糖尿病不同阶段胃运动功能的临床研究

目的 了解在糖尿病（DM）不同阶段胃运动功能的变化及其血糖对胃运动的影响。方法 健康组（HS）20例,2型糖尿病组47例[包括无胃肠症状者12例,有胃肠症状和（或）DM并发症者35例]。采用核素法测定胃排空,并同时测空腹和餐后2h血糖,分析高血糖对胃排空的影响。结果 有胃肠症状或DM并发症患者120min近端胃存留率较健康组增加,全胃T1/2比健康组明显延长;无胃肠症状的DM患者120min近端胃存留率减少,近端胃排空速率明显增加。有胃肠症状DM患者远端胃放射性计数明显增加,食物在胃内分布异常;有胃肠症状DM患者血糖与胃排空指标之间无明显相关性;而无胃肠症状DM患者血糖与胃存留率呈负相关。结论 不同阶段糖尿病患者胃排空功能状态不同,早期胃排空正常或有近端胃排空加速,后期则以排空延迟为主要形式。食物在胃内分布异常是造成DM患者症状的原因之一。推测高血糖加速早期DM胃排空,而DM后期ENS及神经病变等占重要地位。     

胃电刺激治疗难治性胃轻瘫

胃轻瘫即运动障碍引起的胃排空延迟．可分为特发性胃轻瘫以及糖尿病、胃迷走神经切断术等所致继发性胃轻瘫。部分患者对促动力药、止吐剂、以及止痛和营养支持等治疗无效。为此，此研究观察胃电刺激(GES)对常规内科治疗无效的症状性胃轻瘫的疗效及安全性。     

糖尿病性胃病

糖尿病性胃病指糖尿病病人中一些胃肌肉-神经功能障碍(包括胃收缩性、张力和肌电活动的异常),并具有消化不良样的症状。胃排空试验、胃电图及超声等检查有助于诊断。治疗方面调整膳食和控制血糖颇为重要。胃动力增强剂有助于消除症状。     

糖尿病性胃病

糖尿病性胃病指糖尿病病人中一些胃肌肉－神经功能障碍（包括胃收缩性、张力和肌电活动的异常）,并具有消化不良样的症状。胃排空试验、胃电图及超声等检查有助于诊断。治疗方面调整膳食和控制血糖频为重要。胃动力增强剂有助于消除症状。     

糖尿病胃病的诊治进展

糖尿病胃病(DGP)不仅包含胃排空的延迟,还包括上消化道的症状,如腹胀、恶心等.目前它的发病机制不明确,治疗效果欠佳.治疗目的 主要在于加速胃排空,缓解消化道症状,改善血糖控制.最近有证据显示,多种药物及非药物的治疗方法有效,包括胃电针刺激、针灸等.现就DGP的诊治进展作一综述.     

胃电刺激治疗难治性胃轻瘫

胃轻瘫即运动障碍引起的胃排空延迟 ,可分为特发性胃轻瘫以及糖尿病、胃迷走神经切断术等所致继发性胃轻瘫。部分患者对促动力药、止吐剂、以及止痛和营养支持等治疗无效。为此 ,此研究观察胃电刺激 (GES)对常规内科治疗无效的症状性胃轻瘫的疗效及安全性。病人与方法 :病例入选标准 :①每周呕吐 7次以上 ;②胃排空延迟 ;③胃轻瘫症状持续 12月以上 ;④症状难以控制或不能耐受胆碱能激动剂、胃动素受体激动剂、多巴胺受体拮抗剂等 3种胃动力药中的 2种 ,以及抗组胺剂、5 -羟色胺受体拮抗剂、多巴胺受体拮抗剂等 3种止吐药中的 2种。剔除标…     

血糖变化对糖尿病大鼠胃排空功能与胃促生长素表达的影响

目的研究血糖变化对糖尿病大鼠胃排空功能与胃组织胃促生长素（ghrelin）表达的影响，探讨不同病期糖尿病胃排空延迟与胃促生长素表达的关系。方法60只Wistar大鼠随机分为正常对照组（NC组）、糖尿病组（DM组）和胰岛素干预组（INS组）。腹腔注射链脲佐菌素（sTz）制备糖尿病大鼠模型，分别于给药后1和4周用酚红灌胃法检测胃排空；用免疫组化、半定量RT-PCR技术检测大鼠胃组织胃促生长素及其mRNA表达。结果注射STZ1周后，DM组大鼠的胃排空率、胃促生长素积分吸光度及mRNA表达均明显低于NC组和INS组（P〈0．05）。注射STZ4周后，DM组与INS组大鼠的体质量、胃排空率、胃促生长素积分吸光度均明显低于NC组，而胃促生长素mRNA的表达则高于NC组；DM组与INS组之间差异无统计学意义（P〉0．05）。结论短期血糖升高可能通过抑制胃组织胃促生长素表达参与胃排空延迟的发生；而长期高血糖可能通过促进胃促生长素的表达和释放来增加摄食、维持能量平衡。     

糖尿病胃轻瘫的治疗进展

糖尿病胃轻瘫(DGP)是糖尿病常见的并发症,发生率达50%～76%,主要表现为胃排空延缓,临床可见厌食、恶心、早饱、呕吐、腹胀等症状,严重影响患者的生活质量和血糖的控制.目前DGP的发病机制尚未明确,可能与自主神经病变、精神心理因素等有关.DGP的治疗方法较多,包括基础治疗、血糖控制、药物治疗、营养支持、胃电起搏、手术及心理治疗等.本文就上述治疗方法在DGP治疗中的最新研究进展作一综述.     

糖尿病性胃轻瘫的胃动力异常机制

糖尿病性胃轻瘫（diabetic gastroparesis）是糖尿病患者常见的慢性消化道并发症，主要特点为胃动力下降，胃排空延迟．胃电节律紊乱，导致胃潴留。其常见症状包括早饱、恶心、腹胀、呕吐、食欲不振，也可仅有胃动力障碍而无明显症状。目前关于糖尿病性胃轻瘫胃动力学的研究正日益深入，本文就此作一简述。     

胃轻瘫发病机制研究进展

胃轻瘫综合征(简称胃轻瘫)是一种以胃排空延缓为特征的临床症状群.主要表现为早饱、餐后上腹饱胀、恶心、发作性干呕和呕吐等,而有关检查无胃输出道器质性梗阻病变的证据.在临床上十分常见,但其发病机制仍不清楚,可能与血糖浓度、胃肠道神经损害、幽门螺杆菌(HP)感染及胃肠运动不协调等有关.1 血糖作用有统计资料表明:在Ⅰ型和Ⅱ型糖尿病患者,大约50%存在胃液体或/和固体食物排空延迟.Ad-     

Nutrition therapy for diabetic gastroparesis

The management of diabetic gastroparesis often represents a significant clinical challenge in which the maintenance of nutrition is pivotal. Gastric emptying is delayed in 30% to 50% of patients with longstanding type 1 or type 2 diabetes and upper gastrointestinal symptoms also occur frequently. However, there is only a weak association between the presence of symptoms and delayed gastric emptying. Acute changes in blood glucose concentrations affect gastric motility in diabetes; hyperglycemia slows gastric emptying whereas hypoglycemia may accelerate it; blood glucose concentrations may also influence symptoms. It is now recognized that gastric emptying is a major determinant of postprandial glycemia and, therefore, there is considerable interest in the concept of modulating gastric emptying, by dietary or pharmacologic means, to optimize glycemic control in diabetes.     

Gastric emptying in diabetes mellitus: relationship to blood-glucose control.

The application of novel investigative techniques has established that disordered gastric motility is a frequent complication of diabetes mellitus. Thus, gastric emptying of solid or nutrient liquid meals is abnormal in 30% to 50% of randomly selected outpatients with long-standing type 1 or type 2 diabetes. Delayed gastric emptying occurs more frequently than rapid emptying. There is increasing evidence that disordered gastric motility has a major impact on the management of patients with diabetes mellitus by leading to gastrointestinal symptoms and poor glycemic control. Although both gastroparesis and upper gastrointestinal symptoms have been attributed to irreversible autonomic damage, it is now clear that acute changes in the blood-glucose concentration have a major effect on both gastrointestinal motor function and the perception of sensations arising in the gut. For example, there is an inverse relationship between the rate of gastric emptying and the blood-glucose concentration, so that gastric emptying is slower during hyperglycemia and accelerated during hypoglycemia. This article reviews some issues in the etiology, diagnosis, and management of problems associated with gastric emptying in elderly persons with diabetes mellitus.     

Are gastrointestinal symptoms related to diabetes mellitus and glycemic control?

Many patients with diabetes mellitus suffer from upper and lower GI symptoms. The reported prevalence of these symptoms varies among different ethnic groups/populations. The natural history of GI symptoms as well as their pathogenesis in patients with diabetes remains poorly understood, although it is known that gastric emptying is influenced by hyperglycemia, euglycemia, and hypoglycemia. Poor glycemic control over a long period of time can lead to neuropathy and damage the vagus nerve, resulting in diabetic gastroparesis whose signs and symptoms vary in the individual patient. Gastroparesis can further worsen glycemic control by adversely altering the pharmacokinetics of orally administered hypoglycemic agents as well as by altering the delivery of diet-derived calories to intestines from which absorption, subsequently, determines incipient blood glucose, and thus effectiveness of various injectable antidiabetics including various insulins and related insulin analogs. As GI symptoms may overlap with other disorders, including functional dyspepsia, irritable bowel syndrome, and depression, it is important to have such patients/patients with diabetes undergo standardized testing for measuring gastric emptying. Certain medications including metformin, amylin analogues (i.e. pramlintide), glucagon-like peptide 1 analogs (i.e. exenatide, liraglutide), anticholinergic agents, antidepressants, calcium-channel blockers, and others may contribute to GI symptoms observed in patients with diabetes. Given the global diabetes pandemic, it is of utmost importance to not only diagnose and treat present patients with diabetes mellitus and its comorbidities, but also to help prevent the development of further disease burden by educating children and adolescents about healthy lifestyle modifications (avoidance of overeating, portion control, healthy food choices, increased physical and reduced sedentary activity), as changing behavior in adulthood has proven to be notoriously difficult.     

Measurement of gastric emptying in diabetes

There has been a substantial evolution of concepts related to disordered gastric emptying in diabetes. While the traditional focus has hitherto related to the pathophysiology and management of upper gastrointestinal symptoms associated with gastroparesis, it is now apparent that the rate of gastric emptying is central to the regulation of postprandial glycemia. This recognition has stimulated the development of dietary and pharmacologic approaches to optimize glycemic control, at least in part, by slowing gastric emptying. With the increased clinical interest in this area, it has proved necessary to expand the traditional indications for gastric emptying studies, and consider the relative strengths and limitations of available techniques. Scintigraphy remains the ‘gold standard’ for the measurement of gastric emptying, however, there is a lack of standardization of the technique, and the optimal test meal for the evaluation of gastrointestinal symptoms may be discordant from that which is optimal to assess impaired glycemic control. The stable isotope breath test provides an alternative to scintigraphy and can be performed in an office-based setting.The effect of glucagon-like peptide-1 (GLP-1) and its agonists to reduce postprandial glycemia is dependent on the baseline rate of gastric emptying, as well as the magnitude of slowing. Because the effect of exogenous GLP-1 to slow gastric emptying is subject to tachyphylaxis with sustained receptor exposure, ‘short acting’ or ‘prandial’ GLP-1 agonists primarily target postprandial glycemia through slowing of gastric emptying, while ‘long acting’ or ‘non-prandial’ agents lower fasting glucose primarily through insulinotropic and glucagonostatic mechanisms. Accordingly, the indications for the therapeutic use of these different agents are likely to vary according to baseline gastric emptying rate and glycemic profiles.     

Disordered gastric motor function in diabetes mellitus

Summary The application of novel investigative techniques has demonstrated that disordered gastric motility occurs frequently in diabetes mellitus. Gastric emptying is abnormal in about 50% of diabetic patients and delay in gastric emptying of nutrient-containing meals is more common than rapid emptying. The blood glucose concentration influences gastric motility in diabetes. In IDDM patients, gastric emptying is retarded during hyperglycaemia and may be accelerated by hypoglycaemia. Gastroparesis therefore does not necessarily reflect irreversible autonomic neuropathy and blood glucose concentrations must be monitored when gastric motility is evaluated in diabetic patients. There is a poor relationship between gastric emptying and gastrointestinal symptoms and the mechanisms by which abnormal motility causes symptoms are unclear. The introduction of new gastrokinetic drugs has improved therapeutic options for the management of symptomatic patients with gastroparesis considerably. The contribution of disordered gastric emptying to poor glycaemic control is unclear, but the demonstration that the rate of gastric emptying is a major factor in normal blood glucose homeostasis suggests that this is likely to be significant.Abbreviations IDDM insulin-dependent diabetes mellitus - NIDDM non-insulin-dependent diabetes mellitus     

Gastrointestinal motility disorders in patients with diabetes mellitus

Abstract. Disturbed gastric and small intestinal motility is an often overlooked clinical problem. Delayed gastric emptying of liquid and/or solid food in patients with type 1 and type 2 diabetes (gastroparesis diabeticorum) occurs in approximately 50% of the patients. Also, the interdigestive gastric and small intestinal motility is often affected. There is only a weak correlation between symptoms and objectively measurable motor disturbances. Patients with severe upper gastrointestinal symptoms usually have disturbed motility, but most patients with impaired motility are asymptomatic. Recent studies have clearly shown that, in addition to autonomic neuropathy, acute metabolic derangements are likely to contribute to disturbed motility. Elevated glucose levels impair gastric and small intestinal motility during fasting and after food intake. Hyperinsulinemia per se has effects similar to hyperglycaemia on the stomach and small bowel, and may be a mediator of the effects of hyperglycaemia in healthy subjects. The impact of insulin on motility in diabetic patients is still unclear. Treatment of the gastric motility disorder should include a stabilization of gastric emptying. Different therapeutic modes may be useful, e.g. application of prokinetic drugs and optimizing the metabolic situation.     

Botulinum toxin for the treatment of gastroparesis: a preliminary report

Gastroparesis is a disorder of gastric motility that results in delayed gastric emptying. Common symptoms include early satiety, postprandial fullness, epigastric pain, nausea, vomiting, and weight loss. The underlying etiologies of gastroparesis are many and include diabetes, prior gastric surgery, collagen vascular disorders, and a previous viral illness. Up to one third of cases are classified as idiopathic. Treatment typically consists of a change in diet to small volume, frequent meals and the use of the prokinetic agents metoclopramide, cisapride, erythromycin, or domperidone. Botulinum toxin has recently been shown to be effective in treating disorders of smooth muscle hypertonicity in the GI tract. This case report describes three patients with severe gastroparesis whose symptoms persisted despite dietary changes and the use of high dose prokinetic agents. All three were treated with intrasphincteric injection of the pylorus with botulinum toxin and all had significant symptomatic improvement afterwards. Possible mechanisms of action of botulinum toxin on the pylorus and its effects in patients with gastroparesis are discussed.     

胃电图在功能性消化不良患者中的临床应用

功能性消化不良是消化道常见症候群,严重影响患者的生活质量,是21世纪国内外学者研究的热点之一.多数学者认为胃运动障碍可能是功能性消化不良的主要病理生理机制之一,目前胃运动功能的检测手段主要有胃电图、胃排空等,本文对功能性消化不良与胃电图及胃排空之间的关系进行了综述.     

Prevalence and determinants of delayed gastric emptying in hospitalised Type 2 diabetic patients

AIM： To determine the prevalence of delayed gastric emptying （GE） in older patients with Type 2 diabetes mellitus. METHODS： One hundred and forty seven patients with Type 2 diabetes, of whom 140 had been hospitalised, mean age 62.3 ± 8.0 years, HbA1c 9.1% ± 1.9%, treated with either oral hypoglycemic drugs or insulin were studied. GE of a solid meal （scintigraphy）, autonomic nerve function, upper gastrointestinal symptoms, acute and chronic glycemic control were evaluated. Gastric emptying results were compared to a control range of hospitalised patients who did not have diabetes. RESULTS： Gastric emptying was delayed （T50 〉 85 min） in 17.7% patients. Mean gastric emptying was slower in females （T50 72.1 ± 72.1 min vs 56.9 ± 68.1 min, P = 0.02） and in those reporting nausea （112.3 ± 67.3 vs 62.7 ± 70.0 min, P 〈 0.01） and early satiety （114.0 ± 135.2 vs 61.1 ± 62.6 min, P = 0.02）. There was no correlation between GE with age, body weight, duration of diabetes, neuropathy, current glycemia or the total score for upper gastrointestinal symptoms. CONCLUSION： Prolonged GE occurs in about 20% of hospitalised elderly patients with Type 2 diabetes when compared to hospitalised patients who do not have diabetes. Female gender, nausea and early satiety areassociated with higher probability of delayed GE.     

Diagnostic and therapeutic approach to patients with gastroparesis

Gastroparesis is a chronic alteration of gastric motility characterized by symptoms suggestive of mechanical obstruction and delayed gastric emptying in the absence of obstruction. Gastroparesis can be idiopathic or attributable to neuropathy or myopathy as in diabetes mellitus and scleroderma or can occur after vagotomy. Diagnosis is based on symptoms (nausea, vomiting, abdominal distension and early satiety), physical examination (capotement) and on complementary investigations, the procedure of choice being isotope gastric emptying tests. Treatment depends on the clinical repercussions. In most patients, gastroparesis can be controlled by prokinetic drugs, dietary measures, exclusion of drugs that alter gastric emptying, and exhaustive control of blood glucose levels. In patients with severe gastroparesis, hospital nutritional measures (intravenous and/or enteral), gastric decompression and intravenous antiemetic and prokinetic agents are required. Aggressive nutritional therapies (parenteral or enteral nasojejunal nutrition), intrapyloric injection of botulinum toxin, implantation of a gastric stimulation device, or gastrectomy should only be used in patients unresponsive to conservative treatment or if there is selective alteration of gastric motility.