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)

A hybridoma monoclonal antibody against human pepsinogen I was used to develop an enzyme-linked immunosorbent assay for pepsinogen I in serum. In the two-step competitive procedure using antimouse immunoglobulin F(ab')2 fragment coupled to alkaline phosphatase, the measurable assay range was 8-256 micrograms/l. No cross-reactivity with rat pepsinogen 1, human pepsinogen II, gastrin I, bombesin, somatostatin and peptide YY was shown. However, there was slight cross-reactivity (0.09%) with porcine pepsinogen. The coefficients of variation within and between series were 7.6% and 13.0%. This enzyme-linked immunosorbent assay for serum pepsinogen I correlated positively with radioimmunoassay (r = 0.87, n = 92). The concentration range of serum pepsinogen I in 354 healthy controls was 15-100 micrograms/l with a lognormal distribution. Serum pepsinogen I levels were significantly higher in the subjects who developed active duodenal ulcer or active gastric ulcer, but significantly lower in those who had gastric cancer, than in control subjects.
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PMID:Enzyme-linked immunosorbent assay of serum pepsinogen I. 380 50

We investigated the possibility that serum pepsinogen I (PG I) and pepsinogen II (PG II) levels might differ as risk factors for duodenal ulcer and gastric ulcer. From 1967 to 1970, serum was obtained from 7498 Japanese men in Hawaii, and the cohort was followed up to 1981 for the development of peptic ulcer disease. Pepsinogen I and PG II levels in stored serum were significantly higher in the subjects who developed duodenal ulcer (n = 43) or gastric ulcer (n = 115) than in 212 control subjects. The linear trend in risk of each type of ulcer was highly significant for both PG I and PG II. An elevated serum PG I level (greater than or equal to 130 micrograms/L), however, was associated with about a threefold higher odds ratio for duodenal ulcer than for gastric ulcer (8.37 vs. 2.83), whereas an elevated PG II level (greater than or equal to 30 micrograms/L) was associated with about a threefold higher odds ratio for gastric ulcer than for duodenal ulcer (18.21 vs. 6.49). In contrast, the PG I/PG II ratio was significantly lower in the gastric ulcer than in the control and duodenal ulcer cases, and showed a significant linear trend in risk only for gastric ulcer. In addition, a PG I/PG II ratio of less than 4.0, which has been shown previously to be indicative of chronic gastritis, was associated with an almost 10-fold higher odds ratio for gastric ulcer than for duodenal ulcer (7.35 vs. 0.79). The results indicate that an elevated serum PG I level is a major risk factor for duodenal ulcer, whereas an elevated serum PG II level and a low PG I/PG II ratio are major risk factors for gastric ulcer.
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PMID:Elevated serum pepsinogen I and II levels differ as risk factors for duodenal ulcer and gastric ulcer. 394 88

Fundic mucosal pepsinogens reveal six major bands of protease activity on gel electrophoresis and four minor bands. Antral mucosa shows two major bands of activity; the four rapidly moving bands found in fundic mucosa are found in lesser activity in the antral mucosa. Duodenal mucosa shows only one slowly moving band of protease activity. There is a significant difference in the pepsinogen pattern when the uninvolved fundic mucosa of gastric ulcer patients is compared with that of cancer patients.A satisfactory method is described for separating the pepsinogens on column chromatography.
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PMID:The pepsinogens of human gastric mucosa. 458 32

In the United States about four million people have active peptic ulcers and about 350,000 new cases are diagnosed each year. Four times as many duodenal ulcers as gastric ulcers are diagnosed. Approximately 3000 deaths per year in the United States are due to duodenal ulcer and 3000 to gastric ulcer. There has been a marked decrease in reported hospitalization and mortality rates for peptic ulcer in the United States. Changes in criteria for selecting the underlying cause of death might account for some of the apparent decrease in ulcer mortality rates. Hospitalization rates for duodenal ulcers decreased nearly 50 per cent from 1970 to 1978, but hospitalization rates for gastric ulcers did not decrease. Although this decrease in hospitalization rates may reflect a decrease in duodenal ulcer disease incidence, it appears that changes in coding practices, hospitalization criteria, and diagnostic procedures have contributed to the reported declines in peptic ulcer hospitalization and mortality rates. There is no good evidence to support the popular belief that peptic ulcer is most common in the spring and autumn. The most consistent pattern appears to be low ulcer rates in the summer. There is strong evidence that cigarette smoking, regular use of aspirin, and prolonged use of steroids are associated with the development of peptic ulcer. There is some evidence that coffee and aspirin substitutes may affect ulcers, but most studies do not implicate alcohol, food, or psychological stress as causes of ulcer disease. Genetic factors play a role in both duodenal and gastric ulcer. The first-degree relatives of patients with duodenal ulcer have a two- to threefold increase in risk of getting duodenal ulcer and relatives of gastric ulcer patients have a similarly increased risk of getting a gastric ulcer. About half of the patients with duodenal ulcer have elevated plasma pepsinogen I. A small increase in risk of duodenal ulcer is found in persons with blood group O and in subjects who fail to secrete blood group antigens into the saliva. In most Western countries, morbidity from duodenal ulcer is more common than from gastric ulcer, even though deaths from gastric ulcer exceed or equal those from duodenal ulcer. In Japan, both morbidity and mortality are higher for gastric ulcer than for duodenal ulcer.
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PMID:Epidemiology of peptic ulcer disease. 637 41

Serum group I pepsinogen (PG I) levels were measured by radioimmunoassay in patients with peptic ulcer and normal subjects. The mean (+/-S.E.) serum PG I level in 318 normal subjects was 79 +/- 3 ng/ml. The level in males, 87 +/- 2 ng/ml (n = 246), was significantly higher than in females, 72 +/- 4 ng/ml (n = 72). The serum PG I levels in the patients with gastric ulcer and in those with duodenal ulcer were 91 +/- 7 ng/ml (n = 31) and 117 +/- 10 ng/ml (n = 31), respectively. Both values were significantly higher than the value in the subjects with endoscopically normal mucosa (63 +/- 5 ng/ml). No significant change in serum PG I was observed after subcutaneous injection of tetragastrin or after ingestion of meal. A significant correlation was found between serum PG I and stimulated pepsin output, peak pepsin output, and maximal acid output and peak acid output. These findings suggest that serum PG I may be determined by the chief cell mass.
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PMID:Serum group I pepsinogen levels in patients with peptic ulcer and normal subjects. 640 6

We measured serum group I pepsinogen (PG I) levels in subjects with endoscopically normal gastric and duodenal mucosa and patients with peptic ulcer. The release mechanism of PG I into blood stream was also investigated. The mean (+/- S.E.) serum PG I level in 136 subjects with endoscopically normal mucosa was 61 +/- 2 ng/ml and the normal range was calculated to be 30-109 ng/ml from the frequency distribution. In the patients with unoperated recurrent duodenal ulcer, the serum PG I levels remained high with the healing process of the ulcer. On the other hand, in the patients with non-recurrent duodenal ulcer and those with recurrent or non-recurrent gastric ulcer, the serum PG I levels decreased with the healing process of the ulcer gradually and significantly from the value in the active stage. These findings suggest that duodenal ulcer patients with high levels of serum PG I throughout the healing process of the ulcer tend to have the recurrence. Therefore, the serial measurements of serum PG I with the healing process will be helpful for the prediction of ulcer recurrence. Administration of atropine caused a significant decrease in serum PG I in the patients with duodenal ulcer, which suggests the vagal control of PG I release in duodenal ulcer patients.
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PMID:Serum group I pepsinogen (PG I) levels and their changes in the healing process of the ulcer in patients with and without unoperated recurrent ulcer. 647 53

In order to evaluate its clinical usefulness, serum pepsinogen I level was measured in a prospective study in unselected patients affected by endoscopically and histologically confirmed gastric or duodenal diseases. The mean level in controls was 63 +/- 26 ng/ml (M +/- SD) with no statistical difference between males and females, while it was significantly higher in smokers than in non-smokers (respectively 69 +/- 25 and 56 +/- 25 ng/ml). On the average in gastric ulcer patients it overlapped with controls (69 +/- 34 ng/ml), but in prepyloric ulcers its value was higher (81 +/- 45 ng/ml) than that found in ulcer of the gastric corpus (66 +/- 30 ng/ml). Serum pepsinogen I level was significantly higher in duodenal ulcer patients (81 +/- 33 ng/ml), in males as compared to females and in smokers as compared to non-smokers (respectively 91 +/- 32 and 67 +/- 26 ng/ml). Higher than normal values were found in one subject affected by the Zollinger-Ellison syndrome, and in patients with severe renal failure. Low and very low levels were found after partial and total gastrectomies and in A type atrophic gastritis. In the case of duodenal ulcer, serum pepsinogen I determination showed a 16 p. 100 sensitivity and a 96 p. 100 specificity, while for atrophic gastritis it showed an 87 p. 100 sensitivity and a 100 p. 100 specificity. It is concluded that, at present, the most important clinical application seems to be its screening value in the detection of atrophic gastritis and consequently its potential use to detect populations at increased risk for gastric cancer.
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PMID:Diagnostic usefulness of serum group I pepsinogen determination. 662 12

Pepsinogen level, expressed as the potential peptic activity of pepsinogen was determined by a fluorescent microassay using succinyl albumin as substrate, in biopsy specimens from the gastroduodenal mucosa of 95 subjects. The following results were obtained: (1) pepsinogen level in the gastric mucosa becomes progressively higher from pylorus to corpus (p less than 0.001); (2) pepsinogen level in the gastroduodenal mucosa of duodenal ulcer was significantly higher than that of normal mucosa or gastric ulcer (p less than 0.001); (3) the difference in pepsinogen level between the gastric mucosa with and without intestinal metaplasia was statistically significant (p less than 0.01); (4) the correlation between the histology of gastric glands and pepsinogen level was fundic gland greater than intermediate gland greater than pyloric gland (p less than 0.001).
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PMID:Potential peptic activity of pepsinogen of human gastroduodenal mucosa determined by fluorescent microassay method using succinyl albumin. 710 99

A radioimmunoassay (RIA) for human group I pepsinogens (PgI) in serum was developed, using PgI purified from gastric mucosa. The sensitivity (0.7 micrograms/l) and reproducibility of the assay were satisfactory for clinical use. In normal controls, total serum pepsinogen (T-Pg) level was 58.9 +/- 31.7 micrograms/l (mean +/- SD) (PgI, 43.6 +/- 25.0 micrograms/l; PgII, 15.3 +/- 11.1 micrograms/l). Peptic ulcer cases had elevated T-Pg levels (gastric ulcer, gastroduodenal ulcer and duodenal ulcer, in increasing order of magnitude). T-Pg levels were not useful for diagnosis of peptic ulcer because of a large overlap with normal controls. T-Pg levels were low in patients with gastric polyp and in aged subjects. In these groups, the decrease of PgI was more marked than that of PgII.
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PMID:Radioimmunoassay of serum group I and group II pepsinogens in normal controls and patients with various disorders. 715 Dec 78

To evaluate endogenous and exogenous factors affecting the quality of ulcer healing produced by proton pump inhibitors, gastric acid pH, serum gastrin, and serum pepsinogen (PG) I and II were measured in peptic ulcer patients before and after treatment with lansoprazole 30 mg once daily. Lansoprazole achieved more rapid scarring in duodenal ulcer (n = 34), with a healing rate of 97.1% after 6 weeks, than in gastric ulcer (n = 56), with a healing rate of 92.8% after 8 weeks. Scarring was the most rapid in gastroduodenal ulcer (n = 8), with a healing rate of 100% after 8 weeks, but the rate of complete scarring was the lowest (37.5%). Lower gastric acidity and lower PG I:II ratio were associated with poor quality ulcer scarring in patients with gastric ulcers, but the opposite was true for those with duodenal and gastroduodenal ulcers. For gastric ulcers, not only ulcer size but also mucosal atrophy was an important factor in ulcer healing. Smoking and alcohol consumption had little effect on the quality of ulcer healing during treatment. These results suggest that there are a number of differences between gastric ulcers and duodenal ulcers in terms of the quality of ulcer healing after lansoprazole treatment.
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PMID:Factors affecting quality of ulcer healing after lansoprazole treatment. 759 44


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