2018年 · 第38卷第07期

The human intestine contains extremely rich microorganisms, and the total number of genes contained in it is more than 150 times that of the human genome. These microorganisms constitute a complex network of microbial-microbial and microbial-host relationships by competing, complementing, and synergistic with each other. On this basis, the components of intestinal microorganisms are relatively balanced and maintain homeostasis, thus realizing mutual symbiosis with the host. For the host, there are multiple barriers in their gut to maintain homeostasis of intestinal microorganisms. These include: a mechanical barrier composed of mucus layer secreted by intestinal cells and goblet cells that are closely connected on the surface of the gastrointestinal tract, a chemical barrier composed of substances such as antimicrobial peptides produced by epithelial cells, a biological barrier composed of colonized probiotic and symbiotic bacteria in the intestinal tract, and an immune barrier composed of the body's innate immune system and acquired immune system. The above intestinal barriers are an organic and synergistic whole, thus establishing a benign symbiosis between the host and non-pathogenic microorganisms, laying an important foundation for normal intestinal function.

functional gastrointestinal disorders (FGID) are a group of diseases with gastrointestinal symptoms as the main manifestation but lack of biochemical and histopathological abnormalities to explain these symptoms. The earliest recognition of FGID is that these patients have no organic disease, and many symptoms are caused by abnormal gastrointestinal motility^[1]。 With the continuous revision and improvement of the Roman diagnostic and classification criteria, the research on FGID is also in depth. More and more data support that FGID is a disease caused by abnormal brain-intestine interaction. Its pathophysiological mechanism involves motility disorder, visceral hypersensitivity, changes of mucosal and immune function, changes of intestinal flora and abnormal processing function of central nervous system to gastrointestinal afferent signals^[2]。 In some FGID, abnormal motility still occupies the most important position. Correct understanding and objective evaluation of the role of abnormal gastrointestinal motility in FGID is of great significance to choose effective treatment measures.

The human intestine is home to a large number of intestinal microorganisms, including bacteria, fungi and viruses. The order of magnitude of gut bacteria in healthy adults is about 1×10¹⁴With more than 1 000 species. In the past decade, more and more studies have confirmed that the homeostasis of intestinal flora participates in the digestive process, maintains the balance of energy and metabolism of the body, and regulates the immune response. Correspondingly, intestinal flora disorders play an important role in the occurrence and development of various digestive, immune and metabolic related diseases. Studies suggest that intestinal flora can regulate the central nervous system through many ways, including stimulating vagus nerve and releasing neuroendocrine regulators. Intestinal flora and its metabolites not only maintain the normal development of the nervous system, but also participate in the pathophysiological processes of a variety of mental diseases and psychosomatic diseases, and even affect individual social behavior and cognitive function. Studies have found that there are different degrees and characteristics of flora disorders in functional gastrointestinal diseases, IBD, depression, autism spectrum disorder, etc^[1,2]。 Certain bacterial components or their metabolites have the potential to become psychomodulatory drugs. Therefore, the concept of flora-intestine-brain axis is gradually widely accepted as an important supplement and perfection to intestine-brain interaction.

Esophageal pressure monitoring is the basic detection method of esophageal motility disorders. Since the end of the 19th century, esophageal pressure measurement technology has been developed for more than 100 years, from water perfusion pressure measurement to solid state pressure measurement, and the recording method of esophageal pressure monitoring has also developed from traditional linear graph to pressure topography map. Esophageal high resolution manometry (HRM) uses water perfusion or solid-state manometry to detect the pressure of the esophagus through pressure sensors evenly distributed throughout the esophagus, and converts its linear manometry pattern into a color pressure topography map to make it clear at a glance (Figure 1)。 Since the advent of HRM, experts in the field of esophageal motility have been working to categorize the various forms of esophageal motility in HRM. In 2009, led by Peter J. Kahrilas and John E. Pandolfino, esophageal dynamics experts at Northwestern University in Chicago, USA, the first edition of HRM esophageal motility disorder classification standard was published and named "Chicago Classification". This classification summarizes the common esophageal motility manifestations in the process of esophageal motility monitoring. This classification has been continuously updated in clinical practice, and was updated to the third edition in 2015^[1]。 The 3rd edition of the Chicago Classification classifies HRM esophageal motility into 4 categories (Table 1), including gastroesophageal junction outlet obstruction, severe esophageal motility disorder, secondary esophageal motility disorder, and normal esophageal motility. Although the new edition of the Chicago Classification has refined most clinically common esophageal motility disorders, increasing clinical operability and facilitating the diagnosis and treatment of motility-related esophageal symptoms, there are still reports that about 1/3 of patients who undergo HRM examination for pharyngeal and esophageal-related symptoms cannot use the Chicago Classification to classify their motility disorder forms^[2]。 The following mainly describes HRM abnormalities outside the Chicago Classification, including upper esophageal sphincter (UES), proximal esophagus, longitudinal muscle contraction, challenge test, and rumination syndrome.

PPI is the first-line treatment for GERD, but about 40% of patients cannot control their symptoms with PPI treatment, especially patients with non-erosive reflux disease (NERD). At present, it is believed that many factors may be involved in the occurrence of refractory reflux symptoms in PPI, such as insufficient acid suppression, non-acid reflux factors, abnormal esophageal movement and psychological factors^[1]。 Studies report that nearly 1/3 of patients with refractory reflux symptoms may not be GERD, and some of them may be functional heartburn (FH)^[2]。

Acute gastrointestinal hemorrhage is a common acute and severe disease in clinic. Because of the acute onset, large bleeding volume, and difficulty in quickly locating the bleeding site, clinical management is difficult. Interventional diagnosis and treatment of acute gastrointestinal arterial hemorrhage caused by abnormalities of left gastric artery, gastroduodenal artery (GDA) and gallbladder artery have been reported^[1,2]Acute gastrointestinal bleeding caused by rupture of superior pancreaticoduodenal artery (SPDA) and retroperitoneal hematoma caused by rupture of inferior pancreaticoduodenal artery (IPDA) have also been reported from time to time^[3,4,5]。 However, there are few reports on the intervention diagnosis and treatment of gastrointestinal bleeding caused by IPDA rupture at home and abroad^[6,7]。 In this study, 13 patients with acute gastrointestinal hemorrhage caused by IPDA hemorrhage underwent emergency interventional surgery, and embolization was performed to identify the bleeding site. The hemostatic effect was satisfactory, which is reported as follows.

esomeprazole, the 1st levo-isomeric PPI, has higher bioavailability and more consistent pharmacokinetic profile than omeprazole^[1,2]。 At present, domestic esomeprazole sodium for injection has been listed. In this study, the pharmacokinetics and gastric acid control effects of single and multiple doses of esomeprazole sodium for injection in Chinese healthy volunteers were compared between domestic and original research.

In recent years, the incidence of CD has gradually increased, but patients with cytomegalovirus (CMV) infection are rarer in clinical practice, accounting for the proportion of<5%^[1]。 Because CMV infection can aggravate the condition or cause refractory CD, it should be paid attention to clinically. The diagnosis and treatment of a patient with ileocolic CD complicated with CMV colitis by the IBD multidisciplinary diagnosis and treatment team of Beijing Army General Hospital is reported as follows.

A 37-year-old male was admitted to Hebei Provincial People's Hospital on June 9, 2016 due to loss of appetite, weakness of both lower limbs for half a year, aggravation with speech retardation for 2 months. Six months ago, the patient developed weakness of both lower limbs, loss of appetite, accompanied by acid reflux and nausea, and was not treated regularly. Two months ago, he had slow speech and reaction, memory loss, unstable gait, feeling like walking on cotton, numbness at the tips of his fingers and toes, and weight loss of 10 kg compared with before. The above symptoms were progressively aggravated. Past physical fitness. Family history: One sister suffers from cerebrovascular malformation. Physical examination: The tongue was pale red, with tooth marks on the edge of the tongue, and no obvious abnormalities in the heart, lungs and abdomen. Physical examination of nervous system: clear consciousness, normal muscle strength and muscle tone of limbs, tendon reflex of limbs, disappearance of joint position sense, positive Romberg sign and positive bilateral Babinski sign. Laboratory tests: Hemoglobin was 100 g/L, mean red blood cell volume was 110.9 fL, and mean hemoglobin content was 39.1 pg; Serum folic acid was 6.81 nmol/L and vitamin B12 was 76.12 pmol/L;¹⁴C Breath test positive. There were no abnormalities in CT examination of the head and abdomen and plain MRI scan of the head. The surface evoked potentials showed that the waveforms of bilateral tibial nerve P40 and median nerve N20 disappeared. Gastroscopy showed chronic atrophic gastritis (Figure 1)。 Gastroscopic pathological examination: severe chronic inflammation of gastric mucosa, glandular atrophy, intestinal metaplasia of some glands (Figure 2)。 Gastric antrum examination revealed chronic inflammation of the mucosa. Serum factor antibodies were positive, gastrin and parietal cell antibodies were normal. Diagnosis: autoimmune gastritic (AIG), pernicious anemia, subacute combined spinal cord degeneration. After diagnosis, methylcobalamin injection 500 μ g (once/d) was injected intravenously, folic acid 5 mg (once/d) was orally administered, and vitamin B 120 mg (three times/d) was orally administered. After 2 weeks of treatment, the hemoglobin was 128 g/L, the mean red blood cell volume was 108.4 fL, the mean hemoglobin content was 37.2 pg, the serum folate was 35.57 nmol/L, and the vitamin B12 was 1 478 pmol/L. The patient's speech was fluent, anemia improved, appetite recovered, fatigue, numbness of fingers and toes and gait instability improved significantly compared with before. Follow-up: After 1 month of discharge, there was only occasional swelling in both lower limbs, body weight increased by 3 kg, hemoglobin was 147 g/L, mean red blood cell volume was 97.9 fL, mean hemoglobin content was 33.8 pg, serum folic acid was 32.51 nmol/L, and vitamin B12 was 1 365 pmol/L. Quadruple antibodyH.pyloriAfter treatment¹⁴C Breath test negative. By May 2017, the patient had no anemia, leaving mild swelling in both calves, and continued to receive methylcobalamin injection 500 μ g intramuscularly once a month.

A 42-year-old female was admitted to the Department of Gastroenterology of Wuxi Second People's Hospital on January 7, 2017 due to left lower abdominal pain for 1 d. After eating dinner at night, the patient developed paroxysmal left lower abdominal cramps, radiating to the upper abdomen and periumbilical area, accompanied by nausea, abdominal distension, cessation of anal exhaustion and defecation, mild back pain, no hematemesis, hematochezia, and acceptable urine output. She had a history of long-term sedentary, and had a small amount of vaginal bleeding without cause at 10 weeks of pregnancy. She improved after 1 week of progesterone abortion treatment. She raised a son and was in good health. There were two abortions due to unintended pregnancy. Physical examination: blood pressure 120/80 mmHg (1 mmHg =0.133 kPa), consciousness, soft abdomen, mild tenderness in the left lower abdomen, no rebound pain, positive percussion pain in the left kidney area, and no abnormalities were observed. Laboratory test: white blood cell count 8×10⁹/L, the neutrophil ratio was 0.852, and the rapid CRP was 106.8 mg/L; Urine ketone body was 1.5 mmol/L (+ + + +), urine protein (+ +); ALT was 81.0 U/L, AST was 60.0 U/L, AST mitochondrial isoenzyme was 15.1 U/L, creatine kinase isoenzyme was 34.0 U/L, total carbon dioxide was 21.8 mmol/L, GGT was 266.0 U/L, and serum creatinine was 72.6 μ mol/L; The degradation product of fibrin (pro) was 5.73 μ g/mL, the time ratio of activated partial thromboplastin was 0.90, and the D-dimer was 0.98 μ g/mL. Renoureteral ultrasonography showed no abnormalities; CT scan showed that the left colon duct was thickened and there was a small amount of exudation around it. Proposed diagnosis: abdominal pain to be examined, incomplete intestinal obstruction? Abnormal liver function. Fasting, gastrointestinal decompression, cefodizime combined with ornidazole for anti-infection, phloroglucinol for antispasmodic, magnesium isoglycyrrhizinate for liver protection, indomethacin for pain relief, amino acid and vitamin rehydration for supporting treatment. After treatment, the patient's abdominal pain was significantly relieved.

According to the study arrangement of the China Scholarship Council, in December 2017, the author went to the Gastrointestinal Laboratory, GI LAB, University of Mississippi Medical Center, UMMC, USA As a visiting scholar, I mainly investigated and learned the diagnosis and treatment modes and management methods and methods of common gastrointestinal and pancreaticobiliary diseases in the United States. There are indeed many differences between China and the United States in endoscopy, treatment process, and talent training, so I write this article to share it with domestic colleagues.

GERD is a condition in which the contents of the stomach reflux into the esophagus or above into the mouth (including the larynx) or lungs, causing uncomfortable symptoms and/or complications^[1]。 The prevalence of GERD in North America and Europe ranged from 8.8% to 27.8% and in East Asia from 2.5% to 7.8%. The prevalence of GERD in Asian countries was lower than that in Western countries^[2]。 Nevertheless, the prevalence of GERD in China has increased year by year, reaching 3.8% in Hong Kong, nearly doubling in 10 years^[3]The prevalence of GERD in Mainland China is 3.1%^[4]。

Abdominal pain is a common symptom of functional gastrointestinal disease (FGID), and it is an important factor for patients to visit a doctor and affect their quality of life. IBS and centrally mediated abdominal pain syndrome (CAPS) are typical diseases of chronic abdominal pain in FGID. The incidence of IBS is high, about 8.8% worldwide^[1]whose abdominal pain is associated with defecation; However, abdominal pain in CAPS was characterized by persistent or nearly persistent, and the severity was not related to physiological activities such as eating or defecation^[2]。 CAPS has also been referred to as "chronic idiopathic abdominal pain", "chronic functional abdominal pain" and "functional abdominal pain syndrome" in the past. There are few epidemiological studies on CAPS, which may be related to its higher diagnosis difficulty. The incidence of CAPS reported in North America is 0.5% ~1.7%^[2]。 Although the incidence of CAPS is low, it has a significant impact on the quality of life of patients and consumes a large amount of medical resources. CAPS may overlap with IBS, and whether it is an extremely severe form of IBS is still controversial^[3]At present, there is no evidence that chronic, severe IBS abdominal pain is different from centrally mediated gastrointestinal pain diseases (including CAPS), except that the latter has less impact on the intestine.