Search

Background and Aims: The risk of gastric cancer (GCA) is increased in atrophic gastritis. A low serum pepsinogen group I (SPGI) level is a good serologic indicator of atrophic gastritis of the gastric corpus and fundus, and can be used for diagnosis of subjects with atrophic gastritis and of increased risk for GCA. The present study was undertaken to investigate whether SPGI assay and a diagnostic gastroscopy could enable the diagnosis of GCA at an early stage. Material and Methods: The study was carried out as part of the Alpha-Tocopherol, Beta-Carotene Cancer prevention study (ATBC study) in Finland, in which 22,436 male smokers aged 50-69 years were screened by SPGI. Low SPGI levels (< 25 μg/l) were found in 2196 (9.8%) men. Upper GI endoscopy (gastroscopy) was performed in 1344 men (61%) and 78% of these had moderate or severe atrophic corpus gastritis in endoscopic biopsies. A control series of 136 men from the ATBC study cohort with abdominal symptoms, but with SPGI ≥ 50 μg/l were similarly endoscopied, and 2.2% of these had corpus atrophy. Results: Neoplastic alterations were found in 63 (4.7%; 95% CI: 3.6%-5.8%) of the 1344 endoscopied men with low SPGI levels. Of these, 42 were definite dysplasias of low grade, 7 dysplasias of high grade, 11 invasive carcinomas, of which 7 were 'early' cancers, and 3 carcinoid tumors. In the control series, 1 man (0.7%) of the 136 men had a definite low-grade dysplasia. Thus, 18 (1.3%; 95% CI 0.7%-2.0%) cases with 'severe' neoplastic lesions (4 advanced cancers, 7 early cancers and 7 dysplasias of high grade) were found in the low SPGI group, but there were none in the control group. All four patients with advanced cancer died from the malignancy within 5 years (mean survival time 2.5 years), whereas surgical treatment in all those with early cancer or high-grade dysplasia was curative. One of the seven patients with early cancer and two of the seven with high-grade dysplasia died within 5 years, but none died from the gastric cancer. Thus, curative treatment was given to 14 of 18 men in whom a malignant lesion was found in gastroscopy. This is about 15% of all gastric cancer cases (92 cases) which were diagnosed within 5 years after SPGI screening in the 22,436 men. Among the gastric cancer cases of the main ATBC study, the 5-year survival rate was 33% (85% of the non-survivors died from gastric cancer). Conclusions: We conclude that assay of SPGI followed by endoscopy is an approach which can enable the early diagnosis of gastric cancer at a curable stage. [ABSTRACT FROM AUTHOR]

Background: Vitamin E and beta-carotene are considered to decrease the risk of gastric cancer both in humans and in laboratory animals. We studied the effect of dietary supplementation with alpha-tocopherol and beta-carotene on the end-of-trial prevalence of premalignant and malignant lesions of the stomach in older men with atrophic gastritis. Methods: The study was carried out within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC study) in Finland, in which 29,133 male smokers aged 50-69 years were randomly assigned to receive daily 50 mg alpha-tocopherol, 20 mg beta-carotene, both of these agents, or placebo, for 5-8 years. Serum pepsinogen was determined at base line and after 3 years' supplementation to find men with atrophic gastritis. A low serum pepsinogen I level, indicating atrophic gastritis of the corpus area of the stomach, was found in 2132 men. These men were invited to have upper gastrointestinal endoscopy (gastroscopy), which was performed on 1344 subjects after a median supplementation time of 5.1 years. Results: Neoplastic alterations were found in 63 of the men (4.7%): 42 with definite dysplasias of low grade (moderate dysplasia), 7 with definite dysplasias of high grade (severe dysplasia), 11 with carcinomas (of which 7 were 'early' cancers), and 3 with carcinoid tumors. Neither alpha-tocopherol (relative risk, 0.98; 95% confidence interval, 0.57-1.69) nor beta-carotene (relative risk, 1.13; 95% confidence interval, 0.65-1.95) supplementation had any association with end-of-trial prevalence of gastric neoplasias after adjustment for other possible risk factors. The effect was not modified by base-line serum level or dietary intake of vitamins, prevalence of Helicobacter pylori infection, or other covariates. Conclusions: We thus conclude that supplementation with alpha-tocopherol or beta-carotene for 5 years has no major impact on the occurrence of neoplastic changes of the stomach in older male smokers with atrophic gastritis. [ABSTRACT FROM AUTHOR]

We determined the effect of postgastrectomy gastritis on serum pepsinogen I and pepsinogen II concentrations in 108 subjects with subtotal gastric resection. Eleven had normal remnant mucosa, 22 had superficial gastritis, and 75 had atrophic gastritis. In the subjects with superficial gastritis, serum pepsinogen I and II concentrations were significantly higher than in those with normal remnant mucosa, but the ratio of pepsinogen I to II did not differ from normal. In atrophic gastritis, serum pepsinogen I concentrations fell with increasing severity of mucosal damage, but pepsinogen II was persistently raised. Consequently, the ratio of pepsinogen I to II in subjects with atrophic gastritis was significantly lower than in those with superficial gastritis or normal remnant mucosa. Discriminant function analysis revealed that the ratio of pepsinogen I to II, in combination with the absolute level of pepsinogen II, had a sensitivity of 80%, a specificity of 73%, and a positive predictive value of 87% for atrophic gastritis in this population. We propose that the parallel increase in serum pepsinogen I and II concentrations in postgastrectomy superficial gastritis is because of an increased rate of endocrine release of both zymogens from the fundic glands, and that the dichotomy in pepsinogen I and II concentrations in postgastrectomy atrophic gastritis results from the loss of fundic glands, which produce both zymogens, and the appearance of metaplastic pyloric glands, which produce only pepsinogen II. [ABSTRACT FROM PUBLISHER]

Context: Early studies suggested that gastric acidity declines as people age. However, sequelae of achlorhydria are uncommon in older people, making this conventional wisdom unlikely.Objective: To ascertain the prevalence of basal gastric acidity and atrophic gastritis (indicated by serum pepsinogen ratio) in older adults.Design: Cross-sectional study in a volunteer sample.Setting: Retirement communities in suburbs of Kansas City, Mo.Subjects: A total of 248 white male and female volunteers aged 65 years or older living independently.Main Outcome Measures: Presence of basal unstimulated gastric acid was evaluated noninvasively by having subjects swallow quininium resin. Gastric acid with a pH lower than 3.5 releases quinine, which is then absorbed and excreted into urine. Atrophic gastritis was defined as a ratio of serum pepsinogen I/pepsinogen II of less than 2.9.Results: Basal unstimulated gastric content was acidic (pH <3.5) in 208 (84%) of 248 elderly subjects. On retesting 66 subjects (35 normals and 31 hyposecretors), 28 (80%) of 35 had pH less than 3.5 both times, and 22 (71%) of 31 had pH of 3.5 or higher twice; in the remaining 16 subjects, low vs high gastric pH changed between tests. Weighted population prevalence estimates in this sample were 67% for consistent acid secretion, 22% for intermittent secretion, and 11% for consistent gastric pH higher than 3.5. Whereas 14 (67%) of 21 consistent hyposecretors had serum pepsinogen ratios of less than 2.9, indicating atrophic gastritis, only 2 (5%) of 44 consistent or intermittent secretors of acid had ratios in this range (P<.001).Conclusions: In contrast to what is commonly stated, nearly 90% of elderly people in this study were able to acidify gastric contents, even in the basal, unstimulated state. Of those who were consistent hyposecretors of acid, most had serum markers of atrophic gastritis. [ABSTRACT FROM AUTHOR]

In a search for a genetic marker of duodenal ulcer, we measured serum pepsinogen I levels in 168 ulcer patients and 151 of their clinically normal siblings. The ulcer patients tended to have either hyperpepsinogenemia I (pepsinogen I, greater than or equal to 100 ng/mL) or a normal level on a familial basis. Further evidence supporting this separation was the finding that the mean serum pepsinogen I level in the clinically normal siblings of the hyperpepsinogenemic patients was 91.2 ng/mL, significantly higher than the mean level (63.1 ng/mL) in the normal siblings of the normopepsinogenemic I patients. In the hyperpepsinogenemic I families the results of segregation analysis of an elevated pepsinogen I were consistent with autosomal-dominant inheritance of this trait. The genetic basis of normopepsinogenemic I duodenal ulcer was also shown by the familial aggregation of this disorder. These data provide direct evidence for genetic heterogeneity of duodenal ulcer disease. [ABSTRACT FROM AUTHOR]

Human seminal fluid has been shown to contain two pepsinogen fractions with the same electrophoretic mobilities as the group II pepsinogens (Pg II) in gastric and duodenal mucosa. These two fractions have been isolated from seminal fluid by column chromatography on diethylaminoethyl cellulose, gel filtration on Biogel P-150 and preparative acrylamide gel electrophoresis. Rabbit antiserum to the purified seminal pepsinogens formed a single precipitin arc against seminal fluid. This antiserum also formed a single precipitin arc against extracts of gastric and duodenal mucosa with a reaction of identity against all three antigens. Identical results were obtained with an antiserum to gastric Pg II. Neither the antiserum to the seminal pepsinogens nor the antiserum to gastric Pg II reacted against the group I pepsinogens (Pg I). Radioimmuno- electrophoresis with [125I] seminal pepsinogens and antisera against Pg I-Pg Il and human serum revealed radioactivity only in the precipitin arc which formed against Pg II. Radioelectrophoretic analysis of the [125J] seminal pepsinogens produced a single radioactive zone. The results suggest that the pepsinogen preparation obtained from seminal fluid was pure, indicate that the pepsinogens in seminal fluid are electrophoretically and immunochemically identical to Pg II in gastric and duodenal mucosa, and provide further evidence for the existence of two immuno- chemically distinct groups of pepsinogens in man. [ABSTRACT FROM AUTHOR]

Presents the results of studies of hematologic status, assay for nutritional deficiencies and studies of small intestinal function on patients with tropical sprue in Haiti. Survey for deficiency of folate and vitamin B[sub12]; Role of tropical sprue in the development of the anemia and nutritional deficiencies among people in the country; Morphology of tropical sprue.

The peak acid output of the stomach in a group of 71 mothers of spina bifida children and in 71 matched controls was estimated indirectly by the serum level of group I pepsinogens. The mean levels did not differ significantly, suggesting that the conjectured teratogen is not specially acid-labile. The variance was significantly higher in index subjects than in controls, but the interpretation of this finding is not clear. [ABSTRACT FROM PUBLISHER]