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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The author discusses abnormalities in gastric emptying due to diabetes mellitus, and in particular, diabetic gastroparesis, on the basis of his own experience and the relevant literature. Diabetic gastroparesis is a result of a diabetic neuropathy of the vagus. Even in the presence of mild abdominal symptoms, particularly with repeated hypoglycaemic episodes, this condition should be considered and the stomach should be examined readiologically. A diabetic phytobezoar may develop. It may be presumed that these changes are more common than had previously been realized. The author has observed six cases. The gastric atony associated with diabetic coma has to be differentiated from the condition under discussion. Conservative treatment is recommended.
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PMID:[Disturbance of gastric emptying in diabetes mellitus (author's transl)]. 12 11

Diabetic gastroparesis is a complication of diabetes mellitus that usually responds to medical management. We report a patient in whom medical management failed, and a gastrostomy, pyloroplasty, and jejunostomy were done to insure nutrition and to decompress the stomach. We also review the surgical management of this condition.
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PMID:Surgical therapy of diabetic gastroparesis. 273 62

Diabetic gastroparesis is the gastric manifestation of diabetic autonomic neuropathy and may result, on rare occasions, in the formation of a bezoar. This was the case in 3 patients (two women aged 36 and 66 and a 19-year-old man) whose insulin-dependent diabetes was complicated with neuropathy. All patients had marked glycaemic instability apparently related to digestive function. In one patient, a stable normoglycaemic state was obtained by continuous intravenous administration of carbohydrates until the bezoar had disappeared. In the other two patients, who had a long history of neglected digestive disorders, the bezoars provided intractable. In diabetics with dyspeptic symptoms, and particularly when neuropathy is present, it would be advisable to investigate for gastroparesis in order to prevent the development of a bezoar by dietetic and therapeutic measures.
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PMID:[Gastric bezoar in diabetes mellitus. 3 cases (author's transl)]. 729 Sep 42

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

Diagnostic evidence or symptoms of gastroparesis develop in about 20% to 30% of patients with long-standing diabetes. Diabetic gastroparesis is likely caused by autonomic neuropathy involving the nerves that regulate gastric motor function. The following are necessary for diagnosis: thorough history taking and physical examination to eliminate factors that might further delay gastric emptying; esophagogastroduodenoscopy or barium contrast studies to exclude structural abnormalities; and a radionuclide gastric emptying study. The three main agents available for therapy in the United States are metoclopramide (Maxolon, Octamide, Reglan), erythromycin, and cisapride (Propulsid). All have been shown to offer benefit in improving gastric emptying and symptoms, although use of metoclopramide is limited by a significant incidence of side effects. Surgical intervention should be avoided if possible.
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PMID:Diabetic gastroparesis. What to do when gastric emptying is delayed. 815 43

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, caused by an autonomic neuropathy of the vagus nerve, is seen in up to 50% of individuals with diabetes. It results in a delay of gastric emptying that wreaks havoc on glycemic control and also has nutritional implications. Treatment is directed toward ameliorating symptoms and improving nutritional and glycemic control.
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PMID:Methods for treating diabetic gastroparesis. 1198 24

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

Diabetic gastroparesis is a well-recognized delay of gastric emptying in diabetic patients. We assessed the gastric emptying rate in ob/ob mice, a genetic model of obesity and diabetes. The basal gastric emptying rate in 22- to 27-week-old ob/ob mice was significantly lower than that in 10- to 11-week-old ob/ob mice (P<.01). Our results indicate that the ob/ob mice are a useful model not only of glucose intolerance but also of delayed gastric emptying as a diabetic complication.
J Diabetes Complications
PMID:Ob/ob mice as a model of delayed gastric emptying. 1250 53

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


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