The gastric juice urea and ammonia levels in patients with Campylobacter pylori.

The authors studied gastric juice ammonia and urea nitrogen levels to determine how they are altered by gastric Campylobacter pylori (CP) infection. Patients with chronic gastritis (20), peptic ulcer (24), hepatic cirrhosis (10), chronic renal failure (13), or gastric remnant (20) were included. Endoscopic biopsy specimens stained with the Warthin-Starry stain were evaluated for the presence of CP. Blood and gastric juice analysis was performed for 11 of the patients with chronic renal failure and 37 patients from the remaining groups. CP was identified in gastric biopsies from 50 of 87 (57.5%) patients, including 87.5% with peptic ulcer and 40-50% of those with chronic gastritis, cirrhosis, chronic renal failure, or gastric remnant. CP infection had no effect on blood urea nitrogen or blood ammonia levels in any group of patients. The urea nitrogen level of gastric juice was higher in patients with chronic renal failure than in other groups but was not related to CP infection. CP infection was associated with a significant increase in gastric juice ammonia levels, both in patients with chronic renal failure (23.3 mmol/L vs. 2.90 mmol/L; [P less than 0.05]) and in other groups (5.48 mmol/L vs. 1.26 mmol/L [P less than 0.0001]). The authors conclude that elevation of gastric juice ammonia level is an indicator of gastric CP infection.

[A new method of collection of gastric juice from small animals]. / Novaia metodika polucheniia zheludochnogo soka u melkikh zhivotnykh.

A new method is suggested to obtain gastric juice in small animals. This technique is considered to be preferable in comparison with other known techniques as it permits obtaining gastric juice without surgery which is inevitably associated with such unfavourable factors as tissue traumas, pain irritation, inflammation, etc. According to the described technique the gastric juice is collected with the presence of stimulus (dry substance) in the gastric cavity. The animals are not fixed in this case but maintained under ordinary conditions. So, the obtained juice corresponds better to that produced in small animals under physiological conditions than the juice obtained using fistula or by another technique applied up to now.

Chronic atrophic gastritis, gastric pH, nitrites and micronutrient levels in a population at risk for gastric carcinoma.

One hundred and seventy-eight patients at risk for gastric carcinoma had upper gastrointestinal endoscopy. Twenty-seven selected patients with the type B of chronic atrophic gastritis, 32 patients with normal mucosa and 47 non-scoped healthy controls were tested for plasma vitamin C, retinol and tocopherol. The total vitamin C level was also assessed in gastric juice of scoped patients. Micronutrient levels were related to gastric pH, nitrites and gastric mucosal pathology. The study showed a higher level of pH (greater than 4) and high nitrites in gastric juice in patients with chronic atrophic gastritis, gastric malignant and dysplastic lesions. Neither the hypochlorhydria nor gastric nitrites affected the prevalence of C. pylori in gastric mucosa. Low gastric and plasma concentrations of vitamin C observed in patients with chronic atrophic gastritis showed an inverted relationship with pH level, and an inter-relationship of other vitamins with antioxidant properties (vitamins A and E).

[The effect of food products on the endogenous formation of N-nitrosamines in rats]. / Vliianie nekotorykh pishchevykh produktov na éndogennoe obrazovanie N-nitrozaminov u krys.

Data have been presented on carcinogenic N-nitrosoamines (NA) synthesis from precursors in the gastric juice and in the stomach of rats. It is shown that vegetable juices and milk produce an inhibitory effect with respect to NA synthesis in vitro and in vivo, however, food products with high content of fat intensify amine nitrosation.

Reflux gastritis in the intact stomach.

Gastric biopsy specimens from patients who have undergone gastric surgery frequently exhibit foveolar hyperplasia, oedema, vasodilatation and congestion, and a paucity of inflammatory cells as consequences of entero-gastric reflux. Similar, albeit generally milder, changes were found in 47 of 316 (15%) non-surgical patients undergoing endoscopy for dyspeptic symptoms. To relate these changes to bile reflux or other potential gastric irritants the total bile acid concentration was measured in samples of fasting gastric juice, and the use of a symptom questionnaire ascertained the patients' cigarette consumption, use of non-steroidal anti-inflammatory drugs (NSAIDs), and alcohol intake. When patients with reflux gastritis were compared with normal controls (n = 91), significant increases in associated peptic ulceration and NSAID use were found in the group with reflux, but no increases in bile acid concentrations. Indeed, only one patient had evidence of duodenogastric reflux. It is concluded that most cases of "reflux gastritis" in the intact stomach are not due to reflux of bile. Our findings indicate an important pathogenic role for long term NSAID use, in what might be usefully termed type C or "chemical" gastritis.

Continuous 99mTc-HIDA infusion as a method for measuring duodenogastric reflux.

The continuous 99mTc-HIDA infusion test is presented as a method for measuring duodenogastric reflux as well as for studying biliary elimination of the compound when it is administered by constant intravenous infusion. Thirty patients were studied: (a) ten patients with a T tube placed in the biliary tree were used to study the elimination of 99mTc-HIDA in the bile; (b) ten normal subjects were used as a control group; and (c) ten patients were studied who had undergone Billroth I gastrectomy for peptic ulceration. Studies of subjects in groups (b) and (c) were used to assess duodenogastric reflux by this test, correlating it with the measurement of bile acids in gastric juice. When 99mTc-HIDA was administered by constant intravenous infusion it resulted in an increased elimination in bile for the first 80-100 min, and the concentration in bile then remained relatively constant for the rest of the test. With respect to the duodenogastric reflux study group, reflux rates in the patients who had been operated on were higher than those in the control group, with statistically significant differences. Minimum reflux rates were found in the normal subjects. Assessment of reflux by 99mTc-HIDA correlated closely with the results of bile acid concentrations in Billroth I patients (r = 0.75, P less than 0.001) and control subjects (r = 0.85, P less than 0.001). Our results demonstrate that continuous 99mTc-HIDA perfusion is a useful, accurate and objective method for measuring duodenogastric reflux.

Duodenogastric reflux in children: measurement of phospholipids and trypsin in gastric content.

The duodenogastric reflux (DGR) is a suspected cause in some esogastric pathologies in adults: esophagitis, peptic gastric ulcers, stress ulcers, ulcers secondary to drugs, gastric cancer, and gastritis. The toxic substances of the reflux are essentially bile acids, lysolecithin, and trypsin. A number of diagnostic methods have been proposed in the adult. This study suggests a diagnosis technique for DGR in the child. Fasting gastric juice was collected by gastric intubation during 1 h and three substances were measured: phospholipids as markers of biliary reflux, trypsin as a marker of pancreatic reflux, and sialic acid as a marker of the degradation of gastric mucus. The sialic acid enabled us to evaluate some of the toxicity of DGR on the stomach. The study of 49 child subjects permitted us to show the existence, in the normal child, of biliopancreatic markers in the stomach under fasting conditions through a physiological DGR; to define the norms in the child, varying according to three age groups: 0-2 months, 2-12 months, and 1-4 years (the maximum values for an age above 4 years seemed to correspond to those in the adult); and to suggest the existence of a pathological DGR in children with antral gastritis or ulcers.

[Nitrate and nitrite concentrations in gastric juice with regard to the physiologic condition of the gastric mucosa]. / Nitrat- und Nitritkonzentrationen im Magensaft unter Berücksichtigung des physiologischen Zustandes der Magenschleimhaut.

In a random sample comprising 101 test persons (35 without and 66 with gastric disorders) nitrate and nitrite concentrations in gastric juice were determined. It was shown that parameters like pH, physiological stage of gastric mucosa, concentrations of bacteria and fungi in gastric juice or nitrate and nitrite concentrations, fungi and bacteria in saliva do not sufficiently characterize the dynamics of nitrate and nitrite in human stomach.

Relationship between gastrin cell number, serum, antral mucosa and luminal gastrin concentration and gastric acidity in antral atrophic gastritis.

The aim of our study was to investigate the relationship between gastrin producing cell density with antral mucosa, luminal and serum gastrin concentration in antral atrophic gastritis. Our study group consisted of 17 patients: six with mild atrophic gastritis, seven with moderate atrophic gastritis and four with severe atrophic gastritis. None of the patients had type-A atrophic gastritis but the body mucosa was affected by superficial gastritis at various extent in some. A group of 15 healthy subjects served as control. All subjects underwent gastroscopic examination with multiple bioptic sampling. Radioimmunoassay was used for gastrin determination and photomicroscopy for gastrin producing cell density assessment. Electron microscopy was used to assess the gastrin producing granule density index. Patients with moderate and severe atrophic gastritis showed a lower gastric acidity and acid output as compared to control. Serum gastrin did not show significant differences among the groups. In moderate and severe atrophic gastritis, gastrin producing cell granule density index, gastrin producing cell density and antral mucosa gastrin concentration were significantly lower when compared with control and decreased with advancing of the severity of atrophic gastritis. In atrophic gastritis, however, the latter two measurements were not correlated. In moderate and severe atrophic gastritis luminal gastrin concentration significantly increased, compared with control, after the severity of atrophic gastritis. Gastrin producing cell granule density index and luminal gastrin concentration showed a significant correlation with gastric pH. These data suggest that in antral atrophic gastritis with reduced gastric acidity, the decrement of gastrin producing cells is followed by gastrin producing cell hyperfunction with increased luminal release of gastrin.

Pharmacology of pepsinogen secretion: influence of pentagastrin on pepsinogen secretion in man.

To investigate the effect of pentagastrin on serum and urinary pepsinogens and gastric pepsin, eight healthy male volunteers were studied twice during continuous intragastric perfusion with either NaCl 0.9% or 0.1 M HCl in random order. To the perfusate 3 mg/ml phenol red was added as inert recovery marker. Gastric content was aspirated in 15-minute samples, 4 basally and subsequently 6 during continuous i.v. infusion of pentagastrin 1.5 micrograms/kg/h. Furthermore, serum and urine samples were collected immediately before and after each test. Gastric pepsin output increased after pentagastrin. There were no differences in basal or stimulated pepsin output during saline or HCl perfusion despite marked differences in intra-gastric acidity and acid delivery to the duodenum. In addition, no significant changes in serum pepsinogen levels or urinary pepsinogen excretion were observed after pentagastrin infusion. It is concluded that pentagastrin stimulates gastric pepsin secretion directly, but does not stimulate the release of pepsinogens into the systemic circulation.

Duodenogastric reflux before and after surgical or medical therapy for duodenal ulcer.

Duodenogastric reflux was studied in 48 duodenal ulcer patients before and after medical (n = 8) or surgical therapy with either combined truncal vagotomy and gastrojejunostomy (n = 13) or pyloroplasty (n = 12), Polya partial gastrectomy (n = 8), or highly selective vagotomy (n = 7). Seven healthy subjects served as controls. The reflux was assessed both by using 99mTc diethyliminodiacetic acid (HIDA) scintigraphy and by measuring intragastric bile acid levels following endoscopic gastric juice aspiration. Before therapy, duodenal ulcer patients had significantly higher intragastric bile acid concentrations than did normal subjects (p less than 0.001). After truncal vagotomy and drainage, or partial gastrectomy, bile acid levels increased significantly, whereas they remained unchanged after medical therapy. Conversely, they were found to be significantly decreased after highly selective vagotomy. The results of HIDA scan measurements were compatible with those of gastric juice bile acids. We conclude that surgical treatment for duodenal ulcer by highly selective vagotomy is the only form of therapy, among the types considered, that leads to a reduction in duodenogastric reflux. It is of interest that medical therapy of the duodenal ulcer does not improve abnormal duodenogastric reflux, possibly contributing to both the failure of the medical treatment and recurrence of the ulcer.

Risk factors of gastric precancerous lesions in a high-risk Colombian population. II. Nitrate and nitrite.

Gastric nitrite content was studied in relation to precancerous lesions of the stomach in a case-control study conducted in a high-risk Colombian population. The proportion of detectable nitrite in gastric juice and the mean pH were significantly higher among those with precancerous lesions (chronic atrophic gastritis, intestinal metaplasia, and dysplasia) than among the controls (normal and superficial gastritis); the proportion and mean pH increased with the progression of histological changes from normal to dysplasia. Nitrite was not detectable in gastric juice with a pH less than 5.0. A positive association was found between the proportion of detectable nitrite and the risk of gastric precancerous lesions. Odds ratios of 4.39 for intestinal metaplasia and 24.72 for dysplasia remained significant after controlling for confounders. This finding suggests that nitrite may be a precursor of a mutagen that targets gastric epithelial cells.

Physicochemical characterization and biological activity of intrinsic factor in cystic fibrosis.

Absorption of crystalline labeled cobalamin is strongly decreased in cases of cystic fibrosis. In order to determine if this is due to an alteration or a lack of activation of intrinsic factor by proteases, the physicochemical properties and biological activity of intrinsic factor have been studied. Intrinsic factor was purified 800-fold from stimulated gastric juice of cystic fibrosis patients with a yield of 64.2%. Cystic fibrosis intrinsic factor had an estimated Mr of 57,000 in SDS-polyacrylamide gel electrophoresis. Its carbohydrate content resembled that of normal human intrinsic factor, except that the ratio fucose/sialic acid was higher (6.1 and 1.6, respectively) and that the content in N-acetylgalactosamine was decreased. The same alterations in carbohydrate composition were observed for Hc purified from cystic fibrosis saliva. Purified intrinsic factor from cystic fibrosis gastric juice was biologically active in vitro in the presence of ileal solubilized receptor as well as in vivo (Schilling test). The fate of iodinated cystic fibrosis intrinsic factor in guinea pig ileum studied by high-resolution radioautography was similar to that of normal intrinsic factor. In conclusion, despite modifications of the carbohydrate content of the molecule, the biological activity of intrinsic factor is not altered in cases of cystic fibrosis. The malassimilation of crystalline cobalamin observed in cystic fibrosis is due to a mechanism independent from intrinsic factor secretion.

[Sucralfate: the agent of choice in the treatment of peptic ulcer?]. / Sukral'fat: sredstvo vybora v lechenii iazvennoi bolezni?

As many as 72 patients with erosive and ulcerous injuries to the stomach and duodenum were examined for the clinical efficacy of antepsin (sucralfate). Of these patients, 42 were with duodenal ulcer, 10 with gastric ulcer and 20 with erosive gastroduodenitis). Antepsin exerted a beneficial effect on the painful syndrome and on ulcer and erosion healing. The coefficient of the therapeutic efficacy of antepsin in duodenal ulcer patients turned out to be equal to 2.67 that of gastric ulcer to 2.1 and that in patients with gastroduodenitis was 2.6. The drug did not produce any well-defined side effects. In some cases (8.3%), it caused the appearance or enhancement of constipation. Antepsin is indicated not only in ulcer disease but also in duodenogastric reflux, reflux gastritis and reflux esophagitis.

Studies on gastrin in duodenal ulcer.

By immunocytochemical method and radioimmunoassay, the gastrin secreting cells (G cells) and gastrin concentration in antral mucosa, gastric juice and serum in 20 patients with duodenal ulcer (DU) were studied. The number of G cells and gastrin concentration in antral mucosa showed no significant difference as compared with normal control. The number of G cells in patients with DU and antral atrophy was much higher than those with antral atrophy but with DU. It indicated that G cells were increased in number in DU, and the gastrin concentration in gastric juice (271.11 +/- 255.25 pg/ml) was much higher than in sera (74.71 +/- 43.07 pg/ml). G cells were distributed in different parts of pyloric glands, showing that gastrin in gastric juice should come directly from G cells. The disturbance of feedback mechanism in regulating gastric acidity might be an important role in hypersecretion of gastric acid in DU. The increase of gastrin concentration in gastric juice might be closely related to hyperplasia of parietal cells.

[Diagnosis of Campylobacter pylori based on the level of urea in the gastric juice]. / Diagnostika Campylobacter pylori po urovniu mocheviny v zheludochnom soke.

Comparison of urea levels in 3 portions of gastric juice, obtained on an empty stomach, basal, and stimulated, from 28 patients, C. pylori carriers, and 20 patients without C. pylori carriership, has shown that the presence of this bacterium in the gastric mucosa is related not so much with a decrease in the absolute level of urea in the portion collected on an empty stomach but mostly with changes in this parameter in three portions of gastric juice collected in succession. Decreased urea levels in the second portion as against the first one or in the third one as against the two previous ones were detected in 97% of patients with C. pylori carriership. In 100% of patients without C. pylori carriership urea levels in the three portions remained unchanged or were decreasing. The method for measuring urea levels in three portions of gastric juice is recommended for the diagnosis of C. pylori carriership in gastroduodenal diseases.

A characterization of immunoreactive somatostatin in human milk.

In the present work, somatostatin-like immunoreactivity (SLI) in human milk was characterized. In the early postpartum period, SLI levels were highest on the first day after delivery, and then gradually declined. From the fifth day postpartum, SLI levels in milk seemed unchanged. On the fifth day after delivery, milk SLI was significantly (p less than 0.01) higher than plasma SLI (126.3 +/- 11.7 vs. 17.6 +/- 1.1 pmol/L). The results indicate an active transport from blood or synthesis of somatostatin within the mammary gland. Gel filtration studies of skimmed milk, as well as milk exposed to urea and HCl, and aspirated milk from the human premature newborn, revealed that the main portion of milk SLI either represents somatostatin covalently bound to a larger protein, or more likely, a high molecular weight variant of somatostatin.

Basal and somatostatin-stimulated gastric intraluminal prostaglandin E2 in patients with gastric ulcer and with gastric adenocarcinoma.

The effect of somatostatin-14 (SST), at doses utilized in clinical practice, on gastric intraluminal prostaglandin (PG) E2 release was evaluated in 8 endoscopically normal subjects, in 6 patients with benign gastric ulcer and in 8 patients with gastric adenocarcinoma. In normal subjects, SST induced a significant increase in gastric intraluminal PGE2 concentration and output, whereas it did not augment the concentration and output of PGE2 in patients with gastric ulcer and with gastric cancer. The altered PG response to SST stimulation shown by gastric ulcer and gastric cancer patients may be related to a modified cell population in the gastric mucosa and/or to a defective regulation of this local gastric mucosal mediator.