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The pathophysiology, diagnosis, and treatment of diabetic gastroparesis are reviewed, and the mechanisms of action, pharmacokinetics, clinical efficacy, adverse effects, and dosage of metoclopramide, domperidone, and cisapride are described. Diabetic gastroparesis is a state of delayed gastric emptying that reportedly affects 20-30% of diabetic patients. Symptoms include nausea, early satiety, postprandial bloating and fullness, and vomiting. Diabetic gastroparesis has been managed most successfully with drugs that stimulate gastric emptying. Of the three agents studied--metoclopramide, domperidone, and cisapride--only metoclopramide is commercially available in the United States. The clinical efficacy of metoclopramide, domperidone, and cisapride has been well documented in several placebo-controlled trials. Metoclopramide effectively decreases mean gastric emptying time, although tolerance to this stimulation of gastric emptying may develop with long-term therapy. However, symptomatic relief persists with long-term therapy because of metoclopramide's antiemetic properties. Domperidone, which has also been shown to stimulate gastric motility and to possess antiemetic properties, improves symptoms in patients suffering from diabetic gastroparesis. Cisapride appears to have continued beneficial effects on gastric motility with long-term therapy. All three agents have favorable adverse-effect profiles. Although metoclopramide is currently the first-line agent for the management of gastroparesis, domperidone and cisapride both possess properties that may make them useful alternatives in patients who are unresponsive to or cannot tolerate metoclopramide therapy.
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PMID:Use of metoclopramide, domperidone, and cisapride in the management of diabetic gastroparesis. 219 Jul 45

About one-half of patients with insulin- or non-insulin-dependent diabetes have delayed gastric emptying (diabetic gastroparesis). Some of them complain of epigastric pain, nausea, vomiting or postprandial fullness (diabetic dyspepsia), although only a minority are severely symptomatic. Diabetic gastroparesis is clinically relevant not only by virtue of the symptoms induced but also because it may contribute to inadequate glycaemic control and impaired absorption of orally administered drugs. Recent data suggest that abnormal blood glucose control, not only autonomic neuropathy, contribute to the pathogenesis of disordered gastric motility. In most cases diabetic gastroparesis is diagnosed clinically in the absence of demonstrable lesions of the upper gastrointestinal tract. To evaluate gastric emptying, scintigraphy is the 'gold standard'. Gastrokinetic drugs are of help in the treatment of gastroparesis: erythromycin is the first choice in acute presentations and cisapride for chronic symptoms. New macrolides with prokinetic action and devoid of antibacterial properties are very promising and should add another pharmacologic approach to control dyspepsia and gastroparesis in diabetic patients in the future.
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PMID:Gastroparesis and dyspepsia in patients with diabetes mellitus. 749 57

A woman aged 26 with long-standing insulin-dependent diabetes mellitus displayed recurrent periods of nausea, vomiting, abnormal blood sugar levels, weight loss and poor physical condition in spite of a diet and use of propulsive agents. Scintigraphy revealed decelerated gastric evacuation for solid and liquid nutrients. The patient recovered after insertion of a percutaneous endoscopic gastrostomy (PEG) catheter. Diabetic gastroparesis is associated with a vicious circle in which delayed gastric emptying leads to poor glucose regulation with frequent hyperglycaemia, which in its turn adversely affects gastric emptying. Treatment should be aimed at improvement of the gastric motility (for instance by propulsive agents), more accurate glucose regulation and nutritional counselling. If this fails to produce improvement, tube feeding via a permanent nasoduodenal tube or via a PEG catheter constitutes an acceptable alternative for oral nutrition.
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PMID:[Diabetic gastroparesis: is tube feeding an alternative?]. 955 25

Diabetic gastroparesis is a common and debilitating condition affecting millions of patients with diabetes mellitus worldwide. Although gastroparesis in diabetes has been known clinically for more than 50 years, treatment options remain very limited. Until recently, the scientific literature has offered few clues regarding the precise aetiology of gastric dysfunction in diabetes.Up to 50% of patients with diabetes may experience postprandial abdominal pain, nausea, vomiting and bloating secondary to gastric dysfunction. There is no clear association between length of disease and the onset of delayed gastric emptying. Gastroparesis affects both type 1 (insulin dependent) and type 2 (non- insulin dependent) forms of diabetes. Diagnosis requires identifying the proper symptom complex, while excluding other entities (peptic ulcer disease, rheumatological diseases, medication effects). The diagnosis of gastroparesis may be confirmed by demonstrating gastric emptying delay during a 4-hour scintigraphic study. Treatment options are limited and rely on dietary modifications, judicious use of available pharmacological agents, and occasionally surgical or endoscopic placement of gastrostomies or jejunostomies. Gastric pacing offers promise for patients with medically refractory gastroparesis but awaits further investigation. Current pharmacological agents for treating gastroparesis include metoclopramide, erythromycin, cisapride (only available via a company-sponsored programme) and domperidone (not US FDA approved). All of these drugs act as promotility agents that increase the number or the intensity of gastric contractions. These medications are not uniformly effective and all have adverse effects that limit their use. Cisapride has been removed from the open market as a result of over 200 reported cases of cardiac toxicity attributed to its use. Unfortunately, there is a paucity of clinical studies that clearly define the efficacy of these agents in diabetic gastroparesis and there are no studies that compare these drugs to each other. The molecular pathophysiology of diabetic gastroparesis is unknown, limiting the development of rational therapies. New studies, primarily in animals, point to a defect in the enteric nervous system as a major molecular cause of abnormal gastric motility in diabetes. This defect is characterised by a loss of nitric oxide signals from nerves to muscles in the gut resulting in delayed gastric emptying. Novel therapies designed to augment nitric oxide signalling are being studied.
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PMID:Current concepts in diabetic gastroparesis. 1282 60

Diabetic gastroparesis is a long term complication of diabetes mellitus which could basically be defined as dysregulated gastric emptying leading to various pathological, biochemical and clinical changes in absence of any structural changes. Symptoms include nausea, vomiting, bloating, epigastric pain, anorexia, weight loss and so on. For symptomatic gastroparesis prokinetic drugs like metoclopramide, domperidone, cisapride, erythromycin and itcopride are used. Itopride is currently emerging as a prokinetic drug of choice. There is also scope of surgery.
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PMID:Management of diabetic gastroparesis. 1617 96

This review addresses the current concepts in our understanding of the epidemiology, mechanisms, symptoms, clinical consequences, diagnosis and treatment of delayed gastric emptying in patients with diabetes. Upper gastrointestinal symptoms, particularly postprandial fullness, nausea, vomiting and abdominal bloating, occur in 30-50% of patients with diabetes. The use of scintigraphic techniques, and more recently breath test, has shown that as many as 50% of diabetic patients have gastroparesis. Diabetic gastroparesis comprises a decrease in fundic and antral motor activity, a reduction or a lack of the interdigestive migrating motor complex, gastric dysrhythmias, and pylorospasms. The mechanisms involved include: autonomic neuropathy, acute hyperglycaemia, and abnormalities in gastrointestinal hormones and neuropeptides. Other possible contributing factors such as hypothyroidism and H. pylori infection are discussed as well. Because treatment is possible by means of dietary advise, prokinetics or surgical procedures, it is important to identify risk factors for and to diagnose gastroparesis to prevent morbidity by controlling gastrointestinal symptoms, and to enhance glucoregulation. Understanding the current advances is key to the development of novel therapeutic strategies and for making rational choices in the management of diabetic gastroparesis.
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PMID:Current concepts in gastric motility in diabetes mellitus. 1822 Jun 21

Gastroparesis is a disorder of gastric emptying that occurs in the absence of mechanical obstruction. Its cardinal features include nausea, vomiting, bloating, early satiety and discomfort. Weight loss, dehydration, electrolyte disturbances and malnutrition may develop in severe cases. The majority of cases is idiopathic, long standing diabetes mellitus is responsible for about 25-30% of cases. Diabetic gastroparesis may render glucose control extremely difficult, its treatment represents a major challenge. Besides frequent, small meals and psychological support, several drug options are available, however, their efficacy is limited and only a few randomized studies have been performed to date. Prokinetic agents (erythromycin, domperidone, metoclopramide) and antiemetics (phenothiazines, serotonin antagonists, butyrophenones) are the most wide-spread medicaments. Among the novel, recently developed agents, 5-HT4 serotonin receptor agonists and dopamine D2 receptor antagonists are the most promising. Injection of botulinum toxin into the pyloric sphincter resulted in faster gastric emptying and symptom alleviation in some studies. Gastric electric stimulation appears to be one of the most effective options, both low and high-frequency stimulation may alleviate symptoms. Gastrostomy/jejunostomy and other surgical interventions are considered as "last resort".
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PMID:[Gastroparesis and its treatment options]. 1829 33

Gastroparesis, or chronic delayed gastric emptying without mechanical obstruction, affects about 40% of patients with type 1 diabetes and up to 30% of patients with type 2 diabetes. Diabetic gastroparesis (DGP) typically causes nausea, vomiting, early satiety, bloating, and postprandial fullness. These symptoms can be extremely troubling and result in poor quality of life. The diagnosis of DGP is made by documenting the presence of chronic upper gastrointestinal (GI) symptoms, ruling out mechanical obstruction, and demonstrating delayed gastric emptying. The usual treatment for DGP includes dietary modifications, prokinetic agents, and antiemetic agents. Although the majority of patients have mild-to-moderate disease that can be managed using these measures, a substantial percentage of patients have severe DGP that is characterized by inadequate oral intake, malnutrition, weight loss, and frequent hospitalizations. Optimal management of these patients presents a difficult challenge for the clinician, although emerging treatment options, such as gastric neurostimulation, are encouraging. Patients with DGP often present with gastric comorbidities, including gastroesophageal reflux disease, intestinal dysmotility, and fungal and bacterial infections of the GI tract. This monograph will present an overview of the pathophysiology of DGP, review diagnostic testing with a discussion of emerging technology, and present the latest research in treatment options for DGP. In addition, management strategies for refractory DGP and gastric comorbidities will be described.
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PMID:Treatment of patients with diabetic gastroparesis. 2073 35

Diabetic gastroparesis is a disorder that occurs in both type 1 and type 2 diabetes. It is associated with considerable morbidity among these patients and with the resultant economic burden on the health system. It is primarily a disease seen in middle-aged women, although the increased predisposition in women still remains unexplained. Patients often present with nausea, vomiting, bloating, early satiety and abdominal pain. The pathogenesis of this complex disorder is still not well understood but involves abnormalities in multiple interacting cell types including the extrinsic nervous system, enteric nervous system, interstitial cells of Cajal (ICCs), smooth muscles and immune cells. The primary diagnostic test remains gastric scintigraphy, although other modalities such as breath test, capsule, ultrasound, MRI and single photon emission CT imaging show promise as alternative diagnostic modalities. The mainstay of treatment for diabetic gastroparesis has been antiemetics, prokinetics, nutritional support and pain control. In recent years, gastric stimulation has been used in refractory cases with nausea and vomiting. As we better understand the pathophysiology, newer treatment modalities are emerging with the aim of correcting the underlying defect. In this review, what has been learned about diabetic gastroparesis in the past 5 years is highlighted. The epidemiology, pathogenesis, diagnosis and treatment of diabetic gastroparesis are reviewed, focusing on the areas that are still controversial and those that require more studies. There is also a focus on advances in our understanding of the cellular changes that underlie development of diabetic gastroparesis, highlighting new opportunities for targeted treatment.
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PMID:Diabetic gastroparesis: what we have learned and had to unlearn in the past 5 years. 2087 Nov 31

Diabetic gastroparesis is a component of autonomic neuropathy, and is the most common manifestation of gastrointestinal neuropathy. Diabetes is responsible for about one quarter of gastroparesis. The upper gastrointestinal symptoms are often non-specific and dominated by nausea, vomiting, early satiety, fullness, bloating. We also have to look for diabetic gastroparesis in case of metabolic instability, such as postprandial hypoglycaemia. The pathophysiology of diabetic gastroparesis is complex, partly due to a vagus nerve damage, but also to changes in secretion of hormones such as motilin and ghrelin. A decrease in the stem cell factor (SCF), growth factor for cells of Cajal (gastric pacemaker), was found in subjects with diabetic gastroparesis. These abnormalities lead to an excessive relaxation in the corpus, a hypomotility of antrum, a desynchronization antrum-duodenum-pylorus, and finally an abnormal duodenal motility. The treatment of diabetic gastroparesis is based on diabetes control, and split meals by reducing the fiber content and fat from the diet. The antiemetic and prokinetic agents should be tested primarily in people with nausea and vomiting. Finally, after failure of conventional measures, the use of gastric neuromodulation is an effective alternative, with well-defined indications. Introduced in the 1970s, this technology works by applying electrical stimulation continues at the gastric antrum, particularly in patients whose gastric symptoms are refractory to other therapies. Its efficacy has been recently reported in different causes of gastroparesis, especially in diabetes. Gastric emptying based on gastric scintigraphy, gastrointestinal symptoms, biological markers of glycaemic control and quality of life are partly improved, but not normalized. Finally, a heavy nutritional care is sometimes necessary in the most severe forms. The enteral route should be preferred (nasojejunal and jejunostomy if possible efficiency). However, in case of failure especially in patients with small bowel neuropathy, the long-term parenteral nutrition is sometimes required.
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PMID:Gastric electrical stimulation for the treatment of diabetic gastroparesis. 2274 75


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