Serum pepsinogen assays and gastric acid secretion.
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Biomedical subjects
Publications and source records attributed to F Vianello.
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BACKGROUND: Peptic ulcer has multifactorial aetiology, including genetic factors. We have identified a family with pepsinogen Group A levels higher than normal, with a high prevalence of ulcer disease and a low prevalence of Helicobacter pylori infection. AIMS: Performing linkage analysis in the identified family PATIENTS AND METHODS: We examined the segregation of pepsinogens with microsatellite dinucleotide repeat DNA markers along chromosome 11 (D11S480, PYGM) for pepsinogen Group A and along chromosome 6 [D6S105, D6S 1610, TRMI) for pepsinogen Group C. RESULTS: In markers examined along chromosome 11, linkage analysis provided no evidence for significant causal mutation but, controlling for some risk factors we observed that the probability of falling ill, increases. The linkage analysis along chromosome 6 for pepsinogen Group C did not show a uniform genetic profile. CONCLUSIONS: This study evaluates the hypothesis of peptic ulcer inheritance at least in a small group of patients without the common risk factors.
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As a factor favoring relapses, noncompliance is particularly crucial to the treatment of peptic ulcer disease, and greater efforts should be made to eliminate or reduce it. To investigate the reasons for noncompliance, we performed two clinical trials involving a total of 592 patients with duodenal ulcer treated with various H 2 antagonists for 12 months. In the first study, 40.3% of patients with uncomplicated duodenal ulcer were noncompliant, compared with only 4.6% who had had previous bleeding episodes. Compliance in the second study averaged 68%. Major reasons for noncompliance among these patients were an absence of symptoms and an inconvenient dosage schedule. On the basis of our clinical experience and a review of the literature, compliance appears to be higher in patients with previous complications of their disease and when the effectiveness of prescribed drugs does not depend on ingestion with the evening meal.
Glucose Oxidase (GOD) has been covalently bound to functionalized glass cover slips. The surface density of immobilized GOD molecules was measured by a method based on the amperometric determination of Flavin Adenine Dinucleotide (FAD). Atomic Force Microscopy (AFM) images, obtained in aqueous solution for the covalently bound enzyme, show a monomolecular layer of the enzyme on a functionalized glass surface. The catalytic constants were measured for the immobilized GOD and compared with those of the free enzyme.
The clinical course of gastric and duodenal ulcer and the efficacy of H2 blockers in ulcer healing and the prevention of relapse in cirrhotic liver patients were studied. Seventy-four cirrhotic patients with endoscopically proven acute gastric ulcer (30), duodenal ulcer (34) or a combination of both gastric and duodenal ulcers (10) were treated for six weeks with either Cimetidine 800 mg/daily (27) or Ranitidine 300 mg/daily (47). Of the 77 patients 49 (66.2%) were healed after therapy, 11 cases (14.8%) remained unhealed even after two additional cycles of the same treatment and four were lost to follow-up. After an endoscopically proven healing of the active ulcer, 51 patients took part in the long-term study over a mean period of 24 months: 21.5% of the 27 patients were treated with a maintenance dosage of H2 blockers and 29.1% of the 24 patients left without therapy relapsed during the first year. We conclude that the ulcer healing rate with H2 blockers is lower and the relapse rate higher in cirrhotic patients than in the general ulcer population.
The present investigation was undertaken with the aim of evaluating the clinical efficacy on dyspeptic symptoms associated with duodenogastric reflux gastritis of two drugs belonging to two different groups: a prokinetic (cisapride) and a cytoprotective agent (sucralfate). A total of 18 patients with duodenogastric reflux gastritis diagnosed on the basis of symptoms, endoscopy and histology were studied. Nine were given 30 mg of cisapride/daily and 9 4 g of sucralfate/daily for two months according to a randomization list. Pyrosis, epigastric pain, sense of epigastric repletion and foul-tasting mouth were considered on a scale from 0 to 4 attributed by the patient. The total score of dyspeptic symptoms significantly decreased only after cisapride (p less than 0.05). Considering each symptom alone, neither cisapride or sucralfate were able to significantly improve them. Cisapride seems to the better than sucralfate in improving dyspeptic symptoms associated with duodeno-gastric reflux gastritis.
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The effects of Nizatidine, an H2-receptor antagonist, and Misoprostol, a PGE1 analogue, on gastric pH, pepsin, pepsinogen group I and N-acetylneuraminic acid concentration were evaluated in a group of 20 patients with duodenal ulcer. Nizatidine decreased pepsin concentration while it increased gastric pH, although not to a significant degree and left pepsinogen group I and N-acetylneuraminic acid concentration unchanged. Misoprostol did not modify gastric pH, pepsin and N-acetylneuraminic acid values but it increased pepsinogen group I levels. These data support the view that H2-receptor antagonists, especially Nizatidine, and Misoprostol do not directly affect pepsin and/or N-acetylneuraminic acid concentration.
The function of G cells has been mainly evaluated by serum gastrin. A different analytical approach considers the direct determination of gastrin levels (ng/g of wet tissue) in perendoscopic biopsies, but, up to now, the results are contradictory. In the present study we evaluated, by means of a RIA method, the concentration of gastrin (ng/g of protein nitrogen) in homogenized gastroduodenal biopsies in 127 patients with peptic ulcer and in 12 dyspeptic patients. The results demonstrated: 1) a significant gradient of gastrin concentrations among the different anatomical sites, according to the distribution of the G cells; 2) a correlation with serum gastrin levels; 3) a good equivalence of gastrin content in adjacent biopsy specimens. This preliminary report indicates that it is possible directly quantitate tissue levels of gastrin by means of an accurate and simple method.
Several studies have shown an influence of cigarette smoking on serum pepsinogen group I (PGI) levels in duodenal ulcer patients and in control subjects. The elevation of PGI in smokers has just been interpreted as reflecting some degree of smoking-induced inflammation of the gastric mucosa. We have determined fasting serum PGI by radioimmunoassay in 163 healthy subjects investigated by a survey conducted on a sample population of an urban area in the North-East of Italy by means of a random selection based on the public registers of home addresses. The data reported confirmed that PGI levels are increased by smoking in a healthy population. The main contribution of this study consists in demonstrating in a non-selected population an increase of the only parameter up to date claimed to be a possible serological predictive index for ulcer disease.
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