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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The application of novel techniques to quantify gastric motor function and gastric emptying has yielded important insights into the prevalence, pathogenesis and clinical sequelae of gastroparesis. Both acute and chronic gastroparesis occur frequently; gastric emptying of solids is delayed in 30% to 50% of patients with diabetes mellitus, functional dyspepsia and gastroesophageal reflux disease. While many patients with gastroparesis experience upper gastrointestinal symptoms that adversely affect quality of life, the concept that symptoms are inevitably the direct outcome of delay in gastric emptying is now recognized to be overly simplistic. In contrast, the potential impact of gastroparesis on oral drug absorption and blood glucose control in patients with diabetes mellitus has probably been underestimated. While the use of prokinetic drugs (cisapride, domperidone, metoclopramide and erythromycin) forms the mainstay of therapy in symptomatic patients with gastroparesis, a number of novel pharmacological therapies are being evaluated, and preliminary studies using gastric pacing show promise.
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PMID:Gastroparesis: prevalence, clinical significance and treatment. 1177 47

The macrolide antibiotic erythromycin has been known to be associated with increased gastrointestinal motility since its introduction more than 35 years ago. Investigators have, thus, sought to take advantage of this side effect in patients with gastric stasis secondary to long-standing insulin-dependent diabetes mellitus (IDDM). The hormone motilin induces phase 3 contractions of the migrating motor complex (MMC) to induce peristalsis and facilitate gastric emptying in normal subjects. Patients with diabetic gastroparesis lack adequate phase 3 activity to effectively empty gastric contents. Exogenous motilin administered to animals and patients with diabetic gastroparesis has proven useful for promoting gastric emptying. However, motilin is expensive to produce and must be given intravenously. Erythromycin has been shown to induce premature phase 3 activity via stimulation of motilin receptors, so investigators evaluated its efficacy for the treatment of diabetic gastroparesis. Early studies in animals with experimental gastroparesis indicated that erythromycin may be a useful prokinetic agent. Human studies of both intravenous erythromycin and chronic oral erythromycin in patients with diabetic gastroparesis resistant to other prokinetic agents showed that gastric retention was indeed reduced and symptomatic improvement achieved. Even though erythromycin lost some of its prokinetic activity with chronic oral dosing, gastric retention was still significantly reduced compared to placebo or baseline. Although prokinetic agents like metoclopramide, domperidone and cisapride are effective for the treatment of patients with diabetic gastroparesis, tachyphylaxis and adverse effects are obstacles to their use. Erythromycin appears to be both effective and well tolerated in clinical studies. At this time it should be reserved for the treatment of patients with diabetic gastroparesis who are resistant to or intolerant of other prokinetic agents. Future research on erythromycin's long-term safety and comparative efficacy will further define its role.
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PMID:Erythromycin in the Treatment of Diabetic Gastroparesis. 1183 2

There are various reasons for an increased diabetes with type-2 patients. The most frequent reason for hyperglycemia is the metabolic insulin resistance often resulting from a sustaining bad control of metabolism. The problem of insulin resistance can be overcome by making use of high doses of short acting insulin. In case of a subcutaneous insulin resistance, a rare type of insulin resistance, normalising blood sugar can only be achieved by intravenous application of insulin. In many cases there are quite simple reasons for insulin resistance. An erroneous technique of insulin injection is very often attributable for an abnormal need of insulin. With type 2 patients distinctly oscillating blood sugar is anything but normal. Besides a gastroparesis, one needs, in this case, take account of latent autoimmune diabetes of adults (LADA). The most important reasons for hypoglycemia with type-2 diabetes are the following: sulfonylurea and high doses of intermediate-acting insulin.
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PMID:[Increased blood sugar in type 2 diabetes mellitus: what now?]. 1197 31

This review describes recent advances in our knowledge about the pathogenesis and therapeutic approaches to human gastric dysrhythmias. A number of clinical conditions has been found to be associated with gastric slow-wave rhythm disturbances that may relate to the induction of nausea and vomiting. Human and animal studies indicate that multiple neurohumoral factors are involved in the generation of gastric dysrhythmias. Antral distension and increased intestinal delivery of lipids may cause slow-wave disruption and development of nausea. This may be mediated by cholinergic and serotonergic pathways. Similarly, progesterone and estrogen may also disrupt gastric slow-wave rhythm in susceptible individuals. Prostaglandin overproduction in gastric smooth muscle appears to mediate slow-wave disruption in diabetes and with tobacco smoking. On the other hand, central cholinergic pathways play an important role in the genesis of gastric dysrhythmias associated with motion sickness. This may be mediated by vasopressin released from the pituitary. Although it is difficult to ascribe with certainty a causative role of slow-wave rhythm disturbances in the genesis of nausea and vomiting, the search has begun for novel antiemetic therapies based on their abilities to ablate or prevent gastric dysrhythmia formation. This includes the use of prostaglandin synthesis inhibitors, central muscarinic receptor antagonists, and dopamine receptor antagonists. Finally direct gastric electrical stimulation using a surgically implanted neurostimulator has shown promise in reducing emesis in patients with gastroparesis and gastric dysrhythmias.
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PMID:Physiology and pathophysiology of the interstitial cells of Cajal: from bench to bedside. VI. Pathogenesis and therapeutic approaches to human gastric dysrhythmias. 1206 86

Gastroparesis may be related to a variety of underlying disorders, but diabetes mellitus is by far the most common cause. Symptoms of gastroparesis include early satiety, postprandial bloating, nausea and vomiting. Gastric scintigraphy with 99-technetium-labeled low-fat meal is the gold standard method of diagnosing delayed gastric emptying. Dietary measures and prokinetic drugs bring symptomatic relief in most patients. Some patients with severe nausea and vomiting will require antiemetic medications. Few patients will fail medical therapy and will continue to have debilitating symptoms of gastroparesis; such patients may benefit from a venting gastrostomy or a jejunostomy placed surgically, endoscopically, or fluoroscopically. Gastric electrical stimulation is an exiting new approach in the management of gastroparesis. As the treatment of gastroparesis is far from ideal, nonconventional approaches and nonstandard medications are presented.
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PMID:Gastroparesis and its management. 1209 72

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.
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PMID:Botulinum toxin for the treatment of gastroparesis: a preliminary report. 1209 82

The purpose of this article is to present an overview of diabetic gastroparesis, defined as delayed gastric emptying in the absence of mechanical obstruction. Diabetic gastroparesis is a substantial and unrecognized problem. Failure to treat may result in a decreased quality of life and a potential increase for morbidity. The treatment protocol for diabetic gastroparesis combines dietary and pharmacologic measures. This article will discuss normal physiology of gastric emptying along with the pathogenesis of delayed emptying in patients with diabetes. Nursing implications for the care of the patient with diabetic gastroparesis is also presented along with commonly used pharmacologic agents.
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PMID:Understanding diabetic gastroparesis: a case study. 1219 49

In this paper, the influence of food and diabetes on the pharmacokinetics of sodium tungstate in rat was investigated. The compound was administered intravenously (9 mg/kg) and orally in the form of solution (36 mg/kg). An empirical Bayes methodology was used to compute individual pharmacokinetic parameters. Sodium tungstate followed first-order kinetics, and plasma concentration versus time data were described by a two-compartment model. A significant relationship was found between the bioavailability and the status of the animals. Total plasma clearance and elimination half-life averaged 3.1 ml/min/kg and 1.6 h, respectively. Food had some effects on the extent of sodium tungstate absorption. After oral administration, the bioavailability (0.67 versus 0.85), C(max) (6.10 versus 15.2 microg/ml) and AUC (70.7 versus 105 mgh/l) were 20, 60 and 32% lower in fed than in fasted rats, respectively. The presence of cellulose and sulphate anions in rat chow could partially explain the fed state-associated reduction of tungstate bioavailability. In streptozotocin-induced diabetic fed rats, a 25% decrease occurred in AUC and F, and a 14% increase occurred in the elimination rate constant compared with healthy fed rats. These changes could be explain on the one hand, by the increase of liquid consumption and food intake, and on the other hand, by a gastroparesis in the early diabetic rats.
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PMID:Influence of food and diabetes on pharmacokinetics of sodium tungstate in rat. 1242 67

Gastroparesis is a frequent and sometimes life-threatening complication of diabetes mellitus. Autonomic neuropathy seems to be one of the most important mechanisms underlying this entity, together with the other probable pathologies. The present study was performed in order to identify an alternative to gastric scintigraphy as a screening test. The gastric emptying times of 60 subjects (Group 1: 20 insulin-dependent patients, Group 2: 20 non-insulin-dependent diabetes mellitus patients, and Group 3: 20 healthy volunteers) were monitored by gastric scintigraphy. Perception thresholds for cold, heat, and vibration were tested by a quantitative sensory test, and QTc dispersions were calculated from standard electrocardiography recordings. In addition, fasting blood glucose, hemoglobin A1c and urine beta2-microglobulin and microalbumin concentrations were determined for the patient groups. Funduscopic examination was performed by an independent ophthalmologist. Gastroparesis was determined in both patient groups, regardless of fasting blood glucose and hemoglobin A1c concentrations. A strong correlation was observed between nephropathy, retinopathy, and cardiac autonomic denervation (QTc) and gastroparesis. In conclusion, retinal and renal microvasculopathy parameters and cardiac autonomic function tests may be useful for screening diabetic patients for gastroparesis.
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PMID:Diabetic gastroparesis in association with autonomic neuropathy and microvasculopathy. 1253 May 7

Gastroparesis is a common complication of diabetes attributed to autonomic neuropathy. This study investigated whether acute hyperglycemia influences central thyrotropin-releasing hormone (TRH), a well-established brain medullary vagal stimulus, induced gastric acid secretion in overnight fasted, urethane-anesthetized rats. Intravenous infusion of D-glucose (20%, 30% and 40%) dose dependently reduced intracisternal TRH-induced gastric acid secretion (71+/-28 micromol/90 min) by 39%, 90% and 100% respectively. Pretreatment with cholecystokinin(A) (CCK(A)) receptor antagonist devazepide (1 mg/kg) did not influence the inhibitory effect of intravenous glucose (30%). These results indicate that hyperglycemia may have a central effect to antagonize medullary TRH stimulation of vagal outflow to the stomach.
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PMID:Intravenous glucose infusion decreases intracisternal thyrotropin-releasing hormone induced vagal stimulation of gastric acid secretion in anesthetized rats. 1264 56


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