肠道微生态与肠易激综合征:基础与临床

肠道微生态与功能性胃肠病(FGIDs)的关系已成为目前研究热点之一。最新罗马Ⅳ标准指出FGIDs不仅仅是胃肠道疾病,脑-肠互动障碍可能贯穿肠易激综合征(IBS)发病的始终。肠道微生态失衡被认为是导致脑-肠互动障碍的重要始动因素,参与构成菌群-肠-脑轴,成为新兴研究热点。尤其是在IBS的研究中,肠道微生态失衡已被证实与IBS免疫异常和临床症状相关;使用益生菌调节IBS肠道菌群取得良好成效,其他相关菌群干预策略也在不断探索中。     

肠神经系统在功能性胃肠病发病中的作用

肠神经系统对胃肠道运动、分泌和血液供应具有独立的调节作用,功能性胃肠病（FGIDs）的慢性症状如腹泻、便秘和疼痛与肠神经调控的胃肠道功能异常有关。某些FGIDs存在肠神经递质表达异常,甚至神经元退行性改变;肠神经系统与肠道Cajal间质细胞、胶质细胞和免疫细胞连接和功能的异常亦可能参与了FGIDs的发病;脑-肠轴功能紊乱是应激和感染后肠易激综合征的发病机制之一。肠神经系统在FGIDs的发病中具有重要作用,以肠神经为靶点为开发治疗FGIDs的有效药物开辟了广阔的前景。     

功能性胃肠病内脏高敏感与Cajal间质细胞相关性研究进展

目的 功能性胃肠病(FGIDs)是一组常见的消化科疾病,发病机制包括胃肠运动异常、内脏敏感性增高、炎症、脑-肠互动、心理社会因素5个方面.近年研究发现,内脏高敏感性可以被认为是FGIDs的一个生物学指标.胃肠道ICC的数目、分布及超微结构的改变,在功能性胃肠病的发生、发展过程中起重要作用.但要明确诊断ICC异常与功能性胃肠病相关性,并为功能性胃肠病的药物治疗提供新的靶点,仍需做大量相关研究.     

肠道菌群对脑-肠轴和功能性消化不良的影响

肠道菌群是多种消化系统和神经系统疾病的致病因素。研究表明肠道菌群与脑-肠轴具有双向联系,对神经系统发育和功能、胃肠道功能等具有调节作用。功能性消化不良(FD)是常见的功能性胃肠病,其发病机制尚未完全阐明,近年研究表明肠道菌群在FD发病中起有重要作用。本文就肠道菌群对脑-肠轴和FD的影响作一综述。     

基于功能性胃肠病的量表疗效评价研究进展

功能性胃肠病(functional gastrointestinal disorder,FGIDs)又称肠-脑互动异常[1]。成人类的FGIDs包含6类,其在症状上常相互重叠,并且有其共通的病理机制。目前认为FGIDs的"生物-心理-社会模式"是其病理生理决定因素[1]。因此,在FGIDs的临床试验中,主要目标是改善患者所诉的症状和体征。     

中枢神经调节剂在老年功能性胃肠病中的应用现状

功能性胃肠病是一组根据胃肠道症状分类的疾病,其症状产生主要与脑-肠轴功能异常、动力紊乱、内脏高敏感、黏膜和免疫功能的改变、肠道菌群的改变、中枢神经系统处理功能异常相关,在老年患者中发病率较高。单用常规药物治疗该病多难以缓解症状,辅以中枢神经调节剂则可明显改善症状。然而老年人多存在共病状态,因此在应用中枢神经调节剂时,应注意药物种类、剂量和药物间相互作用,避免毒副作用。本文主要对中枢神经调节剂在老年功能性胃肠病患者中对不同转运蛋白和受体的调节机制和作用、临床应用及副反应进行综述,以期对老年功能性胃肠病患者应用中枢神经调节剂提供参考依据。     

肠道菌群与脑-肠轴功能相互影响的研究进展

人体肠道内的菌群参与了许多生理功能的维持和疾病的发生。作为大脑和胃肠道功能相互调节的重要桥梁,脑-肠轴功能的正常发挥是肠道菌群维持稳定的条件。脑-肠轴紊乱可激活肠黏膜免疫,对肠道菌群产生影响,使菌群结构发生改变。反之,肠道菌群结构改变亦会影响神经系统发育,导致脑-肠轴功能紊乱,其中迷走神经和血清代谢物质在脑-肠轴功能的调节中发挥重要作用。本文就肠道菌群与脑-肠轴功能相互影响的研究进展作一综述。     

功能性胃肠病从基础研究进展到临床治疗新理念

功能性胃肠病(functional gastrointestianal disorders, FGIDs)全球发病率高，患者生活质量差，诊断率低，对该类疾病发病机制认知不足，尤其对脑-肠互动及中枢作用的理解不深造成处置不到位及疗效不理想。本文从近年在FGIDs发病机制方面的研究热点和进展及临床难点出发，聚焦在更新FGIDs处置的理念，介绍评估体系，倡导心身同治。     

神经调节在功能性胃肠病发病中的作用及其研究进展

功能性胃肠病是消化系统的常见疾病,其发生与脑-肠轴的异常密切相关.脑-肠轴神经调节过程的紊乱产生了以胃肠道动力改变和疼痛、腹胀为主症的消化系疾病.本文总结了脑-肠轴的神经调节机制和介入治疗进展,探讨了神经调节介入治疗功能性胃肠病的临床研究前景.     

感染后功能性胃肠病及其发病机制

功能性胃肠病（FGIDs）是一类常见胃肠道疾病，其发病和特定症候群与多种因素相关。胃肠道感染和黏膜炎症背景作为FGIDs发病的诱因近年来备受关注。学者们将那些感染后发生的FGIDs称为感染后FGIDs（PI-FGIDs）。本文就感染与FGIDs的关系以及PI-FGIDs发病机制中的动力异常、黏膜免疫改变、肠神经系统改变等内容作一介绍。     

The microbiota-gut-brain axis in functional gastrointestinal disorders

Functional gastrointestinal disorders (FGIDs) are highly prevalent and pose a significant burden on health care and society, and impact patients’ quality of life. FGIDs comprise a heterogeneous group of disorders, with unclear underlying pathophysiology. They are considered to result from the interaction of altered gut physiology and psychological factors via the gut-brain axis, where brain and gut symptoms are reciprocally influencing each other’s expression. Intestinal microbiota, as a part of the gut-brain axis, plays a central role in FGIDs. Patients with Irritable Bowel Syndrome, a prototype of FGIDs, display altered composition of the gut microbiota compared with healthy controls and benefit, at the gastrointestinal and psychological levels, from the use of probiotics and antibiotics. This review aims to recapitulate the available literature on FGIDs and microbiota-gut-brain axis.     

The Brain-Gut-Microbiotal Axis: A framework for understanding functional GI illness and their therapeutic interventions

Functional gastrointestinal disorders (FGIDs), characterized by chronic abdominal complaints without a structural or biochemical cause, are common diseases that are frequently encountered by specialists in internal medicine. Collectively, irritable bowel syndrome (IBS) and functional dyspepsia are estimated to affect up to 22% of the population, and are often associated with additional somatic and pain complaints, all without an obvious structural source [1,2]. An appreciation of the current understanding of the mechanistic basis for these disorders is key to developing treatment goals and optimization of patient management strategies. In recent years, the brain-gut axis increasingly has been recognized as a central factor in the experience of functional abdominal pain disorders, including the most recent Rome IV guidelines which identify FGIDs as disorders of gut-brain interaction [3]. The brain-gut axis (BGA), simply defined, is a complex network of bidirectional communication between the central and enteric nervous systems. This axis broadly includes all the systems involved with communication between the GI tract and central nervous system (CNS), with principle inputs into this network occurring between the CNS, enteric nervous system (ENS), and autonomic nervous systems (ANS), but also includes interfaces with numerous other factors, including endocrine hormones and immune effector cells as well as interactions with the gut microbiota. Perturbances to this system have been found to play a critical role in the development of visceral hypersensitivity, bowel dysregulation, and mood. This review will summarize the principle processes involved in the neurologic and biologic function of the brain-gut axis, our current understanding of its role in functional GI disorders, and potential targets for therapeutic intervention.     

Bile acids and FXR in functional gastrointestinal disorders

Functional gastrointestinal disorders (FGIDs), such as irritable bowel syndrome (IBS) and chronic constipation (CC), are commonly diagnosed conditions in clinical practice which create a substantial global burden. Since the farnesoid X receptor (FXR) and bile acids (BAs) are responsible for maintaining homeostasis in the GI tract, any disturbances in the expression of FXR or the composition of BAs may contribute to the development of the GI symptoms. Alterations in the mechanism of action of FXR directly affect the BAs pool and account for increased intestinal permeability and changes in abundance and diversity of gut microbiota leading to intestinal dysmotility.Current review focuses on the correlation between the FXR, BAs and the composition of gut microbiota and its influence on the occurrence of GI symptoms in FGIDs.     

TRP 超家族与功能性胃肠病

功能性胃肠病(FGIDs)是消化系统常见疾病,其发病机制复杂,症状的产生涉及多种病理生理改变。瞬时受体电位(TRP)通道蛋白可通过多种机制活化,感受细胞内外环境的各种刺激,参与生物体内多种生命活动。本文就TRP超家族与FGIDs之间的联系作一综述。     

抗抑郁药治疗功能性胃肠病的现状

功能性胃肠病（functional gastrointestinal disorders,FGIDs）是消化内科常见的一组疾病.近年来诸多研究表明FGIDs患者存在明显的精神心理异常,其中焦虑抑郁情绪障碍尤为突出,改善精神心理状态的药物对FGIDs有一定的疗效.临床上广泛用抗抑郁药来治疗功能性胃肠病.本文就抗抑郁药治疗功能性胃肠病的有关文献作一概述.     

The canine gastrointestinal microbiota: early studies and research frontiers

ABSTRACT

The canine gut microbiota is a complex microbial population that is potentially related to metabolism, immunologic activity and gastrointestinal (GI) diseases. Early studies revealed that the canine gut microbiota was dynamic, and bacterial populations in the adjacent gut segments were similar, with anaerobes predominating. Metagenomics analysis revealed that nutrient contents in the diet modulated bacterial populations and metabolites in the canine gut. Further research revealed significant correlations between dietary factors and canine gut core microbiomes. Canine GI diseases are closely correlated with gut microbiota dysbiosis and metabolic disorders. Probiotic-related therapies can effectively treat canine GI diseases. Recent studies have revealed that the canine gut microbiota is similar to the human gut microbiota, and dietary factors affect both. Studying canine intestinal microorganisms enables clarifying changes in the canine intestinal bacteria under different conditions, simulating human diseases in dog models, and conducting in-depth studies of the interactions between intestinal bacteria and disease.     

脑肠互动与针刺治疗功能性胃肠病的相关性

功能性胃肠病是临床上常见的消化系统疾病,也是针刺治疗的优势病种.近年来的研究表明,脑肠轴功能失调是功能性胃肠病发病的重要原因,而针刺对脑肠轴的调节作用是其治疗功能性胃肠病的主要着眼点.随着脑功能成像技术的发展和脑肠肽研究的进展,功能性胃肠病与中枢神经系统及脑肠肽代谢相关性的研究日益增多.针灸作为传统中医疗法的一部分,治疗功能性胃肠病疗效显著,被广泛运用于临床.大量研究显示,针刺既能调节中枢神经系统,也能调控脑肠肽代谢.本文拟从中枢神经系统、脑肠肽代谢两方面,探讨脑肠互动与针刺治疗功能性胃肠病的相关性.     

功能性胃肠病的诊治进展

功能性胃肠病（FGIDs）是指具有腹胀、腹痛、腹泻、便秘等消化系统症状但无法以器质性病变或生化异常加以解释的一组疾病。该病极为常见,已成为当前重要公共卫生问题之一。本文结合第六届上海国际胃肠病学会议上有关专家关于功能性消化不良、慢性便秘和肠易激综合征的论述,对上述常见FGIDs的发病机制、诊断和治疗及其研究进展作一介绍。     

Effect of commensals and probiotics on visceral sensitivity and pain in irritable bowel syndrome

The last ten years’ wide progress in the gut microbiota phylogenetic and functional characterization has been made evidencing dysbiosis in several gastrointestinal diseases including inflammatory bowel diseases and irritable bowel syndrome (IBS). IBS is a functional gut disease with high prevalence and negative impact on patient’s quality of life characterized mainly by visceral pain and/or discomfort, representing a good paradigm of chronic gut hypersensitivity. The IBS features are strongly regulated by bidirectional gut-brain interactions and there is increasing evidence for the involvement of gut bacteria and/or their metabolites in these features, including visceral pain. Further, gut microbiota modulation by antibiotics or probiotics has been promising in IBS. Mechanistic data provided mainly by animal studies highlight that commensals or probiotics may exert a direct action through bacterial metabolites on sensitive nerve endings in the gut mucosa, or indirect pathways targeting the intestinal epithelial barrier, the mucosal and/or systemic immune activation, and subsequent neuronal sensitization and/or activation.