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 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effect of erythromycin on gastric emptying in nine patients with gastroparesis following truncal vagotomy and antrectomy, and assessed their clinical response to chronic oral erythromycin. Gastric emptying was evaluated using a solid-phase radio-labeled meal. Patients were studied after erythromycin 200 mg intravenously (N = 9) and after an oral suspension of erythromycin 200 mg (N = 7) each given 15 min after ingestion of the meal. Three parameters of gastric emptying were analyzed: half-emptying time (T1/2), area under the curve, and percent gastric residual at 2 hr. Nine patients were subsequently placed on oral suspension erythromycin 150 mg three times a day before meals (range 125-250 mg three times a day) and symptoms of nausea, vomiting, postprandial fullness, and abdominal pain were assessed before and after erythromycin. Intravenous erythromycin markedly accelerated the gastric emptying (all three parameters studied) of solids (P < 0.01) in seven of nine patients with postsurgical gastroparesis [baseline T1/2 154 +/- 15 min; after intravenous erythromycin, T1/2 56 +/- 17 min (mean +/- SEM)]. Oral erythromycin enhanced (P < 0.05) the gastric emptying rate (T1/2, area under the curve) in five of seven patients (baseline T1/2 146 +/- 16 min; after oral erythromycin, T1/2 87 +/- 20 min). Of the nine patients who were placed on oral maintenance erythromycin, three showed clinical improvement after two weeks. In summary, erythromycin significantly enhances gastric emptying in many patients with vagotomy and antrectomy-induced gastroparesis; however, only a small subset of patients respond clinically to chronic oral erythromycin.
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PMID:Erythromycin enhances gastric emptying in patients with gastroparesis after vagotomy and antrectomy. 795 94

Cisapride induces acetylcholine release in cells of the myenteric plexus, thus promoting gastrointestinal motility. We studied the effects of cisapride on 11 patients with idiopathic gastroparesis. All had negative gastrointestinal endoscopy, normal glucose, and took no drugs capable of influencing motility. Most (9/11) were prior metoclopramide treatment failures. Patients' symptoms were scored (0-60) for pain, satiety, bloating, nausea, vomiting, and heartburn. All underwent a solid gastric emptying study using a Technetium-99-labeled egg meal and received placebo prior to cisapride. There were 10 females and one male with a mean (+/- SE) age of 37.8 +/- 2.6 years. Disease duration was 7.9 +/- 2.8 years. The dose of cisapride was 30-60 mg/day and the duration of therapy was 12.6 +/- 2.6 months (range 2.5-25 months). The symptom score improved on cisapride from 30.9 +/- 3.6 to 14.4 +/- 2.7 (P < 0.002 signed rank test). Emptying half-time improved from 113 +/- 4 min to 94 +/- 6 min, and 46.9 +/- 2.4% food remaining at 120 min decreased to 35.5 +/- 3.6% (both P < 0.05). Emptying half-time in normals was 68 +/- 5 min with 16.9 +/- 2.9% remaining at 120 min. Nine of 11 patients gained weight, with a mean increase of 6.7 +/- 1.6 lb (range 2-12 lb). We conclude that cisapride significantly reduces gastrointestinal symptoms and promotes weight gain in patients with idiopathic gastroparesis and is associated with improvement in solid gastric emptying. The drug is useful in patients who previously failed metoclopramide.
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PMID:Open label study of long-term effectiveness of cisapride in patients with idiopathic gastroparesis. 802 48

Gastroparesis is a chronic gastric motility disorder in which there is delayed gastric emptying of solids plus or minus liquids. Symptoms of gastroparesis may range from early satiety and nausea in mild cases to chronic vomiting, dehydration, and nutritional compromise in severe cases. Diagnosis of gastroparesis is based on demonstration of delayed gastric emptying of a radiolabeled solid meal in the absence of mechanical obstruction. A number of gastrointestinal and systemic disorders may impair gastric motility with resultant gastroparesis. Approximately one third of patients with gastroparesis have no identifiable underlying cause (so called idiopathic gastroparesis). Management of gastroparesis involves four areas: (1) nutritional support, (2) antiemetic drugs, (3) prokinetic drugs, and (4) surgical therapy (in a very small subset of patients). Gastroparesis is often a chronic, relapsing condition; 80% of patients require maintenance antiemetic and prokinetic therapy and 20% require long-term nutritional supplementation. In the near future, the most promising advances in the treatment of patients with gastroparesis will most likely come from the area of combination pharmacological therapy. In the long term, developments in the area of intestinal pacing and intestinal transplantation may offer further treatment options in this difficult disorder.
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PMID:Gastroparesis and the current use of prokinetic drugs. 804 84

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

A 72-year-old woman with chronic fatigue, malaise, weight loss, nausea, and vomiting was treated unsuccessfully for gastroparesis for more than 2 years. Clinical and biochemical features of hypopituitary disease and symptoms of a nonsecreting pituitary tumor had been overlooked and became apparent only after the differential diagnosis of hyponatremia was considered. Transsphenoidal resection of the pituitary tumor and appropriate 1-thyroxine and hydrocortisone replacement returned her gastric emptying time to normal and relieved her symptoms. Primary and secondary deficits of l-thyroxine and cortisol should be considered when making a possible diagnosis of gastroparesis.
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PMID:Case report: reversible gastroparesis in patients with hypopituitary disease. 868 31

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

Disorders of stomach function refer to neuromuscular abnormalities of gastric motility that involve the fundus, corpus, antrum, pylorus, and antroduodenal coordination. Symptoms related to disorders of stomach function are commonly meal-related; "dyspepsia" symptoms of epigastric fullness; or bloating, discomfort, and nausea in the postprandial period. Early satiety and prolonged stomach fullness are often present, and in severe cases the patient may vomit undigested food. Neuromuscular disorders of stomach function should not be considered until structural and metabolic diseases that may also cause these nonspecific symptoms are excluded. A thorough history, routine laboratory studies, ultrasound of the gallbladder and pancreas, and upper endoscopy will exclude the majority of diseases that may cause dyspepsia symptoms. Disorders of gastric neuromuscular function may be detected by solid-phase gastric emptying studies which detect gastroparesis and by electrogastrography which detects abnormalities of gastric myoelectrical activity termed gastric dysrhythmias. Invasive tests to determine abnormalities in gastric motility include intraluminal pressure and gastric tone/compliance recordings. Treatment approaches are limited at the present time and include dietary counseling and gastroprokinetic agents such as metoclopromide, cisapride, and erythromycin. Increased understanding of the pathophysiology of disorders of gastric neuromuscular function will lead to an improved and more rational armamentarium for the treatment of symptoms related to functional disorders of the stomach.
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PMID:Functional disorders of the stomach. 890 32

The median arcuate ligament syndrome (MALS) is characterized by abdominal pain, nausea, and vomiting attributed to compression of the celiac axis by a fibrous band (the median arcuate ligament) connecting the diaphragmatic crura. The pathophysiologic origin of these symptoms is not clearly understood. Theories invoking either a neurogenic or vascular origin for the clinical features associated with MALS have been proposed, but objective evidence to support these theories is lacking. We describe the clinical course and gastric myoelectrical features of a patient with postprandial epigastric pain, weight loss, gastroparesis, and gastric dysrhythmias in whom a diagnosis of MALS was established. Surgical decompression of the celiac axis in our patient resulted in resolution of abdominal pain, return to a full diet within 4 weeks without nausea or vomiting, improvement in radionuclide gastric emptying, and restoration of the gastric electrical rhythm to a normal 3 cycle/min conduction rate. This is the first demonstration of altered gastric myoelectrical activity in a patient with MALS. The regularization of the gastric electrical rhythm in our patient after surgical decompression of the celiac axis would support a neurogenic basis for the symptoms associated with MALS. MALS should be excluded in patients with idiopathic gastroparesis and unexplained epigastric pain.
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PMID:Median arcuate ligament syndrome: a possible cause of idiopathic gastroparesis. 906 84

The effect of long-term cisapride therapy (20 mg orally three times daily for 2 years) on gastric emptying and gastrointestinal symptoms was investigated in 30 patients with severe gastroparesis (24 idiopathic, 6 diabetic). Symptoms were assessed every 2 months, using an overall symptom score based on six symptoms (anorexia, nausea, vomiting, pain, early satiety and bloating), and a 2-year mean overall symptom score was used for analysis. Gastric emptying was measured at 0, 6, 12, 18 and 24 months. Of the 24 patients who completed the study, 10 showed a significant improvement in gastric emptying (P < 0.05) and felt improved on therapy, seven patients showing a > 20% improvement in overall symptom score compared to baseline. Results for 15 patients who underwent at least one follow-up gastric-emptying test showed only a weak correlation between individual symptom score and gastric emptying (r = 0.40). Thus long-term cisapride therapy at the study dose produced long-term symptomatic improvement in 42% of patients with severe gastroparesis, with sustained acceleration of gastric emptying for up to 2 years.
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PMID:Cisapride in the long-term treatment of chronic gastroparesis: a 2-year open-label study. 928 90


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