针灸对比胃肠促动力药治疗功能性消化不良的Meta分析

[目的]系统评价针灸对比胃肠促动力药治疗功能性消化不良(FD)的疗效。[方法]通过检索中国知网(CNKI)、中国生物医学文献数据库(CBM)、PubMed、EMBASE、Cochrane Library等数据库,查找有关针灸对比胃肠促动力药治疗FD的随机对照试验,采用Jadad量表行质量评价,应用RevMan5.3软件行Meta分析。[结果]共16个研究包括1 088例FD患者纳入分析。针灸治疗FD的总有效率显著高于胃肠促动力药(RR=1.18,95%CI=1.11~1.24,P<0.00001)。各项研究均未报道严重不良反应。[结论]针灸用于治疗FD效果优于胃肠促动力药,且安全性较高。由于纳入研究的质量偏低和潜在偏倚,需要高质量、大样本的研究进一步验证结果。     

六味安消胶囊对比胃肠促动力药治疗功能性消化不良的Meta分析

目的系统评价六味安消胶囊对比胃肠促动力药治疗功能性消化不良(functional dyspepsia,FD)的疗效。方法通过中国知网(CNKI)、中国生物医学文献数据库(CBM)、Pub Med、EMBASE、Cochrane Library等数据库,检索有关六味安消胶囊对比胃肠促动力药治疗FD的随机对照试验,采用Jadad量表进行质量评价,应用Rev Man 5.3软件行Meta分析。结果共11个研究包括1 183例FD患者纳入研究。六味安消胶囊治疗FD的总有效率显著高于胃肠促动力药(RR=1.09,95%CI:1.04~1.14,P=0.0006)。各项研究均未报道严重不良反应。结论六味安消胶囊用于治疗FD效果优于胃肠促动力药,且安全性较高。     

健胃促导汤治疗功能性消化不良的临床研究

功能性消化不良(FD)和非溃疡性消化不良(NUD)同义。91年伦敦国际专业会议,有主张称FD较NUD为妥。本病症很常见,目前疗法仍有限,多认为胃肠促动力药较优。中医治疗消化不良有丰富的经验,有多种中药有促胃肠蠕动作用。本文旨在探索发挥中药优势,以传     

促胃肠动力药的作用机制及临床应用研究进展

促胃肠动力药包括很多种类,这类药物有着不同的化学结构及作用机制,对从食管到结肠的胃肠道的不同部位有着不同程度的促动力作用．同时,这类药物对胆道系统的影响也逐渐受到研究者的关注．这类药物对胃肠道及胆道作用机制的研究包括:胆碱能机制、肾上腺能机制、抗多巴胺和抗胆碱脂酶机制、神经体液机制等．促胃肠动力药临床上广泛应用于慢性胃炎、反流性食管炎(GERD)、胃瘫、功能性消化不良(FD)等疾病的治疗．     

健胃促导汤治疗功能性消化不良的临床研究

功能性消化不良(FD)和非溃疡性消化不良(NUD)同义。91年伦敦国际专业会议，有主张称FD较NUD为妥。本病症很常见，目前疗法仍有限，多认为胃肠促动力药较优。中医治疗消化不良有丰富的经验，有多种中药有促胃肠蠕动作用。本旨在探索发挥中药优势，以传统的中医治则完善现代“促动”疗法，提高疗效。     

联用帕罗西汀治疗功能性消化不良36例疗效观察

目的观察联用帕罗西汀治疗功能性消化不良（FD）的临床疗效。方法将门诊72例FD患者随机分成治疗组36例和对照组36例,对照组根据个体化原则给予促动力药和（或）心受体阻滞剂或质子泵抑制剂,治疗组在上述基础上加用帕罗西汀口服治疗。结果治疗组显效26例,有效12例,总有效率为91．7％。对照组显效12例,有效14例,总有效率为72．2％。治疗组与对照组比较疗效差异有统计学意义（P〈0．05）。结论联用帕罗西汀可显著提高治疗功能性消化不良的疗效,不良反应少。值得临床推广。     

促动力药治疗胃食管反流病的循证评价和进展

胃食管反流病（GERD）系胃内容物反流人食管,引起不适症状和（或）并发症的一种疾病,食管下括约肌（LES）功能障碍和胃排空延迟引起胃内容物反流是GERD的主要发病机制。促动力药可通过改善胃食管动力治疗GERD,主要包括多巴眩受体拮抗剂、5-羟色胺（5-HT）。受体激动剂、1-氨基丁酸B型（GABAB）受体激动剂、5型代谢型谷氨酸受体（mGluR5）、选择性胆囊收缩素（CCK）-A受体拮抗剂、胃动素和5-HB部分激动剂。本文就促动力药治疗GERD的循证评价和进展作一慨述.     

养胃定痛汤治疗小儿功能性消化不良疗效观察

目的：观察养胃定痛汤治疗小儿功能性消化不良（FD）的临床疗效。方法：自拟中药养胃定痛汤治疗小儿FD（治疗组）56例,并与用促胃动力药吗丁啉治疗（对照组）50例进行疗效对比。结果：临床疗效,治疗组总有效率为98．21％,对照组78．00％,两组比较差异有显著性意义（P＜0．01）。治疗级对消除腹胀、腹痛,纠正厌食症状的时间均明显短于对照组（P＜0．01）,其中以腹痛消失最明显。临床观察中未发现有明显的不良反应。结论：该方治疗小儿FD较单一胃动力药优越。     

西沙必利治疗功能性消化不良的临床观察

功能性消化不良(FD)是一种常见的症候群,占消化疾病患者的20—40%,在治疗上仍较棘手且意见不一,胃肠促动力药的应用是近年来研究的热门课题。笔者于1995年11月至1996年12月对188例 FD 的病人随机分为两组,分别用西沙必利及吗丁啉治疗,现将资料总结如下。     

功能性消化不良血浆胃动素及体表胃电图临床研究

目的研究血浆胃动素浓度及体表胃电图与功能性消化不良的关系并探讨功能性消化不良的病因．方法功能性消化不良患者及健康志愿者各30例病例组按国际诊断标准选择[1]，并分为动力障碍样型、溃疡样型、反流样型及复合型．对所有受检者空腹、餐后血浆胃动素浓度及同步体表胃电图进行综合分析，并对10例动力障碍样型患者服用促动力药后随访．结果①对30例FD患者分型，动力障碍样型患者空腹血浆MTL水平明显低于对照组（P＜0．01）．②30例FD患者空腹、餐后胃电节律紊乱率均明显高于对照组（P＜0．001）；其餐后胃电振幅较空腹时无明显增加且仍低于对照组（P＜0．01）．结论血浆胃动素浓度异常及胃电活动异常与功能性消化不良关系密切     

Recent insights into digestive motility in functional dyspepsia

Functional gastrointestinal disorders, such as functional dyspepsia (FD) and irritable bowel syndrome, are common pathologies of the gut. FD is a clinical syndrome defined as chronic or recurrent pain or discomfort of unknown origin in the upper abdomen. The pathophysiological mechanisms responsible for FD have not been fully elucidated, but new ideas regarding its pathophysiology and the significance of the pathophysiology with respect to the symptom pattern of FD have emerged. In particular, there is growing interest in alterations in gastric motility, such as accommodation to a meal or gastric emptying, and visceral sensation in FD. The mechanisms underlying impaired gastroduodenal motor function are unclear, but possible factors include abnormal neurohormonal function, autonomic dysfunction, visceral hypersensitivity to acid or mechanical distention, Helicobacter pylori infection, acute gastrointestinal infection, psychosocial comorbidity, and stress. Although the optimum treatment for FD is not yet clearly established, acid-suppressive drugs, prokinetic agents, eradication of H. pylori, and antidepressants have been widely used in the management of patients with FD. The therapeutic efficacy of prokinetics such as itopride hydrochloride and mosapride citrate in the treatment of FD is supported by the results of relatively large and well-controlled studies. In addition, recent research has yielded new therapeutic agents and modalities for dysmotility in FD, including agonists/antagonists of various sensorimotor receptors, activation of the nitrergic pathway, kampo medicine, acupuncture, and gastric electric stimulation. This review discusses recent research on the pathophysiology of and treatment options for FD, with special attention given to digestive dysmotility.     

Ghrelin: a gut hormonal basis of motility regulation and functional dyspepsia

Functional dyspepsia (FD) is a functional gastrointestinal disorder (FGID). Several pathophysiological mechanisms have been indicated as possible etiological factors, such as delayed gastric emptying, impaired proximal gastric accommodation and visceral hypersensitivity. Ghrelin is an important gut hormone. It is a motilin-related peptide that was discovered in the stomach, and it acts as an endogenous ligand of growth hormone secretagogue receptor. Ghrelin plays an important role in the stimulation of food intake and gut motility. Acyl ghrelin stimulates the percentage motor index (%MI) in the antrum and induces fasted motor activity in the duodenum. Des-acyl ghrelin decreases food intake and decrease gastric emptying. Although some studies have demonstrated that plasma acyl ghrelin levels tend to be lower in FD patients than in controls, the association between plasma ghrelin levels and FD remains controversial. Previous reports have demonstrated that hunger sensation was elevated through the administration of ghrelin to patients with FD. However, there have been few clinical reports relating to the administration of ghrelin. Altered gut-brain interactions may underlie the symptoms of FD. Ghrelin may be associated with FD through its effect on the regulation of gut motility. Further studies are needed to examine the effects of ghrelin in FD.     

Treatment of functional dyspepsia

Opinion statement Functional dyspepsia (FD) is a common reason a patient presents with upper gastrointestinal symptoms for medical care. Although treatment of FD remains expensive, the agents are rarely used in a systematic manner; the majority of treatments are empirical and the results short lived once therapy is ceased. This is partly due to the lack of consistent pathophysiologic markers in FD, so therapy is symptom driven. This review appraises the best evidence on available interventions. A structured scheme for deciding on appropriate therapies is to consider the possible putative pathophysiologic mechanisms. Eradicating Helicobacter pylori, if present, is a first-line strategy. In patients who have symptoms suggesting excessive gastric acid secretion, particularly epigastric pain, antisecretory agents are recommended. Prokinetics may confer benefits on symptoms suggestive of upper gastrointestinal dysmotility, like fullness or early satiety. However, their use is limited due to availability issues. The expanding field of psychologic therapies provides a promising avenue of treatment. Complementary medicines are now widely use and their benefits have been suggested in recent controlled trials. Emerging treatments include cholecystokinin 1 blockers, opioid receptor agonists, and serotonergic agents, although their application in FD is in the preliminary stages.     

Practical management approach to gastroparesis

Gastroparesis is a syndrome characterised by delayed gastric emptying in the absence of mechanical obstruction. Symptoms can include early satiety, abdominal pain, bloating, vomiting and regurgitation which cause significant morbidity in addition to nutritional deficits. There is a higher prevalence in diabetics and females, but the incidence in the Australian population has not been well studied. Management of gastroparesis involves investigating and correcting nutritional deficits, optimising glycaemic control and improving gastrointestinal motility. Symptom control in gastroparesis can be challenging. Nutritional deficits should be addressed initially through dietary modification. Enteral feeding is a second‐line option when oral intake is insufficient. Home parenteral nutrition is rarely used, and only accessible through specialised clinics in the outpatient setting. Prokinetic medication classes that have been used include dopamine receptor antagonists, motilin receptor agonists, 5‐HT₄ receptor agonists and ghrelin receptor agonists. Anti‐emetic agents are often used for symptom control. Interventional treatments include gastric electrical stimulation, gastric per‐oral endoscopic myotomy, feeding jejunostomy and gastrostomy/jejunstomy for gastric venting and enteral feeding. In this article we propose a framework to manage gastroparesis in Australia based on current evidence and available therapies.     

Cannabinoids and the gastrointestinal tract

The enteric nervous system of several species, including the mouse, rat, guinea pig and humans, contains cannabinoid CB1 receptors that depress gastrointestinal motility, mainly by inhibiting ongoing contractile transmitter release. Signs of this depressant effect are, in the whole organism, delayed gastric emptying and inhibition of the transit of non-absorbable markers through the small intestine and, in isolated strips of ileal tissue, inhibition of evoked acetylcholine release, peristalsis, and cholinergic and non-adrenergic non-cholinergic (NANC) contractions of longitudinal or circular smooth muscle. These are contractions evoked electrically or by agents that are thought to stimulate contractile transmitter release either in tissue taken from morphine pretreated animals (naloxone) or in unpretreated tissue (gamma-aminobutyric acid and 5-hydroxytryptamine). The inhibitory effects of cannabinoid receptor agonists on gastric emptying and intestinal transit are mediated to some extent by CB1 receptors in the brain as well as by enteric CB1 receptors. Gastric acid secretion is also inhibited in response to CB1 receptor activation, although the detailed underlying mechanism has yet to be elucidated. Cannabinoid receptor agonists delay gastric emptying in humans as well as in rodents and probably also inhibit human gastric acid secretion. Cannabinoid pretreatment induces tolerance to the inhibitory effects of cannabinoid receptor agonists on gastrointestinal motility. Findings that the CB1 selective antagonist/inverse agonist SR141716A produces in vivo and in vitro signs of increased motility of rodent small intestine probably reflect the presence in the enteric nervous system of a population of CB1 receptors that are precoupled to their effector mechanisms. SR141716A has been reported not to behave in this manner in the myenteric plexus-longitudinal muscle preparation (MPLM) of human ileum unless this has first been rendered cannabinoid tolerant. Nor has it been found to induce "withdrawal" contractions in cannabinoid tolerant guinea pig ileal MPLM. Further research is required to investigate the role both of endogenous cannabinoid receptor agonists and of non-CB1 cannabinoid receptors in the gastrointestinal tract. The extent to which the effects on gastrointestinal function of cannabinoid receptor agonists or antagonists/inverse agonists can be exploited therapeutically has yet to be investigated as has the extent to which these drugs can provoke unwanted effects in the gastrointestinal tract when used for other therapeutic purposes.     

ghrelin与功能性消化不良

功能性消化不良（FD）患者尽管未发现胃肠道器质性病变,但是研究提示FD可能存在胃动力、胃排空、胃十二指肠神经调节或内脏敏感性等胃肠道功能的改变。ghrelin作为主要由胃X／A样细胞产生的一种多肽,影响胃的动力、排空和分泌功能。最近的研究表明血清中的ghrelin水平与FD有一定的关系,提示其可能在FD的发病机制中起一定的作用,值得深入的研究。     

Real-time assessment of gastroduodenal motility by ultrasonography

Functional dyspepsia (FD) is a clinical syndrome involving upper abdominal symptoms, the causes of which cannot be identified by conventional diagnostic evaluation. Many pathophysiological factors, such as gastric acid, gastroduodenal motility, gastric accommodation, sensory disturbance, stress and Helicobacter pylori infection, may play a role in the pathogenesis of FD. Dysmotility of the upper gastrointestinal tract has been implicated in the symptoms of FD. In previous studies, antral hypomotility and delayed gastric emptying have been reported as major pathogenetic factors in patients with FD. Although a number of methods have been applied to evaluate gastroduodenal motility in humans, many of them have technical limitations and are too expensive or complex to use in daily clinical practice. Recent technical developments enable one to evaluate gastroduodenal motility by using ultrasonography. Ultrasonography is a simple, noninvasive modality for the assessment of gastric emptying and antral motility in either a liquid or solid meal, along with the examination of duodenogastric reflux.     

FD患者胃十二指肠运动功能的研究

目的通过胃窦十二指肠压力测定，研究功能性消化不良（ＦＤ）患者胃十二指肠的运动功能．方法ＦＤ患者２８例，健康人１３例．采用导管灌注技术测定胃窦和十二指肠的腔内压，消化间期测压３５ｈ，餐后测压１５ｈ．结果在消化间期，２８例ＦＤ中１３例未出现移行运动复合波（ＭＭＣ）３期，１３例健康人１例未出现ＭＭＣ３期，两者相比有显著性差异（Ｐ＜００５）；ＭＭＣ２期和３期收缩的平均频率、平均强度和动力指数，在ＦＤ患者和健康人间相比无差异（Ｐ＞００５）．ＦＤ患者餐后胃窦收缩的频率、强度和动力指数均低于健康对照组（Ｐ＜００５）．结论ＦＤ患者消化间期缺乏ＭＭＣ３期或ＭＭＣ３期延迟出现，餐后胃窦动力减低．     

FD患者红霉素对胃十二指肠动力的影响

目的研究红霉素对功能性消化不良（ＦＤ）患者消化间期胃窦和十二指肠的运动功能的影响．方法ＦＤ患者２０例，采用导管灌注技术测定胃窦和十二指肠的压力，空腹连续测定３５ｈ，若未发现移行运动复合波（ＭＭＣ）３期，于ＭＭＣ１期匀速静滴红霉素２００ｍｇ，滴速６６ｍｇ／ｍｉｎ，测定静滴红霉素期间胃窦和十二指肠的压力．结果空腹测定３５ｈ，８例ＦＤ未出现ＭＭＣ３期，仅１期和２期交替出现，此后在静滴红霉素期间，胃窦和十二指肠均出现了宽大的收缩波，５例出现了ＭＭＣ３期，且各项动力参数值较静滴红霉素前显著增加（Ｐ＜００５）．结论部分ＦＤ于消化间期胃窦和十二指肠缺乏ＭＭＣ３期，动力减低，静滴红霉素能诱发ＭＭＣ３期，促进胃和十二指肠的运动功能     

Dyspepsia: organic versus functional

Dyspepsia is the medical term for difficult digestion. It consists of various symptoms in the upper abdomen, such as fullness, discomfort, early satiation, bloating, heartburn, belching, nausea, vomiting, or pain. The prevalence of dyspepsia in the western world is approximately 20% to 25%. Dyspepsia can be divided into 2 main categories: "organic" and "functional dyspepsia" (FD). Organic causes of dyspepsia are peptic ulcer, gastroesophageal reflux disease, gastric or esophageal cancer, pancreatic or biliary disorders, intolerance to food or drugs, and other infectious or systemic diseases. Pathophysiological mechanisms underlying FD are delayed gastric emptying, impaired gastric accommodation to a meal, hypersensitivity to gastric distension, altered duodenal sensitivity to lipids or acids, altered antroduodenojenunal motility and gastric electrical rhythm, unsuppressed postprandial phasic contractility in the proximal stomach, and autonomic nervous system-central nervous system dysregulation. Pathogenetic factors in FD are genetic predisposition, infection from Helicobacter pylori or other organisms, inflammation, and psychosocial factors. Diagnostic evaluation of dyspepsia includes upper gastrointestinal endoscopy, abdominal ultrasonography, gastric emptying testing (scintigraphy, breath test, ultrasonography, or magnetic resonance imaging), and gastric accommodation evaluation (magnetic resonance imaging, ultrasound, single-photon emission computed tomography, and barostat). Antroduodenal manometry can be used for the assessment of the myoelectrical activity of the stomach, whereas sensory function can be evaluated with the barostat, tensostat, and satiety test. Management of FD includes general measures, acid-suppressive drugs, eradication of H. pylori, prokinetic agents, fundus-relaxing drugs, antidepressants, and psychological interventions. This review presents an update on the diagnosis of patients presenting with dyspepsia, with an emphasis on the pathophysiological and pathogenetic mechanisms of FD and the differential diagnosis with organic causes of dyspepsia. The management of uninvestigated and FD, as well as the established and new pharmaceutical agents, is also discussed.