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Prospective epidemiologic studies among Hawaii Japanese indicate that serum PG I levels below 20 micrograms/1 are highly specific for the presence of intestinal metaplasia and the intestinal type of gastric cancer; but this test shows a low level of sensitivity. Substitution of the PG I/PG II ratio for the PG I level results in a modest improvement in the level of sensitivity at the expense of some loss in specificity. Antral gastritis and intestinal metaplasia are gastric cancer precursors in this population. Abnormally low values of serum PG I or the PG I/PG II ratio predict high stage tumors in the majority of cases. It therefore does not seem likely that estimates of serum pepsinogen are likely to increase the frequency of the diagnosis of early intestinal type carcinoma of the antral portion of the stomach in this population.

Radionuclide labeled gastric emptying was compared with plasma paracetamol (acetaminophen) concentration measured by fluorescence polarization immunoassay. A significant correlation was found between both gastric emptying half-time of radionuclide (t1/2) and % isotope remained in the region of the stomach and paracetamol absorption kinetic parameters. The strongest correlation was found between t1/2 and the time required to reach the peak plasma level of paracetamol (r = 0.680, p less than 0.01). This study indicates that simple paracetamol marker method has enabled an indirect quantitative measurement of gastric emptying by sampling at varying time intervals.

Sheep and calves prepared with separated, innervated pouches made from the acid secreting region of the abomasum were given single or multiple infections of Ostertagia spp and comparisons were made of the secretory changes of parasitised and non-parasitised mucosa by means of cannulas placed in the abomasum and pouch. Contrary reactions of the parasite-free pouches and infected main part of the abomasum are described and explained in terms of a two-part hypothesis. The inhibitory effect on acid secretion of the abomasum (resulting in its contents being pH 5 to 7) was postulated to be due to the direct suppressive effects of substances released locally by parasites or injured host tissues, whereas increased secretion of the hormone, gastrin, was thought to account for the stimulatory effects of infection on acid secretion from the pouches. In sheep treated with anthelmintic and then reinfected the inhibitory effects on abomasal pH were not obtained. The hypersecretion from the pouches still persisted.

Biopsy specimens have been taken from five standard sites in the stomach and from the duodenal bulb in order to investigate the association of gastritis and duodenitis with duodenal ulcer. Twenty patients with chronic duodenal ulcer were investigated in this manner and in addition had gastric secretion tests and a radio-immune assay of serum gastrin under differing conditions. The patients were then treated either by a truncal vagotomy and pyloroplasty (TVP) or by a highly selective vagotomy without a drainage procedure (HSV). All the investigations were repeated three months postoperatively. Duodenal ulcer was usually associated with gastriitis, although this varied in extent and severity from patient to patient. In nearly all the patients, gastritis was present at the pyloric end of the stomach and along the lesser curve. In more than half of the patients, gastritis was also present in the body of the stomach but the fundus was usually spared. Chronic duodenitis was found in the duodenal bulb in all these patients. After vagotomy there was a marked increase in both the extent and severity of the proximal gastritis in both treatment groups but the distal gastritis remain almost unchanged. There was little change in the incidence of duodenitis after vagotomy but its severity was lessened. No correlation was found between the peak acid output (PAO) in response to Histalog and the severity of the gastritis or the duodenitis either before or after operation, with one exception. The postoperative PAO was significantly less in those patients who developed a severe proximal gastritis after vagotomy. No relationship was found between the severity of the distal gastritis and the levels of serum gastrin. No correlation was found between either the basal or peak acid output and the corresponding serum gastrin levels before or after vagotomy.

A study was made of the time course of changes in gastrin, insulin and ACTH concentration in the peripheral blood in the course of the development of a specific dynamic food action. Eighteen normal subjects and 78 patients with peptic ulcer, chronic gastritis and chronic enterocolitis were entered into the study. It was demonstrated that apart from digestion stimulation, food intake acted as the most important factor changing the hormonal level in the body. Studies of the blood level of hormones in the course of food intake in patients allowed the detection of various deviations from normal occurring in hormonal secretion.

Content of fucose and of fucosylated protein fractions was studied in blood serum of healthy donors as well as in blood serum of patients with chronic gastritis and with stomach cancer. Concentration of fucose was increased in blood serum under conditions of the tumor generalization. At the same time, content of fucosylated albumin was elevated within early steps of stomach cancer, while the content of fucosylated globulins was decreased. Estimation of albumin-bound fucose might be used in diagnosis of stomach cancer.

Fasting serum gastrin was determined in 35 Chinese patients with various types of chronic gastritis and in 23 Chinese control subjects. The mean (+/- S.D.) fasting serum gastrin levels for 13 patients with chronic atrophic gastritis, 16 patients with chronic gastritis and six patients with acute-on-chronic gastritis were 32.1 (+/- 38.9) pg./ml., 36.1 (+/- 23.2) pg./ml. and 33.7 (+/- 19.4) pg./ml., respectively. The mean (+/- S.D.) fasting serum gastrin levels for the whole gastritis group (35 patients) and the control group were 34.2 (+/- 28.8) pg./ml. and 24.6 (+/- 13.7) pg./ml., respectively. Statistical analysis showed that the mean basal serum gastrin levels of the three gastritis groups did not differ significantly from control subjects and with each other.

As part of an ongoing cohort study of gastric cancer precursors in Nariño, Colombia, blood levels of ascorbic acid, vitamin E, retinol, pre-albumin, retinol binding protein and carotenoids were measured and correlated with histopathologic findings of gastric biopsies. Carotene levels in both sexes and vitamin E levels in males were significantly lower in subjects with gastric dysplasia than in subjects with normal mucosa and subjects with less advanced gastric lesions (chronic atrophic gastritis and intestinal metaplasia). No other significant correlations were found.

A method of assay for the circulating intrinsic factor antibody type I (IFA1) and for the serum vitamin-B12 level by the use of hog intrinsic factor has been developed. The results, the sources of error being taken into consideration, are in agreement with the values obtained by the generally accepted methods of ARDEMAN--CHANARIN for IFA1 and of WIDE--KILLANDER for the serum vitamin-B12 level. Parallel with the increase in the frequency of circulating IFA1, the serum vitamin-B12 level was found to decline in normal individuals as well as in patients with atrophic gastritis or pernicious anaemia. The method is suitable for the assessment of vitamin-B12 deficiency and lends itself to screening of patients tending to pernicious anaemia.

The ratio of pepsinogen I to pepsinogen II in the circulation decreases progressively with increasing severity of atrophic gastritis of the fundic gland mucosa. Fasting blood was obtained from 359 free-living and institutionalized elderly people (age range, 60 to 99 years). A pepsinogen I/pepsinogen II ratio less than 2.9, indicating atrophic gastritis, was found in 113 (31.5%) subjects. The prevalence of atrophic gastritis increased significantly with advancing age (P less than .05). Within the atrophic gastritis group, 84 had a pepsinogen I level greater than or equal to 20 micrograms/L, indicating mild to moderate atrophic gastritis, and 29 had a pepsinogen I level less than 20 micrograms/L, indicating severe atrophic gastritis or gastric atrophy. A significant increase in the prevalences of elevated serum gastrin levels (P less than .005), low serum vitamin B12 levels (P less than .005), circulating intrinsic factor antibody (P less than .005), and anemia (P less than .025) was observed with stepwise increases in severity of atrophic gastritis. Subjects with atrophic gastritis exhibited a lower mean serum vitamin B12 level (P less than .05) and a higher mean folate level (P less than .05), but no difference was detected in mean hemoglobin levels or serum levels of iron, ferritin, retinol or alpha-tocopherol. It is concluded that serum pepsinogen I and pepsinogen II levels can be used to determine the prevalence and severity of atrophic gastritis, that atrophic gastritis is common in an elderly population, and that atrophic gastritis is associated with vitamin B12 deficiency and anemia. Further, higher folate levels in atrophic gastritis may be related to an accumulation of 5-methyl tetrahydrofolate in serum due to vitamin B12 deficiency and/or greater folate synthesis by the intestinal flora resulting from bacterial overgrowth secondary to hypo- or achlorhydria.

The effect of a rational diet and of antiulcerous diets containing a proteinic-mineral enrichment (in an amount of 20--30 g) on the clinical symptomatology, the peripheral blood picture and some biochemical blood serum characteristics in patients with atrophic gastritis and duodenal ulcer was studied. In cases of atrophic gastritis with hypoferremia the proteinic enrichment was incorporated in the diet (rational) in an amount of 80--90 g per day. Control observations were conducted over analogous groups of patients receiving the same diets, but without proteinic enrichment. These observations continued over a period of 30--40 days. Thanks to a high content of easily assimilated iron and a well-balanced amino acids composition the proteinic-mineral enrichment has been found to be a valuable food product that is capable of favourably influencing the hemopoietic function of the organism and improving the blood proteins composition. Most patients with atrophic gastritis and peptic ulcer tolerate well the products and meals carrying additions of the proteinic enrichment.

The numbers of T lymphocytes, helper and suppressor T lymphocytes, were measured in peripheral blood of 10 patients, 13 patients with gastric cancer and 20 normal controls. T lymphocyte subpopulations were enumerated by the use of monoclonal antibodies OKT3 (pan-T lymphocytes), OKT4 (helper/inducer lymphocytes) and OKT8 (cytotoxic/suppressor lymphocytes) in an indirect immunofluorescence technique. Furthermore, the possible pharmacological modulation of 10(-4) histamine and 10(-4), 10(-6) M cimetidine of T lymphocyte subsets was investigated. Lymphocyte subpopulations were found to range in normal values in patients with ulcer and chronic gastritis. A marked decrease of OKT3 and OKT8 positive lymphocytes was noted in patients with gastric cancer, whereas OKT4 lymphocytes from the three groups of patients to histamine and cimetidine resulted in no significant changes of lymphocyte subsets.

Four patients with erosive hemorrhagic gastroduodenitis were found to have high fibrinolytic activity of the gastric juice. No increase in the fibrinolytic activity could be demonstrated in the circulating blood, but the values found for fibrinogen, plasminogen and alpha2-macroglobulin were low. A high content of FDP was found in the serum. All patients had a markedly decreased content of factor XIII. Platelet count and other coagulation components were normal. These findings were interpreted as signs of local fibrinolysis in the diseased parts of the gastrointestinal canal. The bleeding stopped after oral and intravenous administration of a fibrinolytic inhibitor (AMCA Cyclokapron) and of factor XIII-containing concentrate. In bleeding from gastroduodenal ulcer and esophageal varices, no increase in gastric fibrinolytic activity was found. It is suggested that the high local fibrinolytic activity in the stomach in erosive gastritis together with the low content of factor XIII contributes substantially to the hemorrhage in this condition. These observations may lead to a revision of the treatment of such cases.

The sulfation of gastrin in serum, antrum and duodenum was studied in 22 normo- and 20 hypergastrinemic patients. The ratio between gastrin-17 and gastrin-34 was measured in antrum and duodenum. The degree of sulfation was reduced in the antrum of hypergastrinemic patients (35.3 +/- 1.3%, mean +/- SEM) compared with 48.0 +/- 2.1% in normo-gastrinemic patients (p less than 0.001). The degree of sulfation in serum and duodenum was similar to that of the antral gastrins in all patients. The percentage of gastrin-34 in antrum was increased (7.3 +/- 0.7%) in hypergastrinemic compared with 4.9 +/- 0.3% in normogastrinemic patients (p less than 0.01). In the duodenum the percentage of gastrin-34 was similar in normo- and hypergastrinemia. When classified according to clinical diagnosis, sulfation of antral gastrin was normal in duodenal ulcer (47.6 +/- 4.5%) but decreased in gastric ulcer (36.7 +/- 1.6%, p less than 0.01) and pernicious anemia (31.3 +/- 1.9%, p less than 0.001) compared with 48.2 +/- 2.2% in control patients. In pernicious anemia a larger proportion of antral gastrins occurred as gastrin-34 (8.2 +/- 0.9%) compared with 4.8 +/- 0.4% in control patients (p less than 0.01). Our study suggests that both sulfation and proteolytic processing of the gastrin precursor is diminished in hypergastrinemia of antral origin.

A pathophysiological role of gastrin has been established only in the Zollinger-Ellison-Syndrome. Hypergastrinemia may be found in cases with prenicious anemia, atrophic gastritis and after all forms of vagotomy; furthermore in the excluded antrum syndrome, the short bowel syndrome, in renal insufficiency, pyloric stenoses and after oral or parenteral administration of calcium. The role of gastrin in the pathogenesis of duodenal ulcer is unknown.

The concentration of the NH2-terminal fragment of gastrin-17 in serum was determined by radioimmunochemistry. Two antisera were used, one specific for the COOH-terminus and the other for the NH2-terminus of gastrin-17. The NH2-terminal gastrin-17 immunoreactivity in unfractionated serum correlated well with the amount of fragment found after gel filtration of the same sera (p less than 0.001). In healthy subjects (no. = 100), the NH2- and COOH-terminal gastrin immunoreactivity was 8 +/- 1 and 20 +/- 1 pmol/l (mean +/- SEM), respectively. In patients with acute duodenal ulcer (no. = 30) and acute gastritis (no. = 10) the NH2-terminal immunoreactivity was fourfold increased compared with in healthy subjects (p less than 0.001), whereas the COOH-terminal was identical, the NH2- and COOH-terminal concentrations being 33 +/- 7 and 22 +/- 2 pmol/l in duodenal ulcer and 35 +/- 6 and 21 +/- 1 pmol/l in acute gastritis. Other groups of patients had NH2- and COOH-terminal gastrin concentrations in serum similar to those measured in healthy subjects. The results suggest that gastrin cells process gastrin-17 abnormally during the acute phase of duodenal ulcer and gastritis.

32 children (mean age 12 years, range 6-18) with non-specific abdominal pain and Campylobacter pylori positive gastritis received a six week course of daily oral amoxycillin (50 mg/kg) and tinidazole (20 mg/kg). Before treatment and one month after stopping treatment, endoscopic biopsy samples were taken from the antral mucosa and serum C pylori IgG antibody, pepsinogen I, and gastrin levels were measured in fasting blood samples. One month after treatment 30 children (94%) were cleared of C pylori and gastritis had resolved in 27 (84%) and was improved in the remaining 5. Serum IgG, pepsinogen I, and gastrin levels were significantly decreased after treatment. Of 12 children assessed at six months, 9 remained free of C pylori. Increases or decreases in IgG level indicated clearance or recurrence, respectively, of C pylori.

Forty-two patients with pernicious anemia (PA) and 35 patients with achlorhydria but without PA were investigated by means of serum gastrin determination and estimation of circulating parietal cell and thyroidal autoantibodies. In 38 of the 77 patients, gastroscopic and histopathological examinations of the antral and corpus mucosa were performed. The patient groups were similar with regard to distribution of high and normal serum gastrin levels, the frequencey of autoantibodies and antrum-sparing atrophic gastritis. In the present selection of patients, therefore, the achlorhydria group was supposed to represent a precursor state of the group with PA. A minor proportion of patients with severe atrophic gastritis of the antrum as well as of the corpus mucosa was found in the two groups.

The serum level of pepsinogen I (PG I) and pepsinogen II (PG II), and the PG I/PG II ratio were compared with the surface area of the fundic mucosa, as determined endoscopically by the Congo red staining method. Reduction in the area of the fundic mucosa due to gastritis was associated with stepwise reduction in the PG I levels and the PG I/PG II ratios. Reduction in the area of the fundic mucosa was also associated with decreases in the basal acid output, maximal acid output (MAO), the basal pepsin output and the stimulated pepsin output. The best sensitivity and specificity levels for the diagnosis of normal mucosa and severe gastritis were obtained with the PG I/PG II ratio and the MAO. A retrospective study of 58 patients with gastric cancer and 162 cancer-free patients showed that a PG I/PG II ratio identified 86.2% of all carcinomas and 87.5% of early carcinomas. Although this test gave a positive rate of 36% among the cancer-susceptible age group controls, its use would lower the cost of mass screening by targeting a smaller test population.