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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood serum insulin, glucagon, pepsinogen, trypsin was studied by radioimmunological methods in 95 patients with ulcer disease. Fasting values and values 1 and 2 hours after a standard breakfast (1212 kcal) were evaluated. It was established that all patients showed a statistically valid increase of the basal level of glucagon while patients with gastric ulcer showed an increase of the basal insulin level. Use of a test breakfast showed reserve and compensatory capacities of the hormonal pancreatic function. Patients with gastric and duodenal ulcer revealed an increase of the pepsinogen level under conditions of basal secretion and after a test breakfast.
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PMID:[Pancreatic hormonal function and proteolytic activity in peptic ulcer]. 208 6

Anatomically, functionally, and clinically, peptic ulcer patients are a heterogeneous group of subjects. These patients can be classified according to the anatomic localization of the niche. The functional state of the gastric mucosa was studied in 30 gastric ulcer patients, 25 duodenal ulcer patients, and 10 normal controls. The classification of the first group was based on Johnson's criteria, with the following results: 10 individuals were type I, 10 were type II, and 10 were type III. Pepsinogen I levels and gastric acid secretion were measured in all 65 subjects under basal conditions and after subcutaneous pentagastrin stimulation. Both basal and stimulated serum pepsinogen I values were significantly higher (p less than 0.05) in gastric ulcer type III patients than in the other four groups. These values in gastric ulcer type I were similar to those of the controls. Gastric ulcer type II patients showed an intermediate functional state similar to that of duodenal ulcer patients. In both gastric ulcer type II and duodenal ulcer patients, the basal and stimulated pepsinogen I levels were significantly higher (p less than 0.05) than those found in controls, whereas the basal serum gastrin levels were similar in the five groups. In conclusion, different HCl and pepsinogen I secretory patterns, with functional heterogenicity of the gastric mucosa, are shown here for the anatomically defined gastric ulcer subsets.
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PMID:Different HCl and pepsinogen I secretion patterns in anatomically defined gastric ulcer subsets. 233 56

Ability to taste phenylthiocarbamide is genetically determined and has been investigated as a possible genetic marker for disease. This study examined phenylthiocarbamide taste sensitivity in gastric and duodenal ulcer disease. The study sample included 164 patients with gastric ulcer, 134 with duodenal ulcer, and 299 community controls. Eight concentrations of phenylthiocarbamide in distilled water were obtained by binary serial dilution. The lowest concentration distinguished by taste from distilled water defined taste threshold. Bimodality of threshold distributions distinguished nontasters from tasters. Comparisons of patients with controls gave odds ratios of nontaste in gastric ulcer and duodenal ulcer of, respectively, 0.7 (P greater than 0.1) and 1.3 (P greater than 0.03). The power of detecting at least a twofold difference between patients and controls in the odds of nontaste was 80%. Nontaste was more common in duodenal than in gastric ulcer patients (odds ratio = 2.0, P = 0.02). Taste sensitivity was unassociated with other genetic factors related to ulcer--ABO blood group, secretor status, and serum pepsinogen 1 level. The difference between gastric and duodenal ulcer patients in the ability to taste phenylthiocarbamide may be genetic; however, this study's inability, despite substantial power, to detect at least a twofold difference between patients and controls suggests that if phenylthiocarbamide taste sensitivity is a genetic factor in peptic ulcer, the relationship is weak.
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PMID:Phenylthiocarbamide taste sensitivity in chronic peptic ulcer. 234 42

Ninety-seven consecutive patients with gastric surgery for peptic ulcer were studied; 86 had duodenal ulcer (DU), and 11 gastric ulcer (GU). DU patients were surgically treated by proximal vagotomy, proximal vagotomy and pyloroplasty, truncal vagotomy and pyloroplasty, or truncal vagotomy and antrectomy. All GU patients were operated on by the Billroth I method. Serum pepsinogen I(S-PG I), serum pepsinogen II (S-PG II), basal acid output (BAO), and maximal acid output (MAO) were determined before and 3 months and 1 year after the operation. The mean preoperative S-PG I concentration in DU patients (154 +/- 7 micrograms/l; mean +/- SE) was significantly higher than that (97 +/- 9 micrograms/l) in GU patients (p less than 0.001). A significant decrease in the mean S-PG I concentration in DU patients was seen 3 months (92 +/- 6 micrograms/l) and 1 year (66 +/- 4 micrograms/l) after the operation (p less than 0.001). This change did not depend on the type of vagotomy. However, this decrease was not seen in all individual patients as it was in BAO values. Moreover, the mean BAO decrease was much greater at 3 months (7% of the preoperative value) and 1 year (23%) after the operation than the respective decrease in S-PG I concentration. There was also no correlation between S-PG I and acid output (BAO and MAO) before and after the operation. In GU patients the decrease in mean S-PG I value after the Billroth I operation was smaller than in DU patients after vagotomy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of vagotomy and antrectomy on serum pepsinogens I and II. 235 72

In this revision article it was tried to focus on the role played by pepsinogen/pepsin since its discovery until its practical use. Pepsinogen determination as the gastric acid secretion has different basal or stimulated secretion levels in the peptic ulcer, gastritis, etc. The methods for pepsinogen determination are evaluated, verifying that, in spite of radioimmunoassay utilization another methods less sophisticated have been used successfully. The pepsinogen seric levels (PSL) after stimulation with Histalog, discriminate the patients suffering from duodenal ulcer from normal individuals, and they are higher among men than women. A parallelism is made between pepsinogen-I and II finding out pepsinogen-I higher level in smoking individuals. The pepsinogen-I is increased in the duodenal ulcer and II in the gastric ulcer and both of them bent to be characterized as a genetic marker for peptic ulcer. Finally, the main clinical applicability for PSL group I determination is the detection of atrophic gastritis considering its potential for gastric malignancy.
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PMID:[Pepsinogen I and duodenal ulcer]. 306 7

The role of pepsin in the pathogenesis of peptic ulcer has been the subject of intense study and debate for many years. Two difficulties inherent in distinguishing between the role of acid alone vs acid and pepsin are that a) acid-containing gastric juice always contains pepsin, and, b) that hydrogen ion concentration (pH) is a major determinant of the activity of pepsin. However, studies in animal models of peptic ulcer indicate clearly that pepsin, in combination with acid, produces much more severe and more extensive mucosal damage than acid alone. Recent interest in pepsin and its precursor, pepsinogen, has stemmed from the finding that each is remarkably heterogeneous, and that the heterogeneity has a genetic basis. Results of studies using radioimmunoassays specific for the 2 major forms of pepsinogen, pepsinogen I and pepsinogen II, have shown that serum levels of pepsinogen I and pepsinogen II, and the ratio of pepsinogen I to pepsinogen II, can be used as noninvasive probes of gastric mucosal structure and function, indicators of the genetics and heterogeneity of duodenal ulcer, and as markers of increased risk for duodenal ulcer and gastric ulcer.
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PMID:Pepsinogens, pepsins, and peptic ulcer. 311 99

Serum pepsinogen I and pepsinogen II levels in 369 healthy controls, 38 duodenal ulcer, 30 gastric ulcer and 46 stomach cancer including 21 early and 25 advanced gastric cancer patients were measured by enzyme-linked immunosorbent assays using pepsin moiety-reacting monoclonal antibodies to pepsinogens I and II. Serum pepsinogen I and pepsinogen II levels were higher in the duodenal and gastric ulcer groups than in the control. Although there was no significant difference in serum pepsinogen II between stomach cancer and control, serum pepsinogen I was significantly lower in the former than in the latter and also in advanced gastric cancer than in early gastric cancer. A specific negative correlation of serum pepsinogen I with patient age was observed in stomach cancer but not in peptic ulcer or control groups. Receiver operating characteristic analysis was performed and indicated that serum pepsinogen I, compared with serum pepsinogen II or the pepsinogen I/pepsinogen II ratio, is the most effective marker for stomach cancer.
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PMID:Enzyme-linked immunosorbent assays for serum pepsinogens I and II using monoclonal antibodies--with data on peptic ulcer and gastric cancer. 316 82

We measured serum pepsinogen I (sPG-I) in 269 patients undergoing upper GI endoscopy and then classified by endoscopic diagnosis, gastric mucosal histology, and smoking habit. Both ulcer-free and duodenal ulcer smokers had significantly higher sPG-I levels than their non-smoking controls. In contrast, sPG-I values were not different in smokers and non-smokers with gastric ulcer. In ulcer-free smokers the overall increase in sPG-I simply reflected the high prevalence of patients with superficial gastritis and elevated sPG-I levels. Conversely, in duodenal ulcer smokers the increase in sPG-I, which was related to the number of cigarettes smoked daily, was not an epiphenomenon of concomitant gastritis. The smoking-induced increase in sPG-I in duodenal ulcer is proposed to reflect an augmented pepsin secretory capacity, which can be of aetiologic significance in the association between cigarette smoking and duodenal ulcer.
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PMID:Serum pepsinogen I elevation in cigarette smokers. 339 33

The present study explored the 24-hr variations in serum gastrin and pepsinogen in clinically healthy subjects and in patients with gastric ulcer, duodenal ulcer, and erosive gastroduodenopathy. Time-qualified data were analyzed by means of cosinor procedures. Significant changes in rhythmometric properties were documented in patients with peptic disease when compared to clinically healthy subjects. In essence, it was discovered that gastric ulcer patients exhibit a higher mesor and amplitude for both gastrin and pepsinogen, whereas duodenal ulcer patients and those with erosive gastroduodenopathy show only a significant increase in the pepsinogen mesor. These characteristics are so specific in the groups investigated that one can hypothesize that the disorders in the circadian rhythmicity of gastrin and pepsinogen have a role in determining the clinical manifestations of peptic disease.
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PMID:Peptic disease and 24-hr patterns of serum gastrin and pepsinogen. 360 74

One hundred and forty-four patients with apparently benign gastric ulcer were endoscopically followed up in order to evaluate the outcome of the lesion. Particular attention was given to: (a) detect possible delay in diagnosing gastric cancer; (b) ascertain the frequency of association with epithelial dysplasia; (c) establish the role of markers, such as serum pepsinogen group I (PGI), and gastric juice CEA in predicting gastric ulcer evolution. Endoscopic and bioptic check-ups were carried out during the first year at 3, 6 and 12 months after endoscopic healing of the ulcer, and then at every symptomatic recurrence. Ten patients (6.9%) were found to present histological evidence of malignancy (within 3 months in six cases, between 6 and 12 months in three cases, and after 41 months in the rest). Four cases were early gastric cancers, and six had shown dysplastic changes of the mucosa at the edge or scar of the ulcer. Serum PGI levels were not significantly different in gastric cancer patients, while gastric juice CEA levels were sharply increased compared to those of gastric ulcer patients: nine out of ten patients had values above normal range. These data suggest that: (a) there may be some delay in diagnosing gastric carcinoma, and gastric ulcer patients should be controlled routinely more than once; (b) the presence of dysplasia indicates the need for prolonged follow-up, because of the high risk of association with or evolution into gastric cancer, and because of the higher number of early gastric cancer detections that this protocol allows; (c) further support in monitoring patients "at risk" may be afforded by gastric juice CEA determination.
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PMID:Early and advanced gastric cancer during follow-up of apparently benign gastric ulcer: significance of the presence of epithelial dysplasia. 369 32


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