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

Gastropathy on the basis of mesenteric arterial ischemia can be masked in presentation as the typically more benign entities of gastritis, gastric ulceration, or gastric atony. Gastritis and ulceration are commonly associated with stress, hyperacidity, Helicobacter pylori infection, or medication injury. Gastric atony is less commonly seen and usually attributable to diabetes mellitus, vagotomy, or mechanical gastric outlet obstruction. Gastric ischemia as a cause of gastropathy is an underappreciated phenomenon with a particularly poor prognosis in which early diagnosis is essential to potentially successful intervention. Seven patients with ischemic gastropathy are described; all are women, aged 41 to 71 years, smokers, with hypertension. Nausea, vomiting, weight loss, and gastrointestinal bleeding were the common presenting symptoms. All patients had endoscopic or autopsy-proven gastric ulcerations or necrosis, and two patients had proven gastroparesis. Four of five patients with ischemic gastritis died within 3 months of diagnosis despite vascular reconstruction. The two patients with gastroparesis underwent aorto-celiac bypass and are well 9 and 20 months, respectively, after operation. Treatment results were distressingly unsatisfactory, especially in those patients in whom gastritis rather than gastroparesis was the presenting problem. Although the high mortality of mesenteric ischemia is well described, little documentation of gastric ischemia exists in the literature. This entity is generally not considered in the differential diagnosis of gastritis, ulceration, or gastroparesis. Empirically, an early diagnosis and treatment may improve the survival in this select patient group.
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PMID:Lethal nature of ischemic gastropathy. 848 53

Cutaneous electrogastrography was performed in nine healthy volunteers and in 43 patients presenting with various clinical conditions known to be associated with gastric motor disorders, including: 24 with functional dyspepsia, nine with longstanding diabetes mellitus, five with recent nausea/vomiting, three with pyloric stenosis, one with post-vagotomy gastroparesis, and one with idiopathic gastric distension and atony. The electrogastrography signal was recorded during 1h pre-prandial period and 1h after eating. The electrogastrography dominant frequency and power were determined using running spectral frequency analysis and the time-course of electrogastrography was evaluated in a pseudo three dimensional graphic. The electrogastrography dominant frequency was divided into four bands: 1. Bradygastria (0-2.4 cpm); 2. Normal (2.4-3.9 cpm); 3. Tachygastria (4.0-9.9 cpm); 4. Duod-resp (10.0-15.0 cpm). The percentage of the dominant electrogastrography power into those four frequency bands was determined. Electrogastrography was considered normal if functional dyspepsia was normal in more than 65% of the time. The electrogastrography was normal (dominant frequency into 3 cpm range in > 65%) in: 9/9 healthy volunteers, 3/3 pyloric stenosis, 4/5 nausea/vomiting, 3/9 diabetes mellitus, 13/24 functional dyspepsia. Gastric dysrhythmias were present in > 35% of the electrogastrography recording in: 1/5 nausea/vomiting, 11/24 functional dyspepsia, 6/9 diabetes mellitus, 1/1 post-vagotomy gastroparesis, 1/1 gastric distension and atony. Persistent tachygastria (> 10%) was found in: 1/1 gastric distension and atony (90% electrogastrography), 1/1 post-vagotomy gastroparesis, 1/5 nausea/vomiting, 6/9 diabetes mellitus, 6/24 functional dyspepsia. It was concluded that electrogastrography is a non-invasive, well-tolerated, reliable means of recording gastric myoelectric activity and gastric dysrhythmias. Patients presenting with gastric motor disorders, with chronic dyspeptic symptoms, or acute nausea may present transitory or persistent gastric dysrhythmias.
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PMID:[Myoelectric gastric activity using cutaneous electrogastrography--electrogastrogram]. 854 Aug

We reviewed the discharge records of all diabetic ketoacidosis hospitalizations over 30 months for the presence of clinically significant upper gastrointestinal hemorrhage. Of 284 hospitalizations in 193 patients, hemorrhage occurred in 26 hospitalizations (9%) in 25 patients (13%). None required invasive therapy to achieve hemostasis, and there were no bleeding recurrences and no deaths due to bleeding. Endoscopy in eight revealed esophagitis in all (five had erosions or ulcerations), one Mallory-Weiss tear, five with gastritis (mild in four), four with duodenitis (one erosive), one duodenal ulcer, and no gastric ulcers. Hemorrhage patients had a longer diabetes duration (14.85 vs 9.16 years, P < 0.02), and more nephropathy (40% vs 11%, P < 0.001), retinopathy (28% vs 12%, P < 0.03) and gastroparesis (36% vs 10%, P < 0.002) than those without hemorrhage. Ulcer medication (42% vs 23%, P < 0.03) or anticoagulant (12% vs 1%, P < 0.005) but not nonsteroidal antiinflammatory drug usage (12% vs 12%) was higher in the hemorrhage group. Admission glucose (P < 0.02), BUN (P < 0.04), and creatinine (P < 0.02) levels were higher in hemorrhage patients, but arterial pH, serum ketones, hemoglobin, platelet count, and coagulation values were not. Hemorrhage patients required more blood transfusions (27% vs 10%, P < 0.003) and intensive care unit admissions (69% vs 43%, P < 0.009). Total (15% vs 3%, P < 0.003) and intensive care unit mortality (22% vs 6%, P < 0.026) were higher in the hemorrhage group. We conclude that upper gastrointestinal hemorrhage complicates 9% of diabetic ketoacidosis hospitalizations. Blood transfusion may be required, but the bleeding is self-limited and not severe. The most common lesion is erosive esophagitis. Hemorrhage correlates with glucose level, admission to the intensive care unit, duration of diabetes, the presence of diabetic complications, and portends a high non-bleeding-related mortality.
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PMID:Prevalence, etiology, and prognostic significance of upper gastrointestinal hemorrhage in diabetic ketoacidosis. 856 40

The pathophysiological mechanisms responsible for diabetic gastroparesis remain unclear. Diabetes mellitus occurs spontaneously in 90% of a partially inbred colony of BB/W rats. This animal model resembles human insulin-dependent diabetes and is suitable for investigating the mechanism of diabetic gastroparesis. Diabetic BB/W rats were killed 6 mo after the onset of diabetes. Muscle contraction experiments and [3H]acetylcholine release studies were performed with muscle strips of the gastric body. Biochemical measurements of inositol trisphosphate (IP3) and protein kinase C (PKC) in gastric muscle were performed to characterize abnormalities of the intracellular signal transduction system in gastric myocytes. Circular muscle contractions in response to direct myogenic stimulants, carbachol (10(-7) - 10 (-3)M) or substance P (10(-7) - 10(-5)M), were significantly impaired in diabetic BB/W rats compared with controls. Similarly, muscle contractions in response to NaF (10 mM), a direct stimulant of G proteins, were also impaired in diabetic BB/W rats. In contrast, muscle contractions in response to KCl (25-75 mM) were similar between control and diabetic BB/W rats, indicating normal voltage-dependent Ca2+ entry in muscle strips obtained from diabetics BB/W rats. [3H]acetylcholine release from gastric myenteric plexus in response to electrical transmural stimulation remained intact in diabetic BB/W rats. In separate studies, we demonstrated that carbachol (10(-6) - 10(-4)M) -induced IP3 responses were significantly reduced in diabetic rats compared with control. In addition, there was also impairment of translocation of PKC in diabetic BB/W rats. These observations indicate that myogenic impairment occurred in diabetic BB/W rats. This resulted from altered intracellular signal transduction involving abnormal IP3 production and PKC translocation.
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PMID:Impaired intracellular signal transduction in gastric smooth muscle of diabetic BB/W rats. 863 6

Gastroparesis is delayed gastric emptying of either solids or liquids, which occurs in the absence of mechanical obstruction. Although associated with many diseases, the most frequent cause of gastroparesis is diabetes mellitus. It is estimated that up to 50% of diabetic patients may have this problem. Symptoms of gastroparesis include postprandial nausea, epigastric pain/burning, bloating, early satiety, excessive eructation, anorexia and vomiting. The vomiting associated with gastroparesis often has the following two features: (1) emesis of undigested foods ingested more than four hours previous; and (2) emesis of undigested foods in the middle of the night or in the morning prior to eating breakfast. It is important to recognize and treat gastroparesis not only to decrease symptoms but also to prevent bezoar formation and nutritional deficiencies as well as to improve glycemic control in brittle diabetics. The purpose of this article is to review the physiology of gastric emptying and to use this information to understand the pharmacological therapies for this debilitating problem.
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PMID:Gastroparesis: current management. 878 40

Gastric emptying is delayed in 30%-50% of patients with longstanding diabetes mellitus. The prevalence of disordered gastric emptying in patients with "early" Type 2 diabetes is controversial, but it has been suggested that gastric emptying is often accelerated. The pathogenesis of delayed gastric emptying in diabetes is poorly understood. It is, however, clear that acute changes in the blood glucose concentration have a major effect on gastric motor function and gastric emptying. There is an inverse relationship between the rate of gastric emptying and the blood glucose concentration, so that emptying is slower during hyperglycaemia and faster during hypoglycaemia. The motor dysfunctions responsible for delayed gastric emptying in patients with diabetes are heterogeneous. There is a high prevalence of upper gastrointestinal symptoms in diabetes. However, the correlation between symptoms and delay in gastric emptying is poor. Recent studies indicate that the blood glucose concentration modulates the perception of some sensations arising from the gastrointestinal tract. In both normal subjects and patients with diabetes the blood glucose response to oral carbohydrate and gastric emptying are related and there is evidence that modulation of the rate of gastric emptying, by dietary or pharmacological means, could be used to optimise glycaemic control. The use of prokinetic drugs, particularly cisapride, is currently the most effective approach to the treatment of symptomatic patients with gastroparesis. An improved understanding of the pathophysiology of both symptoms and delayed gastric emptying is fundamental to the development of more effective treatments.
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PMID:Gastric emptying in diabetes: an overview. 889 65

The gastric emptying function tests were carried out in eight patients with pancreatic diabetes, who were classified into two groups according to the coefficient of variation in the R-R interval in ECG (C.V. R-R) on the normal subjects: < or = the mean - 2SD (the autonomic nerve dysfunction group: AND+ group) and > the mean - 2SD (the autonomic nerve normal group: AND- group). Both the gastric emptying of liquid food by the acetaminophen method and that of solid food by the isotope method were significantly reduced in the AND+ group than in the AND- and normal groups. In addition, a significant correlation was found between the C.V. R-R and the serum acetaminophen concentration (a 45 min value) and the % gastric retention of isotope (a 120 min value). The above results demonstrated that even pancreatic diabetes might be complicated by gastroparesis diabeticorum among autonomic nerve dysfunction. There was a close relation of delayed gastric emptying to the C.V. R-R in ECG or an index of the vagus nerve function.
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PMID:Study of gastric emptying in patients with pancreatic diabetes (chronic pancreatitis) using acetaminophen and isotope. 901 26

Electrical responses of gastric smooth muscles produced by transmural nerve stimulation, acetylcholine, norepinephrine, or K-free solution were investigated in streptozotocin-induced diabetic rats, using intracellular microelectrode techniques. In muscles from diabetic rats, 1) the resting membrane potential remained unchanged, 2) slow waves disappeared or were markedly reduced in amplitude, 3) the excitatory junction potential was absent, and in most cases only an inhibitory junction potential of reduced amplitude was elicited, 4) the amplitude of the hyperpolarization generated after superfusion with K-free solution was reduced, 5) the sensitivity of the acetylcholine-induced membrane depolarization was increased, and 6) the norepinephrine-induced hyperpolarization was reduced because of functional loss of alpha- and beta-adrenoceptors. Thus diabetes mellitus caused functional impairment of neuromuscular transmission, reduced the maximum activity of the electrogenic pump, increased the sensitivity of muscarinic receptors, reduced the sensitivity of adrenoceptors, and reduced the myogenic activity in gastric smooth muscles. These alterations in the properties of smooth muscle may be involved in the diabetes-induced gastroparesis.
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PMID:Electrical responses of gastric smooth muscles in streptozotocin-induced diabetic rats. 903 79

The influence of diabetic hyperglycemia on solid gastric emptying in rats was examined. Diabetes was produced by streptozotocin (STZ, 40 mg/kg i.v.), and diabetic hyperglycemia was observed from 1 day after the STZ injection. The gastric emptying of glass beads in the diabetic rats was significantly delayed compared with that in age-matched control rats at 1, 3 and 7 days after diabetes induction. A slight decrease in gastric emptying was observed in the diabetic rats from 2 to 52 weeks after the diabetes induction. We also investigated the influence of gastroprokinetic agents on STZ-induced diabetic gastroparesis and subdiaphragmatic vagotomy-induced gastroparesis in rats. The selective 5-HT3 receptor antagonists ramosetron (YM060), YM114 (KAE-393), granisetron and ondansetron, and the substituted benzamides (5-HT4 receptor agonist/5-HT3 receptor antagonists) cisapride mosapride and SC-53116 dose-dependently enhanced gastric emptying in normal rats. These compounds also reversed the impairment of diabetic gastroparesis rats at 7 days after the STZ injection, but higher doses were required. The solid gastric emptying in subdiaphragmatic vagotomized rats was also delayed. Ramosetron and the substituted benzamides cisapride and zacopride partially reversed the gastroparesis in the vagotomized rats. These results suggest that acute hyperglycemia is important mechanism for the delay of solid gastric emptying in diabetic rats. It is also suggested that selective 5-HT3 receptor antagonists and substituted benzamides enhance gastric emptying not only in normal rats but also in diabetic and vagotomized rats.
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PMID:Effects of gastroprokinetic agents on gastroparesis in streptozotocin-induced diabetic rats. 922 2

Our understanding of the nature of diabetic gastroparesis has advanced in the last decade due to new investigational procedures (electrogastrography, visceral evoked potential recording), and transferring these insights into clinical routine will be our task in the future. Meanwhile, the clinical relevance of gastroparesis--whether overt or silent--remains unquestioned: proper gastric emptying is a prerequisite for adequate metabolic control, and its disturbance may result not only in further progression of the chronic complications of the disease, but also in the false assumption that these patients are not compliant with their doctor's management--the patients just may have delayed emptying of their stomach without noticing it.
Diabetes 1997 Sep
PMID:Pathophysiology of diabetic gastroparesis. 928 4


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