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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over a one-year period, 95 children and adolescents presenting with epigastric pain and/or vomiting, and without associated risk factors for development of peptide disease, underwent endoscopic antral biopsies for pathologic diagnosis and to detect presence of Campylobacter ss. pylori (C. pylori). Additional biopsies of the esophagus, stomach, and duodenum were obtained for histologic evaluation. C. pylori was identified in 16 patients (16.8%), all of whom had evidence of acute and/or chronic gastritis. Significant discriminating factors between C. pylori-positive and -negative subjects included age at presentation (positive vs negative = 14.6 vs 9.9 years, P less than 0.01), biopsy-confirmed gastritis (100% vs 30.4%, P less than 0.001), and diagnosis of duodenitis alone (0% vs 46.8%, P less than 0.001). Risk for bacterial colonization was significantly higher in the presence of endoscopic gastritis (P less than 0.001). Among C. pylori-positive patients, none responded to standard antiulcer therapy (H2-receptor antagonists, antacids). Symptomatic and histologic remission was achieved utilizing combined therapy with bismuth subsalicylate and antibiotics. Seven of 79 C. pylori-negative patients with biopsy-proven gastritis who responded poorly to antisecretory therapy had the organism identified in follow-up antral biopsies; these patients improved clinically following treatment for C. pylori. These data suggest that C. pylori is a significant factor in the etiology of upper gastrointestinal tract inflammatory disease in pediatrics, and presence of the organism should be evaluated, particularly in children with evidence of acute and/or chronic gastritis.
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PMID:Campylobacter pylori-related gastrointestinal disease in children. Incidence and clinical findings. 279

We have identified ten children who developed gastritis after prolonged anticonvulsant therapy that included either valproic acid or divalproex sodium. Presenting symptoms were primarily feeding difficulties, including anorexia and refusal to eat. Vomiting was present in two thirds of the patients, with diarrhea, weight loss, and abdominal pain occurring less frequently. Occult blood in stool samples was a late development. All patients responded to therapy with H2-receptor antagonists, oral antacids, or both, with prolonged treatment often necessary to prevent relapse. Although gastrointestinal tract side effects are common with the initiation of valproate sodium therapy, feeding difficulties after long-term treatment are less common. Gastritis should be suspected in children receiving valproate therapy when feeding difficulties arise, particularly if the symptoms are persistent or recurrent.
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PMID:Gastritis with valproate therapy. 289 28

Experimentally, the gastric and the duodenal mucosa can both be damaged by acute exposure to small intestinal juice. Though chronic exposure to bile causes mucosal erythema and hyperplasia, the gastric mucosal barrier is not damaged. Duodenogastric reflux is relevant in the pathogenesis of postoperative bilious vomiting and probably of "alkaline" reflux esophagitis. The exact mechanism of mucosal damage has not been established. Duodenogastric reflux is likely to be irrelevant in the pathogenesis of (microscopic) gastritis, of gastric ulcer, and of reflux esophagitis without previous gastric surgery.
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PMID:[Is a duodenogastric reflux of pathogenic significance?]. 305 2

Twelve partially gastrectomized subjects who have consecutively undergone total biliary diversion for severe bilious vomiting were studied before and after operation in order to assess the effects of surgery on gastric histology and enterogastric reflux. Before and six months after operation, the following protocol was performed: (1) blood examinations including serum basal gastrin; (2) endoscopy with multiple gastric biopsies; and (3) quantitation of bile acids in the gastric aspirate. Of the preoperative symptoms, bilious vomiting and heartburn completely disappeared postoperatively in all the subjects. Fasting bile reflux was significantly reduced (bile reflux was annulled in six and considerably lowered in the remaining six subjects), and erythema of the gastric mucosa completely disappeared in all the subjects after diversion. Among histological findings, while a significant regression of foveolar hyperplasia was found both in the perianastomotic area and in the body of gastric remnant, none of the other aspects identifiable in postgastrectomy gastric mucosa (chronic gastritis changes included) were affected by diversion. These results show that biliary diversion is effective in correcting reflux, bilious vomiting, erythema, and foveolar hyperplasia of the gastric mucosa and confirm the suggested relationship between bile reflux and gastric foveolar hyperplasia.
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PMID:Short-term effects of bile diversion on postgastrectomy gastric histology. 316

Paraesophageal hiatal herniation and pyloric obstruction were diagnosed in a pup with a history of vomiting. Findings of contrast radiography included esophageal reflux, delayed gastric emptying time, and paraesophageal herniation. Exploratory celiotomy revealed increased firmness of the pylorus and a primary defect in the esophageal hiatus, which allowed gastric herniation. Nissen fundoplication was performed following reconstruction of the esophageal hiatus, and pyloroplasty was performed to relieve the gastric outlet obstruction. Pyloric biopsy findings were consistent with a diagnosis of chronic gastritis. Recovery from surgery was initially unremarkable; however, the dog died suddenly 3 weeks after surgery. Necropsy revealed a large diaphragmatic hernia adjacent to the esophageal hiatus; the hernia had resulted in incarceration of the abdominal organs. The hiatal hernia reconstruction remained intact and was not the cause of the diaphragmatic disruption.
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PMID:Paraesophageal hiatal hernia and pyloric obstruction in a dog. 320 61

A survey of the histology of gastric biopsies in 501 dogs, consisting of 19 clinically healthy dogs and 482 vomiting dogs is presented. Whole stomachs of four young clinically healthy laboratory dogs were used as controls. Eleven percent of forceps biopsies were unsuitable for examination; all suction biopsies were of good quality. Slight to severe gastritis was found in 168 vomiting dogs (35%), whereas five dogs (26%) of the clinically healthy group showed a mainly slight gastritis. Superficial and diffuse gastritis were the most prominent findings in the 168 dogs with gastritis. A single type of gastritis was found in 114 dogs, a combination of different types in 54 dogs. Gastric atrophy was seen in 23 (5%) vomiting dogs and in three (15%) clinically healthy dogs, atrophy with a slight to severe fibrosis in 21 (4%) vomiting dogs, and in 84 (17%) vomiting dogs and two (11%) healthy dogs, gastric fibrosis was present. Carcinomas were seen in 26 vomiting dogs, of which 17 also had gastritis. A differential diagnosis of granulomatous gastritis/carcinoma had to be made in one case. Seven dogs showed a lymphosarcoma, and in six other dogs a differential diagnosis of lymphosarcoma and/or gastritis was made. One adenomatous polyp was seen. In one clinically healthy dog an adenomyoma was diagnosed. Ulceration was found in 24 dogs, but only five of these lacked other lesions. Other biopsy findings were pseudopyloric metaplasia, hyperplasia, cysts, calcification and edema. Some dogs showed "antralization".
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PMID:The histological appearance of peroral gastric biopsies in clinically healthy and vomiting dogs. 334 2

The clinical course of a child who developed an adenocarcinoma of the stomach at 11 years of age is described. At 6 years of age, the child was evaluated for abdominal pain, weight loss, and vomiting. She was found to have hemorrhagic, atrophic gastritis, achlorhydria, and panhypogammaglobulinemia. The gastritis improved with corticosteroid therapy, but relapsed each time that the steroid dosage was tapered. The clinical course was marked by severe growth failure, recurrent infections, and intermittent abdominal pain. Radiographic studies done when the patient was 11 years of age demonstrated a large fungating mass on the lesser curvature of the stomach. Endoscopy and biopsies done 1 year previously had not revealed any sign of malignancy. A radical gastrectomy was performed. Microscopic studies revealed multifocal adenocarcinoma of the stomach with no evidence of invasion of the submucosa or local lymph nodes. The patient died of Candida septicemia and pneumonia 6 months after the gastrectomy. There was no evidence of recurrence of the tumor on autopsy. The relationship between common variable immunodeficiency and gastrointestinal disease is described.
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PMID:Multifocal adenocarcinoma of the stomach in a child with common variable immunodeficiency. 338 60

Excessive Enterogastric reflux following partial gastrectomy is believed to be responsible for bilious regurgitation, vomiting, nausea, and epigastric pain. At endoscopy, striking erythema and inflammatory changes of the gastric mucosa may be seen. The nonsurgical treatment for this syndrome is unsatisfactory. Because of the potential pathogenetic role of regurgitating bile acids, lysolecithin, and pancreatic secretions, it seemed relevant to find out whether prostaglandin E2 (PGE2) in a dose of 0.5 mg qid could protect the gastric mucosa from further damage and thereby lead to symptomatic improvement. The results of this controlled doubled-blind crossover trial, comparing PGE2 and placebo, in the treatment of postgastrectomy reflux gastritis reveal no significant differences between PGE2 and placebo with regard to symptoms, endoscopic features, and histologic evidence of inflammatory changes. Thus, prostaglandin E2 in the dose used appears incapable of improving postgastrectomy reflux gastritis in patients with mild to moderate degrees of this entity.
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PMID:Double-blind crossover trial of prostaglandin E2 in postgastrectomy reflux gastritis. 354 41

In order to help clarify the clinical importance of chronic erosive gastritis, we describe our experience of 28 patients with this disorder who were seen over a 2-yr period. Twenty patients were male. Twenty-four patients presented with abdominal pain, for which no cause other than chronic erosive gastritis was found in 20 patients. Ten patients had pain for more than 1 yr. Three patients presented with painless vomiting. The antrum was involved in 27 patients and the body in 17 patients. There was no correlation between the number of erosions and the duration of symptoms. Double contrast barium meal was positive in nine of 21 patients. Of 19 patients treated with cimetidine, 15 improved clinically and six of eight had endoscopic improvement. The treatment of choice is unknown and controlled trials are needed. Symptoms in patients with chronic erosive gastritis appear to be due to the gastritis itself rather than to associated lesions.
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PMID:Chronic erosive gastritis: a clinical study. 356 32

Six patients with alkaline reflux gastritis postoperative were treated between 1977 and 1984 by Roux-en-Y diversion. All of the patients had a typical history of mild epigastric burning pain and bilious vomiting. The diagnosis was reached by endoscopic results of the gastric mucosa. The pain, complaints and the macroscopically apparent gastritis subsided completely after surgery but the histological manifestations of gastritis improved though no disappear. In four cases we used the Roux-en-Y procedure; in two, the Henley jejunal loop with the Soupault-Bucaile, technique. All patients were vagotomized for the fear recurrent peptic ulceration if increased the acid secretion. One patient was most complex because after derivation with Roux-en-Y developed severe diarrhea and was necessary to change to loop jejunal Henley and reversed 10 centimeter the jejunal loop at 1 meter from Treitz angle.
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PMID:[Postoperative alkaline reflux gastritis]. 357 20


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