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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tests of gastric secretion are seldom diagnostic in the investigation of gastric and duodenal ulceration, but they can provide evidence that is helpful in arriving at a diagnosis. Common tests include basal acid output, pentagastrin-stimulated maximal and peak acid output, and the Hollander test. There is some evidence that they may be useful in selecting the type of operation for peptic ulceration. Indications for performing these tests relate to the Zollinger-Ellison syndrome, duodenal ulcer, recurrent dyspepsia after operation for duodenal ulcer, and decisions concerning the choice of operation for peptic ulcer. In order to perform these functions they must be properly conducted and interpreted; they are simply an adjunct to clinical judgement, and complementary to other laboratory tests.
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PMID:Clinical usefulness of gastric acidity studies. 16 33

Sixty-one cases of the Zollinger-Ellison syndrome, encountered over a 2-year period, have been treated with cimetidine, half of them for over 1 year. Two-thirds of the patients responded to 300 mg of the drug every 6 hr by mouth. Others required up to 600 mg every 6 hr. In adequate doses the drug was highly effective: it controlled pain and dyspepsia, restored weight, abolished diarrhea, and allowed healing of ulcers and other inflammatory conditions. Missed or reduced doses led to rapid return of symptoms. Progression of the basic neoplastic process, with associated secretory drive, was unimpeded. Patient acceptance of the drug was 100 percent, and apart from minor transient abnormalities, gynecomastia (5 cases) and liver dysfunction (3 cases), which resolved while treatment continued, no serious adverse effects were seen. Of 61 patients 48 are still on the drug, 3 who were well controlled were treated surgically, 5 died for reasons unrelated to therapy, and 5 had significant problems. The drug provides an alternative to total gastrectomy and can be recommended with confidence for the suitably selected patients. The drug was also beneficial in some cases of the short bowel syndrome, systemic mastocytosis, and endogenous hyperhistaminemia due to leukemia.
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PMID:Report on the United States experience with cimetidine in Zollinger-Ellision syndrome and other hypersecretory states. 62 Sep 13

The quantification of mucus glycoproteins (GPs) faces paramount difficulties in terms of methods and interpretation. Mucus glycoprotein erosion, however, might be quantified in gastric juice by measurement of GP-bound sialic acid. Basal sialic acid content was low in normal healthy subjects (N) and in nonulcer dyspepsia (NUD) patients. They were five to six times higher in duodenal ulcer (DU), or more in Zollinger-Ellison patients. Pentagastrin stimulation induced a five- to sixfold rise in N and NUD patients although it did not affect DU patient sialic acid contents. Relationships between sialic acid content and pepsin output in DU indicate that pepsin exerts a variable mucolytic activity depending on disease evolution. In addition to pepsin, duodenogastric reflux exerts a potent mucolytic effect. Therapeutically, highly selective vagotomy without recurrent ulcer markedly reduced mucus erosion. The reduction of mucus erosion by protective drugs has been observed in some cases but in other cases sialic acid measurement did not allow to verify a protective effect. Adherent mucus analysis by high-performance liquid chromatography (HPLC) should allow one to appreciate GP fractions qualitatively. Combination of both methods should allow further determination of the mucus protective role, simultaneously investigating the adherent mucus quality and eroded GPs.
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PMID:Assessment of mucus glycoprotein erosion by measurement of sialic acid in gastric secretions: pathophysiologic and therapeutic aspects. 194 Jan 93

The heterogeneity of muscarinic receptors has been well supported by differential characteristics between pirenzepine and atropine both in receptor binding and in whole tissue pharmacology studies. Under these conditions pirenzepine has been classified as a selective receptor antagonist with high affinity for M1 receptors. The antisecretory properties of pirenzepine on gastric acid and pepsin secretion may be attributed to the antagonistic activity of the drug on muscarinic M1 receptors of gastric intramural plexuses, whereas the effect on parietal muscarinic M2 receptors seems of less importance. Additional inhibitory mechanisms on gastric secretion may be represented by pirenzepine-induced increase in somatostatin release from gastrointestinal system. Significant cytoprotective properties of pirenzepine have been observed on a variety of experimentally induced peptic ulcerations. This protective activity may be due to pirenzepine-induced increase in gastric mucosal blood flow as well as to the increase in gastric transmural electric potential difference. In accordance with this pharmacodynamic profile of pirenzepine, numerous clinical studies have revealed its efficacy in the treatment of both duodenal and gastric ulcerations. In addition to this, the clinical usefulness of the drug has been demonstrated in Zollinger-Ellison syndrome, in stress ulceration, in acute gastrointestinal bleeding as well as in gastritis, duodenitis and non-ulcer dyspepsia. In most of the studies pirenzepine has been found to be well tolerated with a low incidence of antimuscarinic effects which may occur at salivary, ocular, cardiac and urinary sites. The clinical use of pirenzepine alone or in association with H2 blockers is recommended in the treatment of peptic ulcer patients, in the case of acute gastrointestinal haemorrhage and in patients non responders to H2 antagonists.
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PMID:[A selective antimuscarinic agent: pirenzepine. Review of its pharmacologic and clinical properties]. 257 37

In the Zollinger-Ellison syndrome, symptoms and complications are due to hypersecretion of acid, and the first therapeutic step is to suppress the acid secretion. Long-term treatment with histamine H2-receptor antagonists was compared with omeprazole treatment. A total of 30 consecutive ZES patients were treated continuously with H2-receptor antagonists. During long-term treatment, a marked tachyphylaxis was noted, more than 50% of the patients had periods of dyspepsia, recurrent ulcers were found in 10 patients and in 16 a decline in the action of the H2-receptor antagonist required a change to omeprazole after a median duration of 36 months. A total of 22 patients were treated with omeprazole. During long-term treatment, the dose could be reduced slightly. Inhibition of acid secretion was maintained in all cases, and none had dyspeptic symptoms. The median duration of treatment was 18 months, with a range of 1-120 months (H2-receptor antagonists) and 27 months with a range of 1-66 months (omeprazole). No side-effects were seen with omeprazole.
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PMID:Effects of omeprazole on acid secretion and acid-related symptoms in patients with Zollinger-Ellison syndrome. 257 12

'Acid-related disorders' is a term used to describe a whole range of conditions from the Zollinger-Ellison syndrome, where acid is entirely responsible for the problems, to aerophagia and motility-type non-ulcer dyspepsia, where acid plays little if any role in the dyspeptic symptoms. Careful evaluation of the patient's symptoms is required to establish the basis for the dyspepsia and from that, careful selection can be made for any investigations that might be needed. These symptoms are the basis for advising on the most effective management--but as many doctors and patients erroneously attribute dyspepsia solely to acid, it is all too easy for inappropriate treatment to be offered. Acid is not the only cause of dyspeptic symptoms. Dyspepsia is a very common complaint with many causes. Acid and pepsin are often held responsible for these symptoms, by both the medical profession and the lay public. The term, 'acid-related disorders' is used to embrace this wide variety of conditions in which acid may play a part. However, in spite of current folklore, it is a spectrum of conditions ranging from situations where acid is crucial to conditions where acid may play little part.
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PMID:Acid-related disorders: what are they? 324 3

A case of Zollinger-Ellison syndrome with some peculiar aspects is described. The disease started with painless dyspepsia, watery diarrhea, relevant loss of body weight and absence of peptic ulcer. After a steroid treatment performed at home without any rationale, diarrhea stopped totally for 18 months and body weight returned to normal. Subsequently, the disease recurred with more typical clinical characters: juxtapyloric ulcer, increase in serum gastrin levels and positive secretin test, presence of gastrinomas at angiography. The monitoring of gastric pH showed a persistent hyperacidity during medical treatment with H2 and muscarinic antagonists. The localization of gastrinomas was extrapancreatic, at the root of jejunal mesentery. Excellent results were obtained by surgical treatment which consisted in resection of the principal neoplastic masses with total gastrectomy. The patient's general conditions after two years are good.
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PMID:[Description of a case of Zollinger-Ellison syndrome]. 632 67

Endocrine cells of the gastric oxyntic mucosa, and especially the enterochromaffin-like (ECL) cells, are the progenitors of gastrin-promoted proliferative lesions whose tumorigenic potential largely depends on the background condition in which they arise. Hypertrophic gastropathy due to the familial multiple endocrine neoplasia (MEN-1)-associated or sporadic Zollinger-Ellison syndrome (ZES), diffuse chronic atrophic gastritis restricted to the corpus-fundus (type A CAG), with or without associated pernicious anemia, and Helicobacter pylori-related multifocal chronic atrophic gastritis are the usual background for such growths. The endocrine cell lesions have been classified as pseudohyperplasia (cell clustering unassociated with cell proliferation), hyperplasia (diffuse, linear, micronodular, adenomatoid), dysplasia (enlarged, adenomatous or fused micronodules, microinfiltration, nodular growth), and neoplasia (intramucosal or invasive carcinoids). The entire spectrum of endocrine cell proliferation, from hyperplasia to dysplasia and neoplasia, has been observed in MEN-ZES and diffuse type A CAG. Both hyperplastic and pseudohyperplastic changes occur with some frequency in the H. pylori-related chronic gastritis associated with ulcer disease or dyspepsia. However, because no progression to dysplastic or neoplastic lesions has thus far been documented in these latter conditions, their role in gastric endocrine cell tumorigenesis appears negligible.
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PMID:Hyperplastic, dysplastic, and neoplastic enterochromaffin-like-cell proliferations of the gastric mucosa. Classification and histogenesis. 776 35

With rare exception, peptic ulcers can now be classified as either Helicobacter pylori-related, induced by nonsteroidal anti-inflammatory drugs (NSAIDs), or related to Zollinger-Ellison syndrome. Helicobacter pylori-related ulcers can be treated by eradication of H pylori or by traditional therapies, including antisecretory drugs or sucralfate. Successful eradication of H pylori requires compliance with a multidrug regimen. Therefore, candidates should demonstrate substantial motivation. In general, the greater the degree of ulcer recurrence or resistance, the stronger the indication for H pylori eradication. Sucralfate is effective in healing H pylori-related duodenal ulcers, and H2 receptor antagonists heal H pylori-related duodenal and gastric ulcers. Omeprazole provides faster healing of H pylori-related ulcers, and is particularly useful in treating large gastric ulcers. Dyspepsia induced by NSAIDs and NSAID-related endoscopic erosions are managed by stopping NSAID use or reducing the dosage; administering NSAIDs with meals; and administering H2 receptor antagonists in full split-doses. NSAID-induced duodenal ulcers and small gastric ulcers can be healed with full split-doses of H2 receptor antagonists, even while the NSAID is continued. Large (> 5 mm) NSAID-induced gastric ulcers are most efficiently treated with omeprazole, particularly if the patient continues to take the NSAID.
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PMID:An etiologic approach to management of duodenal and gastric ulcers. 828 53

Since the mid-seventies, it is possible to treat peptic ulcers and reflux oesophagitis with acid secretion inhibitors. The most important medicaments are H2-receptor antagonists (cimetidine was registered in 1977) and proton pump inhibitors (1988: omeprazole). Surgical treatment of these conditions is almost a thing of the past. Many Dutch researchers played an important part in clinical research of acid secretion inhibitors; the first studies of effect and safety were done in patients with severe overproduction of gastric acid (Zollinger-Ellison syndrome) and in those with severe reflux oesophagitis. At present the most important syndromes in which acid secretion inhibitors are used are gastroesophageal reflux disease, gastric or duodenal ulcers and acid-related dyspepsia.
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PMID:[25 years of gastric acid blockers]. 1062 49


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