.

The 4th Beijing Forum on Integrated Medicine of Traditional Chinese and Western Medicine for Gastrointestinal Function and Motility Diseases, sponsored by the Digestive Integrated Medicine Branch of China Association for the Promotion of Traditional Chinese Medicine Research and hosted by Wangjing Hospital of Chinese Academy of Chinese Medical Sciences, Beijing Jishuitan Hospital and Peking University First Hospital, was held in Beijing on July 5th, 2015. The conference was initiated by Professor Ke Meiyun, Professor Yang Yunsheng and Professor Wei Wei, and co-chaired by Professor Zhang Xuezhi and Professor Lan Yu. Western medicine experts represented by Academician Fan Daiming, Professor Ke Meiyun and Professor Liu Xinguang, and Chinese medicine experts represented by Professor Wei Beihai and Professor Tian Delu attended the conference, with more than 200 participants.

The 51-year-old male was admitted to the hospital on August 19, 2014 due to upper abdominal distension and pain for 1 month. He was in good health. Gastroscopy showed biliary reflux gastritis, duodenitis, and positive for Helicobacter pylori. Fecal occult blood test was positive and tumor marker levels were in the normal range. Upper abdominal enhanced CT showed no significant abnormalities. Colonoscopy revealed multiple polyps of the colon. After antibacterial treatment and polypectomy, the fecal occult blood test was negative and he was discharged from hospital on September 7th. The patient still had distension and pain in the upper abdomen, and repeated nausea and vomiting of bile-like fluid, which worsened after eating, and was significantly thinner than before. He was hospitalized again on September 14th. The physical examination showed positive vibration sound, and gastrointestinal decompression and drainage of gastric juice and bile>1 000 mL/d were performed. Abdominal standing X-ray showed no abnormalities. Reexamination enhanced CT (Figure 1) and abdominal angiography (Figure 2), duodenal horizontal stenosis with anterior mesenteric vascular compression, considering mesenteric vascular compression syndrome. After enhanced intravenous nutrition and conservative medical treatment, there was no improvement. Upper gastrointestinal lipiodol angiography showed that the horizontal part of the duodenum was narrowed and the contrast medium could not pass. After taking prone position, the contrast medium could pass, but the junction between the ascending part of the duodenum and the jejunum was narrowed and the contrast medium could not pass, seeFigure 3Considering the existence of lesions at the junction of duodenum and jejunum, malignant tumors could not be ruled out, so surgical exploration was decided. During the operation, a tumor was seen at the junction of the ascending duodenum and the jejunum, with a maximum diameter of about 3 cm, seeFigure 4Involving serosa, corresponding intestinal stenosis and obstruction, swollen lymph nodes in the mesenteric, decreased adipose tissue between the mesenteric blood vessels and the abdominal aorta, partial compression of the horizontal part of the duodenum, no abnormalities were found in the exploration of the rest of the small intestine and colon, no obvious metastases in the liver, pelvic cavity and abdominal aorta, and no ascites in the abdominal cavity. Postoperative pathological diagnosis (Figure 5) shows medium to poorly differentiated adenocarcinoma of the small intestine, invading the extraserous adipose tissue, and tumor thrombus is seen in the vessels. There was no involvement of cancer tissue in the upper and lower excised ends, 5 of the 16 lymph nodes in the surrounding adipose tissue showed metastatic cancer tissue, and 2 cancer nodules were seen. Immunohistochemical examination showed negative cytokeratin 7, positive cytokeratin 20, CEA, villin, cytokeratin 19, CA19-9, and CD34 vessels, and about 85% positive for Ki-67 antigen. The patient recovered well after operation, without nausea and vomiting, and had normal food and appetite after discharge. After 1 month, the body weight increased by about 5 kg at the follow-up visit.

A 21-year-old female was admitted to the hospital in September 2014 due to intermittent diarrhea for 7 years. Since 2007, the patient has intermittent watery diarrhea, 2 to 10 times/d, 200 to 500 mL/time, and food residues can be seen in the feces. The symptoms are more than those after eating irritating food or catching cold. Symptoms can be relieved after about 1 week of infusion treatment in the local hospital (details are unknown), and the attacks will repeat within 7 years, with an interval of 2 weeks or 2 months. In 2010, gastroscopy in a foreign hospital showed superficial gastritis and duodenal lymphoid follicular hyperplasia, enteroscopy showed nodular hyperplasia of ileal mucosa, and pathology showed chronic inflammatory reaction of ileal mucosa. Patients are prone to upper respiratory tract infections since childhood, more than 6 times a year. Physical examination: vital signs stable, BMI 18.1 kg/m²Rough skin, anemic appearance, pale conjunctiva, mild periumbilical tenderness, no rebound pain, muscle tension, bowel sounds 5 times/min. Blood routine: WBC count 4×10⁹/L, Hb 76 g/L, PLT count 392×10⁹/L. Blood smear: RBCs vary in size, some irregular in shape, and the center light stained area is enlarged. Bone marrow smear showed active myeloproliferation and iron deficiency anemia. Albumin was 33~48 g/L, and the ratio of albumin to globulin was 2.7. There was no abnormality. Fecal examination: negative for routine and occult blood, positive for Sudan III staining, negative for bacterial and fungal culture, negative for acid-resistant staining, negative for Clostridium difficile culture and toxin determination, negative for parasites and eggs, negative for giardiola antigen and cryptosporidium antigen, negative for suspension drop test and Shigella dysenteriae culture. D xylose absorption test 0.5 g/5 h. Serum gastrin and somatostatin receptor imaging was negative. IgG 2.41 g/L, IgA 0.22 g/L, IgM normal. Determination of serum IgG subclasses: IgG1 2 640 mg/L (normal value 4 900~11 400 mg/L), IgG 2 433 mg/L (normal value 1 500~6 400 mg/L), IgG3 normal, IgG4 3 mg/L (normal value 80~1 400 mg/L). B lymphocytes, CD4 positive T lymphocytes and CD8 positive T lymphocytes were normal. Abdominopelvic enhanced CT and three-dimensional reconstruction of small intestine: multiple lymph nodes of different sizes in retroperitoneal and mesenteric roots, splenomegaly, and no abnormalities in small intestine. Chest CT: multiple lymph nodes in bilateral axillary. Total gastrointestinal angiography showed excessive small intestinal peristalsis, and some small intestinal mucosal folds were slightly thickened with filling defects (Figure 1)。 Gastroscopy showed nodular bulge of the duodenum (Figure 2)。 Pathology: Acute and chronic inflammatory reaction of mucosa, local lymphoid tissue hyperplasia (Figure 3)。

A 63-year-old male was admitted to the hospital on 6 June 2014 due to abdominal distension, diarrhea and 3 months of wasting. Since March 2014, the patient had abdominal distension, accompanied by diarrhea, 3 to 4 times/d, accompanied by anorexia, fatigue, and weight loss, and weight loss of 8 kg within 3 months. Before admission, abdominal and pelvic CT showed local intestinal dilatation and gas-liquid level; Colonoscopy showed inflammatory reaction of the rectum. Symptomatic treatment is not effective. Previous fatty emulsion allergy, heavy smoking history, family history of cancer. Physical examination: blood pressure 90/61 mmHg (1 mmHg =0.133 kPa), thin body, anemic appearance, no difference in heart and lung, soft abdomen, active intestinal sounds. The patient's blood routine WBC count after admission was 4.84×10⁹/L, neutrophils 0.475, monocytes 0.12, lymphocytes 0.40, Hb 94 g/L, PLT 386×10⁹/L; urine, fecal routine (–); Albumin 31 g/L, LDH 109 U/L; Normal kidney function; PT 17.0 s, activated partial thromboplastin time 55.2 s, D-dimer 0.24 mg/L. Screening for fecal etiology was negative. Antinuclear antibody negative. Serum protein electrophoresis M protein 10.60 g/L, M protein percentage 15.5%. Serum immunofixation electrophoresis: IgM kappa chain positive (+); The free light chain kappa3 was 530 mg/L, the free light chain lambda was 81.4 mg/L, and kappa/lambda was 43.4. Blood smears showed red blood cells varying in size, with large red blood cells visible. Bone marrow smear: red blood cells are arranged in a line-like manner, and the proportion of lymphocytes is increased. Suspected lymphoplasma cells account for 0.01 in the smear, seeFigure 1。 Bone marrow biopsy: There is a significant increase in hematopoietic tissue in bone marrow tissue, and more small lymphocytes of B phenotype can be seen in hematopoietic tissue. Consider B-cell lymphoma or leukemia, seeFigure 2。 Bone marrow immunohistochemistry showed CD117 (-), CD138 (-), CD15 (+), CD20 (+), CD3 (focal +), CD34 (vascular +), CD38 (scattered +), myeloperoxidase (+), Ki-67 index 0.40; Special staining showed Congo red (–), potassium permanganate Congo red (–). Colonoscopy showed multiple white spots at the end of the ileum, and colonoscopy pathology showed chronic inflammatory reaction in the small intestinal mucosa (end of ileum), with more focal lymphocytes and plasma cells aggregating in the lamina propria, mainly B lymphocytes, seeFigure 3。 Immunohistochemistry showed AE1/AE3 (-), CD10 (partial +), CD138 (-), CD20 (partial +), CD23 (+), CD3 (-), CD5 (partial +), cyclin D1 (partial +), Ki-67 index 0.15. positron emission computed tomography (PET) examination showed increased metabolism of multiple lymph nodes throughout the body, abnormally increased metabolism of bone marrow and spleen throughout the body, and colonic involvement was not excluded, seeFigure 4。 Final diagnosis: non-Hodgkin lymphoma (NHL), exact classification as lymphoplasmacytic lymphoma (LPL). At the time of writing, the patient had completed 2 courses of R-CHOP regimen chemotherapy, had transitioned to normal diet, defecated 2 to 3 times/d, had yellow soft stools, had no abdominal pain, diarrhea, nausea, vomiting and other discomfort, had a body weight increase of about 5 kg, and anemia was significantly improved (Hb 121 g/L). The patient remains under follow-up.

A 23-year-old female, Manchu nationality, was admitted to the hospital on 28 January 2014 due to persistent abdominal distension and pain for 1 month, aggravated with increased abdominal circumference for 1 week. One month ago, the patient felt persistent distension and pain in the middle and upper abdomen without obvious trigger, irrelevant to diet, radiating to the right shoulder and low back, aggravated in the lateral position, accompanied by progressive decrease in appetite, and the symptoms did not improve after self-administration of omeprazole. Nearly 1 week after admission, the patient had aggravated distension and pain in the upper abdomen, and developed lower abdominal pain, which was aggravated during exercise, and the conscious abdominal circumference increased progressively. Outpatient abdominal ultrasound suggested possible cirrhosis and massive ascites; CT scan of upper abdomen showed ascites and slightly thickened stomach wall; Gastroscopy revealed chronic superficial gastritis and was admitted to hospital for further treatment. Since the onset of the disease, the patient's appetite and food intake have decreased, the body weight has increased by 5 kg in the past 1 month, the defecation is normal, the urine output has not decreased, and the color is yellow. No nausea, vomiting, no fatigue, weight loss, no diarrhea, melena, blood in the stool, no facial edema, foamy urine, lying down at night, no decreased urine volume, no edema of both lower limbs, no fever, night sweats, chest tightness, shortness of breath. She has no special past history and is a nurse. She has been exposed to chemotherapy drugs such as oxaliplatin, irinotecan, fluorouridine, fluorouracil and epirubicin for 2 years. Normal menstrual history, unmarried, childless, denying family history of hereditary diseases, tuberculosis and other infectious diseases and contact history.

There are not a few patients who need long-term PPI clinically, such as refractory GERD and intractable peptic ulcer, all of which need oral standard dose of PPI to be maintained^[1]； The use of PPI to prevent gastrointestinal bleeding caused by antiplatelet drugs and other NSAIDs is also increasing. Such drugs are used more and more widely, and even in certain symptoms or diseases there is the possibility of abuse. However, clinicians may have little understanding of the potential risks associated with long-term (usually>1 year) PPI use. In recent years, there have been some related large-scale and high-quality observational research results. This paper summarizes the latest research on the adverse reactions of long-term use of PPI. Because there are few studies on the application of PPI in children at present, it will not be discussed for the time being.

myeloid differentiation factor 88 (MYD88) is a key adaptor in the TLR signaling pathway, which can activate the NF-κ B signaling pathway after TLR and IL stimulation. In recent years, research has found that,MYD88 gene has activating mutations or abnormal expression in lymphohematopoietic tumors and many solid tumors, which plays an important role in tumorigenesis and development, and may become an important therapeutic target. The relationship between MYD88 and TLR signaling pathway and its role in digestive system tumors are reviewed.

According to the data in the 2012 China Cancer Registry Annual Report, there are 3.12 million new cancer patients and 2.7 million deaths in my country. Cancer is surpassing the incidence trend of cardiovascular and cerebrovascular diseases and becoming the first cause of death^[1]。 The incidence rate of colorectal cancer ranks third among malignant tumors in urban areas of our country, and it is also rising rapidly in rural areas of our country, now ranking fifth^[1]。 Colorectal cancer accounted for 10.56% and 7.80% of the morbidity and mortality of malignant tumors, ranking 3rd and 5th, respectively^[1]。 Clinical emphasis is placed on early detection, early diagnosis and early treatment, but at present, imaging technology has shortcomings in the early diagnosis of colorectal cancer, such as MRI, CT and positron emission tomography-computed tomography (PET-CT) examination costs are relatively expensive, and the imaging changes can only be made when the tumor tissue develops to a certain extent, and the diagnosis cannot be confirmed; Air barium double contrast contrast radiography, transrectal ultrasound and endoscopy can be painful, and patients often refuse. In addition, the sensitivity and specificity of serum tumor markers and fecal occult blood tests were not high. In recent years, it has been found that miRNA is closely related to the occurrence and development of colorectal cancer. Because colorectal cancer cells can be excreted with feces after shedding, the detection of fecal miRNA may be a new method for early screening and diagnosis of colorectal cancer. This paper reviews the correlation between miRNA and colorectal cancer, and the progress of fecal miRNA detection in diagnosis and screening.