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

The main clinical signs of three dogs with Zollinger-Ellison syndrome were vomiting, diarrhoea, poor appetite and weight loss. The diagnosis was confirmed by histological examination and by gastrin immunocytochemistry. Gastrin was extracted from pancreatic tumours of two dogs. Gastrin-component III predominated in one dog while gastrin-component II and gastrin-component III were demonstrated in almost equal amounts in the other dog. In one dog serum gastrin concentration was high. Postmortem examination revealed pancreatic tumours in all three dogs and metastases in the regional lymph nodes and liver in two. The pancreatic tumours contained three patterns of growth: solid, trabecular and acinar. Electron microscopy of liver metastases showed cells with secretory granules. In all three dogs there was an erosive oesophagitis and thick gastric mucosa caused mainly by glandular proliferation. Two dogs had erosions and ulcers in the duodenum, one also in the first part of the jejunum. Villous atrophy and cellular infiltration of the duodenal mucosa were found in all dogs.
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PMID:Zollinger-Ellison syndrome in three dogs. 624 88

Billroth II resection was carried out in 1000 duodenal ulcer patients in the period 1948-1956. Twenty-two to thirty years later, gastroscopy and biopsy was performed in 196 of 423 survivors. Chronic atrophic gastritis appeared in 93 per cent of the cases, 47 per cent showed slight and 46 per cent severe changes. Seven per cent had normal mucosa. The microscopic grade of gastritis proved to be independent of age, alcohol and tobacco consumption and serum gastrin. No correlation between clinical status, such as dumping, diarrhoea, vomiting and pain, haematological parameters and the microscopic grade of gastritis, could be found. It is suggested that gastritis might be caused by reflux of bile, pancreatic and intestinal juices, and that postgastrectomy symptoms and anaemia do not depend on the microscopic grade of gastritis.
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PMID:Causes and clinical significance of gastritis following Billroth II resection for duodenal ulcer. 686 Sep 6

Infantile hypertrophic pyloric stenosis is a relatively common condition and there is some recent evidence that the incidence is increasing in this country. Gastric outlet obstruction is caused by hypertrophy of the pyloric smooth muscle and the clinical presentation is with non-bilious vomiting starting at the age of 3-4 weeks. The diagnosis can usually be made by palpation of the hypertrophied pylorus. Operation has now superseded medical treatment as the treatment of choice but meticulous assessment and correction of fluid and electrolyte imbalance is essential preoperatively. The operation of pyloromyotomy as described by Ramstedt in 1912 is simple and effective, but attention to detail is necessary if minimal morbidity and zero mortality are to be achieved. Untreated, the mortality is high but, after successful treatment, these babies are healthy and normal, so that treatment is both worth while and gratifying. The aetiology is obscure; a polygenic pattern of inheritance has been shown to be a predisposing factor, but the postnatal precipitating factors are less defined. Early hopes that the hormone gastrin might prove to be the key have not been sustained by more recent research, but the role of other gastrointestinal hormones awaits clarification.
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PMID:Infantile hypertrophic pyloric stenosis: a review. 703 56

The hypothesis that reflux of upper intestinal content, particularly of bile acids (BA), is responsible for a unique postgastrectomy syndrome, alkaline reflux gastritis, was tested on 28 occasions in 21 postoperative patients (14 symptomatic patients, 7 controls). Parameters evaluated: recumbent (rec.), upright, p.c. intragastric pH, {BA}, net BA reflux per hour, specific BA fractions, fasting and p.c. gastrin, maximal acid output (MAO), gastric emptying of solids by delta-scintigraphy), and the severity of nonstomal histologic gastritis, the "gastritis score," graded 0-15 by an independent senior pathologist. For the entire group, gastritis severity correlated positively with intragastric {BA} and net BA reflux per hour, both in recumbency and p.c. Five symptomatic patients demonstrated rec. and p.c. {BA} and net BA reflux per hour greater than two standard deviations from comparable mean values in control patients. They differed significantly from the remaining symptomatic patients as follows: increased intragastric {BA} and net BA reflux per hour, increased intragastric pH and decreased MAO. They also demonstrated a more severe grade of gastritis. Lithocholic acid was present in their reflux content significantly more often. Bilious vomiting was also more frequent. No other differences could be identified, either objectively or clinically, between the symptomatic groups. Four patients with excessive reflux underwent Roux-en-Y revision and restudy 6-22 months later. BA reflux was completely abolished, histologic gastritis improved, hematocrit rose, MAO increased, and gastric emptying slowed. Burning pain, bilious vomiting, and symptoms of esophageal reflux were eliminated. Vomiting and nausea were improved. Diarrhea was unchanged. The objective criteria outlined can identify symptomatic postgastrectomy patients with a greater than normal reflux and gastritis. Clinical criteria alone cannot. Revisional surgery in these patients eliminates reflux, improves gastritis, and produces symptomatic improvement. The hypothesis under consideration is strengthened but not proven.
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PMID:Alkaline reflux gastritis. An objective assessment of its diagnosis and treatment. 741 26

We evaluated in children with abdominal complaints the prevalence of Helicobacter pylori gastric and duodenal colonization and the histological features of gastric and duodenal mucosae. Fifty patients, aged 1-17 years, underwent upper endoscopy for recurrent abdominal pain, vomiting and/or gastrointestinal bleeding. With serological, bacteriological and/or histological methods twenty-eight children were demonstrated to be Helicobacter pylori-positive. No statistically significant differences were observed with regard to age, sex and indication to perform endoscopy. Eighty-two percent of Helicobacter pylori-positive patients had gastritis and/or duodenitis. The Helicobacter pylori-positive children had higher Helicobacter pylori specific IgG levels than the Helicobacter pylori-negative ones (p < 0.001). No statistically significant differences were found between Helicobacter pylori-positive and Helicobacter pylori-negative subjects, for gastrin and pepsinogen I. Since the frequency of Helicobacter pylori infection in children with gastrointestinal complaints is high, in patients undergoing upper endoscopy, the sistematical examination of bioptic samples for bacteriological and histologic procedures is of great importance.
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PMID:[High incidence of Helicobacter pylori infections in an endoscopic pediatric patient series]. 780 63

Many patients with acid-peptic disease have idiopathic gastric acid hypersecretion defined as a basal acid output > 10.0 meq/hr; however, a significant proportion have basal acid outputs > 15.0 meq/hr, which is within the range found in Zollinger-Ellison syndrome. Although idiopathic gastric acid hypersecretion is more common than Zollinger-Ellison syndrome, it is important that these two disorders be differentiated because of differences in treatment and natural history. In the present study, we compared 124 patients with idiopathic gastric acid hypersecretion and 137 patients with Zollinger-Ellison syndrome. There were no significant differences with regard to age at diagnosis, history of upper gastrointestinal hemorrhage, nausea, vomiting, and family history of duodenal ulcer and other acid-peptic disease. However, significant differences were observed between patients with idiopathic gastric acid hypersecretion and patients with Zollinger-Ellison syndrome with regard to percentage of males: 77% compared to 64% (P = 0.008), mean serum gastrin: 60 pg/ml compared to 3679 pg/ml (normal < 100 pg/ml) (P < 0.001), mean basal acid output: 15.4 meq/hr compared to 47.0 meq/hr (P < 0.001), mean age at onset of symptoms: 33 years compared to 41 years (P < 0.001), mean duration of symptoms before diagnosis: 11 years compared to five years (P < 0.001), percentage with abdominal pain: 67% compared to 82% (P = 0.00004), percentage with diarrhea: 12% compared to 75% (P < 0.000001), percentage with pyrosis: 58% compared to 40% (P = 0.003), percentage with duodenal ulcer: 53% compared to 74% (P < 0.000001), and percentage with esophagitis: 31% compared to 42% (P = 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Idiopathic gastric acid hypersecretion. Comparison with Zollinger-Ellison syndrome. 802 53

We report an impressive case with Zollinger-Ellison syndrome (ZES), in which stress-induced sympathetic discharge influenced serum gastrin. Our patient was a 35-yr-old female who complained of frequent and massive vomiting (more than 4000 ml of gastric juice) which was aggravated especially by psychosocial stress. Basal hypergastrinemia (1900 pg/ml) was found after the admission. The most striking finding was that laboratory stress dramatically increased serum gastrin (from 1900 to 5400 pg/ml) and plasma noradrenaline (from 180 to 1130 pg/ml). Mental arithmetic stress further enhanced hypergastrinemia (5800 pg/ml) with a concomitant increase in plasma noradrenaline (1240 pg/ml). Neostigmine (10 micrograms/kg im) also increased serum gastrin up to 6100 pg/ml but propranolol (40 micrograms/kg i.v.) reduced these elevations (noradrenaline: 990 pg/ml, gastrin: 5000 pg/ml). In this case, the effect of stress on serum gastrin mimicked the effect of catecholamine infusion in ZES. These findings suggest that psychological stress induces serum gastrin secretion via beta-adrenoceptor with exacerbation of symptoms in some cases with ZES.
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PMID:Impact of stress on serum gastrin in Zollinger-Ellison syndrome. 836 43

The ferrets' responsiveness to several known and putative emetic agents was evaluated using a variety of agents that were injected subcutaneously and/or intravenously. Apomorphine was consistently emetic at relatively high doses (100 micrograms/kg) when injected subcutaneously in large male ferrets (> or = 1.4 kg). The responsiveness to apomorphine was anomalous in that subcutaneous injections produced a more consistent response than intravenous ones. In addition, ferrets rapidly become tolerant or tachyphylactic to subcutaneously administered apomorphine. Area postrema ablation, but not abdominal vagotomy, rendered ferrets refractory to the emetic effects of apomorphine. This species, relative to dog and humans, proved to be insensitive to a variety of pharmacologic agents including angiotensin II, gastrin, histamine, Leu-enkephalin, neurotensin, serotonin, and vasopressin. Cisplatin elicited forceful retching and emesis. Emetic responses were obtained with substance P and Met-enkephalin in individual animals but were inconsistent. Sensitivity to DAGO [D-Ala2,MePhe4,Gly-ol5 enkephalin] was variable. Results of this study indicate that the ferret is not an optimal model for all forms of emesis.
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PMID:Behavioral studies of emetic sensitivity in the ferret. 849 72

Feeding problems, anorexia and vomiting are common in infants and children with chronic renal failure (CRF), and play a major role in the growth failure often found in this condition. However, the gastroenterological and nutritional aspects of CRF in children have received little attention, hence therapeutic interventions are usually empirical and often ineffective. Gastritis, duodenitis and peptic ulcer are often found in adults with CRF on regular haemodialysis and following renal transplantation. Despite persistent hypergastrinaemia, gastric acid secretion is decreased rather than increased in most of these patients, and active peptic disease appears to be promoted by the removal of the acid output inhibition (neutralisation of gastric acid by ammonia) that follows active treatment. Helicobacter pylori, on the other hand, does not seem to play a significant role in the pathogenesis of peptic disease in CRF. Gastro-oesophageal reflux has been found in about 70% of infants and children with CRF suffering from vomiting and feeding problems, and thus appears to be a major problem in these patients. In a number of symptomatic patients with CRF, gastric dysrhythmias and delayed gastric emptying have also been found; hence there appears to be a complex disorder of gastrointestinal motility in CRF. Serum levels of several polypeptide hormones involved in the modulation of gastrointestinal motility [e.g. gastrin, cholecystokinin (CCK), neurotensin] and the regulation of hunger and satiety (e.g. glucagon, CCK) are significantly raised as a consequence of renal insufficiency, and can be reverted to normal by renal transplantation. Furthermore, several other humoral abnormalities (e.g. hypercalcaemia, hypokalaemia, acidosis, etc.) are not uncommon in CRF. By directly affecting the smooth muscle of the gut or stimulating particular areas within the central nervous system, all these humoral alterations may well play a major role in the gastrointestinal dysmotility, anorexia, nausea and vomiting in patients with CRF. Specific pharmacological and nutritional interventions should thus be considered for the treatment of vomiting and feeding problems in CRF.
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PMID:Gastrointestinal function in chronic renal failure. 874 22

To investigate changes in motility of the extrahepatic biliary system associated with emesis, we measured the volume of the gallbladder and flow resistance through the sphincter of Oddi, as well as antral and duodenal contractilities before and during retching in decerebrate paralyzed dogs. Motilities of the gallbladder, sphincter of Oddi, duodenum and antrum were enhanced with most episodes of fictive retching elicited by stimulation of the central part of the severed dorsal, as well as the ventral trunk of the thoracic vagus nerve. These enhanced motilities persisted until the end of retching. Motilities of the sphincter of Oddi and duodenum were sometimes transiently depressed at the beginning of retching. This depression in the sphincter continued for only 13 +/- 1.0 s, while the gallbladder contraction continued for 65 +/- 3.4 s. Motilities were rarely enhanced by vagal stimulation when retching was not elicited. These changes in motilities were abolished by bilateral vagotomy. The serum gastrin level was increased just after and 10 min after retching only when the ventral vagal trunk remained intact, while the plasma cholecystokinin level was not changed with retching. These results suggest that bile evacuation is interrupted with emesis despite contraction of the gallbladder during retching, since the sphincter of Oddi also contracts simultaneously.
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PMID:Changes in extrahepatic biliary motilities with emesis in dogs. 878 85


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