Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was carried out to develop a scoring system for the diagnosis of gastric adenocarcinoma (GAC). A total of 686 subjects, 150 patients with GAC, 182 with gastric ulcer, 127 with duodenal ulcer, and 227 subjects with negative findings, were enrolled. Analysis of the likelihood ratio (LR) showed that patients with advanced age, ulcer in the stomach, low serum levels of pepsinogen I (PGI), low PGI x gastrin values, and low PGI/gastrin ratio were likely to have GAC. Of these indicators, the serum PGI level had the greatest weight, with a LR of 7.59 for the group with a level < 30 ng/ml. A scoring system combining serum PGI level, Helicobacter pylori seropositivity, and gastric ulcer status was derived, using a logistic regression model. This scoring system was found to be better than any one-parameter criterion for diagnosing GAC after evaluation by the area under the receiver operating characteristic curve (0.84; 95% confidence interval, 0.81-0.88) or by specificity-fixed sensitivity (sensitivity 0.82 at specificity 0.72, sensitivity 0.87 at specificity 0.66, sensitivity 0.96 at specificity 0.44). This scoring system may be potentially useful as a new model for the noninvasive diagnosis of GAC in the future.
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PMID:Diagnosis of gastric adenocarcinoma using a scoring system: combined assay of serological markers of Helicobacter pylori infection, pepsinogen I and gastrin. 777 44

In order to investigate the clinical usefulness of human pepsinogen I (PGI) as a noninvasive diagnostic tool for gastric lesions, 92 healthy volunteers, 87 patients with a gastric ulcer and 94 patients with gastric carcinoma, verified by histologic examinations, were enrolled. The serum level of PGI in each patient was measured by radioimmunoassay. Mean serum PGI levels were 95.4 +/- 39.4 ng/mL in patients with gastric ulcers, 77.6 +/- 29.3 ng/mL in healthy volunteers, and 52.1 +/- 26.5 ng/mL in patients with gastric carcinoma. Statistically significant differences (p < 0.01) existed between the two groups. Various factors which affect serum PGI levels, including age, sex, smoking habit, blood type, and Helicobacter pylori (H. pylori) infection, were also analyzed in each group. The serum levels of PGI were not affected by gender or blood type in any of the three groups (p > 0.05). A negative correlation of serum PGI levels with age was observed in patients with carcinoma (r = -0.43, p < 0.01). Smokers in the gastric ulcer group had significantly higher levels of PGI than nonsmokers (106.2 +/- 35.9 ng/mL vs 83.2 +/- 32.3 ng/mL, p < 0.05). A significantly higher PGI concentration was found in both H. pylori infected asymptomatic volunteers and gastric carcinoma patients (82.9 +/- 29.8 ng/mL vs 67.6 +/- 26.0 ng/mL, and 56.5 +/- 26.7 ng/mL vs 43.6 +/- 24.3 ng/mL, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum levels of pepsinogen I in healthy volunteers and patients with gastric ulcers and gastric carcinoma in Taiwan. 790 45

Helicobacter pylori (Hp) infection is thought to play an important role in for the pathogenesis of atrophic gastritis and even gastric carcinoma. The ratio of Pepsinogen I/II (P I/II) also shows good correlation with atrophic gastritis and gastric ulcer. Since many hemodialysis (HD) and renal transplantation patients suffer from gastrointestinal problems, we investigated the importance of Hp infection and P I/II in these patients. Serum Hp IgG was measured by EIA. Pepsinogen titer was measured with antipepsinogen antibody-bearing beads and anti-pepsinogen antibody. Hp positive HD patients accounted for 50.7% of the subjects. Of the renal transplantation patients, 23.5% were positive with lower values than the HD patients. The value of P I/II in all patients with a high Hp positive titer also was low (under 3). In conclusion, serum IgG antibody to Hp and P I/II exhibit good correlation and both are useful for the diagnosis of atrophic gastritis in chronic renal failure.
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PMID:[Importance of Helicobacter pylori infection and pepsinogen titer in hemodialysis and renal transplantation patients in Japan]. 807 24

This study was aimed to investigate the association of restriction fragment length polymorphisms (RFLPs) for pepsinogen genes with peptic ulcer disease. Eighty unrelated controls, 61 patients with gastric ulcer, and 57 patients with duodenal ulcer were studied. No genetic polymorphisms for pepsinogen A were detected by EcoRI digestion in Japanese subjects but a 100 base pairs insertion-deletion RFLP for the pepsinogen C gene was observed. The allele frequencies of the large (3.6 kilobase EcoRI fragment) and the small fragment (3.5 kilobase EcoRI fragment) were 80.6% and 19.4% respectively in controls, 55.4% and 44.6% in patients with gastric body ulcer, 79.4% and 20.6% in patients with gastric angular ulcer, 71.4% and 28.6% in patients with gastric antral ulcer, and 75.4% and 24.6% in patients with duodenal ulcer. The allele frequency of the small fragment was significantly higher in patients with gastric body ulcer than in controls and in patients with gastric angular or antral ulcer. The genotypes which possessed the small fragment were significantly more frequent in patients with gastric body ulcer (78.4%) than in controls (33.8%) and in patients with gastric angular or antral ulcer (37.5%). These results suggest that there is a significant association between the genetic polymorphism at the pepsinogen C gene locus and gastric body ulcer, and that the pepsinogen C RFLP is a useful marker of the genetic predisposition to this disorder. These results also indicate genetic heterogeneity of gastric ulcer disease, and suggest that the pepsinogen C RFLP may be a useful subclinical marker to explain the differences in genetic aetiologies of gastric body ulcer and gastric angular or antral ulcer.
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PMID:Pepsinogen C gene polymorphisms associated with gastric body ulcer. 809 9

In 25 patients with duodenal ulcer, before treatment and after three weeks, and another 30 days of treatment with ranitidine, plasma concentrations were determined of IgA, IgG, IgM immunoglobulins, and of 10 other proteins. In comparison to the control group of 20 persons, a statistically significant decrease was found in the concentration of alpha 2-M, prealbumins, and IgG, as well as a significant increase of alpha 1-AT, C4 complement component, and a non-significant increase of coeruloplasmin, haptoglobin and IgM. During the treatment a tendency was observed for an increase of IgG and IgM level, as well as a statistically significant decrease of alpha 1-AT, C4, and coeruloplasmin concentration. The treatment exerted no effect on the decreased level of alpha 2-M. It was accepted that the tendency for an increase of IgG and IgM level was due, most probably, to the immunostimulating action of ranitidine, and the changes of concentrations of other parameters induced by the treatment were related to the presence and healing of the ulceration. The observed decrease of alpha 2-M level was probably due to binding of alpha 2-M to pepsinogen whose blood level was increased during gastric ulcer.
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PMID:[Changes of IgA, IgG and IgM immunoglobulins and of 10 other plasma proteins in patients with duodenal ulcer treated with ranitidine]. 824 88

A modification of Berstad's spectrophotometric method was tested and proved capable of detecting pepsin concentrations in mucosal perendoscopic biopsy homogenates. The relationship between this parameter and pepsin in gastric juice and pepsinogen group I in serum and in biopsy homogenates was analyzed. From the biochemical point of view, the assay was found sufficiently accurate. Mucosal pepsinogen group I, but not mucosal pepsin, concentration was found higher in gastric and duodenal ulcer patients than in controls. Patients with corpus-fundic gastric ulcer showed significantly lower mucosal pepsin and mucosal pepsinogen group (PG) I. Aging and smoking did not influence either parameter but male duodenal ulcer subjects presented higher mucosal pepsinogen group I concentration. The lack of any relationship between serum and mucosal PG I and between pepsin in gastric juice and in mucosa raises a question, at least in methodological terms, about the validity of using serum pepsinogen group I and pepsin as indicators of peptic output.
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PMID:Pepsin concentration in gastroduodenal biopsy homogenates in chronic ulcer disease. 831 12

At the turn of the century, duodenal ulcer rose from rarity to affect 10% of males in their life time, subsequently declining in some countries such as UK, levelling off in others such as Germany, and continuing to increase in still others such as Hong Kong. The annual incidence per 1000 population varies from about 1 in Japan to 1.5 in Norway, 1.8 in USA and 2.7 in Scotland, and the frequency also varies within many individual countries, such as Australia, China and India, and among races such as a higher prevalence among whites than blacks in USA and among Chinese than Javanese in Indonesia. Ulcer frequency is higher in winter months, and this appears universal, being true in cold as well as in warm countries. Most places report a rise of ulcer rates among the elderly in recent decades. The male to female ratio also varies geographically, for example from 1:1 in USA to 18:1 in India, and with time such as moving from 2:1 to 1:1 in the last two decades in USA, and the duodenal ulcer to gastric ulcer ratio varies widely from place to place, for example from 0.8 in Japan to 19:1 in Africa and 32:1 in India. Placebo healing rates also differ geographically, ranging from 5% in Philippines to 78% in Mexico. These epidemiological data can only be explained by the presence of multiple aetiological factors, including analgesics, society stress, cigarette smoking, Helicobacter pylori, dietary factors, and genetic factors. Three lines of evidence support a genetic role: family studies, twin studies and blood group studies. Family aggregation occurs more commonly in patients with early-onset (< 30 yr) of symptoms. Blood group O prevalence is more associated with late-onset of symptoms. Other genetic markers include nonsecretor status, HLA antigens, phenylthiocarbamide taste sensitivity, and alpha-1-antitrypsin. Genetic syndromes such as MEN I also support a genetic role and give insight into pathogenetic mechanisms. The best physiological marker is still hyperpepsinogenemia I, which is transmitted by autosomal dominance, despite recent report of lower serum pepsinogen 1 after healing of Helicobacter pylori associated gastritis.
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PMID:Epidemiology and genetics of peptic ulcer. 835 24

To investigate the effect of the location of the ulcer crater on the serum levels of pepsinogen I (PGI), pepsinogen II (PGII) and the ratio of PGI/PGII, these parameters were determined in 161 healthy controls, 29 patients with gastric ulcer in the gastric body (GU-I), 65 with coexistent gastroduodenal ulcer (GU-II), 104 with gastric ulcer in the prepyloric region (GU-III), and 116 with duodenal ulcer (DU). Serum PGI levels were significantly higher (P < 0.01) in patients with GU-III (110.6 +/- 65.1 ng/mL), GU-II (100.0 +/- 46.6 ng/mL), and DU (92.2 +/- 35.2 ng/mL) than in the controls (77.4 +/- 31.4 ng/mL), while there were no significant differences between GU-I (82.5 +/- 36.3 ng/mL) and the controls. Patients with gastric ulcer in any region had significantly higher (P < 0.01) serum PGII levels (GU-I, 20.0 +/- 15.7 ng/mL; GU-II, 15.5 +/- 10.9 ng/mL; GU-III, 14.3 +/- 10.0 ng/mL) than the controls (10.6 +/- 6.0 ng/mL) and the patients with DU (10.0 +/- 5.5 ng/mL), whereas no significant differences existed between the latter two. The ratio of PGI/PGII in GU-I (5.86 +/- 3.90) was significantly lower (P < 0.01) than any other group (controls, 8.83 +/- 4.70; GU-II, 8.33 +/- 4.99; GU-III; 9.64 +/- 6.13; DU, 10.45 +/- 4.49), while patients with DU it was significantly higher (P < 0.01) than any other groups. These findings indicate that peptic ulcer is comprised of a heterogeneous group of diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum pepsinogen I and pepsinogen II, and the ratio of pepsinogen I/pepsinogen II in peptic ulcer diseases: with special emphasis on the influence of the location of the ulcer crater. 852 5

Non-invasive diagnosis of gastric adenocarcinoma (GAC) is usually difficult due to the low sensitivity and specificity of serologic markers,including pepsinogens and gastrin. For the improvement of the diagnostic values of these markers, a "recursive partitioning and amalgamation" algorithm was employed to construct a decision protocol. A total of 636 subjects including 161 healthy subjects, 163 patients with GAC, 196 with gastric ulcer and 116 with duodenal ulcer were enrolled. Serum levels of gastrin, pepsinogen I, pepsinogen II, and the ratio of pepsinogen I / pepsinogen II were determined for each of the subjects. The proposed "decision tree" classifies subjects into five subgroups with different risks of GAC and peptic ulcer, based on the information of age, serum pepsinogen and gastrin levels. Using this novel analysis system, an expected probability of GAC or ulcers could be obtained. Patients with an age > 62 years and a serum level of pepsinogen I < or = 33 ng/ml were strongly indicated for further confirmatory tests of GAC. This treestructured analysis is also helpful in clarifying the interactions between various serologic markers and demographic factors.
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PMID:A novel tree-structured analysis for non-invasive diagnosis of gastric adenocarcinoma. 866 56

The human gastric mucosa contains five isozymogens of pepsinogen (pepsinogens PGA1-PGA5), two isozymogens of gastricsinogen (gastricsinogens PGC6-PGC7) and zymogens of cathepsins. Ratios between some individual pepsins or pepsinogens are very important from a diagnostic point of view. The ratio of pepsinogen 3 to pepsinogen 5 is significant marker of gastric cancer and gastric ulcer. High-performance ion-exchange chromatography is an easy and fast method for determination of ratios between individual proteolytic zymogens in human gastric mucosa and thus could serve for additional diagnosis of gastric diseases.
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PMID:High performance liquid chromatography enables fast determination of ratios between individual proteolytic enzymes in human gastric mucosa. 871 9


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