[Studies on the gastric juice, gastric radiograms and appetite of patients undergoing chemotherapy for pulmonary tuberculosis. I. Gastric juice].
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BACKGROUND: Amoxicillin and clarithromycin are key antibiotics in proton pump inhibitor-based Helicobacter pylori eradication therapies. AIMS: To study gastric mucus and tissue concentrations and collect basic data about optimal antibacterial doses. METHODS: Plasma, gastric mucosa and gastric juice antibiotic concentrations were measured following either low- or high-dose amoxicillin (750 or 1000 mg b.i.d.) and clarithromycin (400 or 500 mg b.i.d.) given in combination with omeprazole 20 mg bid to 12 male volunteers in an open crossover design. Gastric juice and mucosal biopsy collection was performed either 2 (n=6) or 6 hours (n=6) after dosing. RESULTS: Amoxicillin concentrations 2 hours after high dosage were gastric juice > gastric body > antral mucosa > plasma. At 6 hours, plasma and gastric juice concentrations were still above the MIC for amoxicillin-susceptible bacteria but no antibiotic was detectable in mucosa samples. Clarithromycin concentrations after high dosage were gastric juice > mucosa > serum; all above the MIC for clarithromycin-susceptible bacteria at both 2 and 6 hours. CONCLUSIONS: Both dosage regimens provided effective antibiotic concentrations in gastric juice at 2 hours. After dosing, both antibiotics demonstrated high gastric tissue concentrations via local diffusion while clarithromycin also provided sustained delivery (6 hours) via gastric mucosa penetration.
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Gastric juice contains both pancreatic group I phospholipase A2 (PLA2-I) and synovial-type group II phospholipase A2 (PLA2-II), which may play a crucial role in Helicobacter pylori infection and gastric mucosal injury. PLA2-I present in gastric juice is derived from pancreatic acinar cells. The cellular source of PLA2-II found in gastric juice is unknown. A specific cell type of the intestinal mucosa, the Paneth cell, is known to secrete PLA2-II. The purpose of the present study was to define the source of PLA2-II present in gastric juice. For this purpose, gastric juice was collected from 29 individuals during gastroscopy, and mucosal biopsies were taken from the antrum and body of the stomach and from the duodenum as well as from the jejunum of individuals with resected stomach, for immunohistochemical detection of PLA2-II. The concentration of bilirubin in the gastric juice samples was determined to identify duodenogastric regurgitation. The PLA2-II content was significantly higher in bilirubin-positive than in bilirubin-negative gastric juice samples. PLA2-II was localized by immunohistochemistry in Paneth cells in three patients with areas of intestinal metaplasia of the gastric mucosa and in Paneth cells of duodenal and jejunal mucosa in all patients, but not in any other epithelial cell type of the mucosa of the stomach or the small intestine. Inflammatory cells did not contain PLA2-II. The current results suggest that PLA2-II found in gastric juice is derived from the Paneth cells of the small intestinal mucosa.
The experiment was performed in order to evaluate the beta-glucuronidase activity in gastric juice and gastric mucosa of rats submitted to protein-free diet. A group of 36 young adult male wistar rats was fed a protein-free diet ad libitum for five weeks; a second group of 36 wistar rats ingested a purified isocaloric 12,5% casein diet for the same period. The concentration of proteins in plasma, gastric juice and gastric glandular mucosa and the beta-glucuronidase activity in the gastric juice and gastric glandular mucosa were determined. Protein deficient rats had lower plasma protein concentration and also a lower protein concentration in gastric juice and gastric mucosa. In these animals there was no significant change of beta-glucuronidase activity in the gastric juice, but there was a significant increase of the specific enzimatic activity in the gastric mucosa. The results suggest that protein restriction in young adult rats affects the gastric mucosa. The increase of the specific beta-glucuronidase activity might be due to heightened local catabolism or to a comparatively more severe protein depletion.
UNLABELLED: The aim of this study was to examine the amount of endogenic histamine measured simultaneously in the plasma, gastric juice and gastric mucosa in habitual smokers and nonsmokers and to suggest possible implications of the obtained results. METHODS: 48 individuals were selected for this test. None of them suffered from any symptoms of ulcer disease. 28 were habitual cigarette smokers, 20 were nonsmokers who had never smoked. The tests were carried out standard conditions. Each patient underwent endoscopy. Gastric juice was taken by catheter via endoscopes, and biopsy specimens were taken for microscopic examination and establish histamine levels, which were also measured in plasma. Blood samples were taken before endoscopy. RESULTS: The levels of endogenic histamine in plasma and gastric juice were significantly higher in habitual smokers than in nonsmokers, especially in plasma. In the tissue of both groups no statistically significant differences were observed, but the histamine level was slightly higher in nonsmokers. CONCLUSION: The amount of histamine in plasma, as well in gastric juice, is may be connected with habitual cigarette smoking, and its level in tissue may also depend on smoking.
A rapid, selective and sensitive HPLC assay has been developed for the simultaneous analysis of clarithromycin, its 14-hydroxy-clarithromycin metabolite, and its decladinose acid degradation product, in small volumes of rat gastric juice aspirate, plasma and gastric tissue. Sample were extracted with n-hexane/2-butanol (4:1) and the internal standard was roxithromycin. A Kromasil ODS 5 micrometer(75x4.6 mm I.D.) column was used with a mobile phase consisting of acetonitrile/aqueous phosphate buffer (pH 7, 0.086 M) (45:55 v/v). The column temperature was 30 degrees C and coulometric detection was used at 850 mV using a screen voltage of 600 mV. The analysis time was less than 8 min. The limits of quantitation for clarithromycin, 14-OH clarithromycin and decladinose clarithromycin were 0.15 microgram ml(-1) or lower in plasma (0.05 ml); 0.16 microgram ml(-1) or lower in gastric juice (0.2 ml); and 0.51 microgram g(-1) or lower for gastric tissue (0.25 g). The method was linear up to at least 20.3, 15.4 and 12.5 microgram ml(-1) for clarithromycin, 14-OH-clarithromycin and decladinose, respectively, in gastric juice aspirate and plasma and up to 40.6, 30.9 and 25.0 microgram g(-1) in gastric tissue. The assay was applied to the measurement of clarithromycin, 14-OH-clarithromycin and, for the first time, decladinose clarithromycin in pharmacokinetic studies of gastric transfer of clarithromycin in individual rats.
BACKGROUND: Intragastric growth of non-Helicobacter pylori bacteria commonly occurs during acid-suppressive therapy. The long-term clinical consequences are still unclear. AIM: To investigate the luminal and mucosal bacterial growth during gastric acid inhibition, in relation to the type and duration of acid-inhibitory treatment, as well as to concomitant H. pylori infection. METHODS: A total of 145 patients on continuous acid inhibition with either proton pump inhibitors (n=109) or histamine2-receptor antagonists (H(2)RAs, n=36) for gastro-oesophageal reflux disease, and 75 dyspeptic patients without acid inhibition (control group) were included. At endoscopy, fasting gastric juice was obtained for pH measurement and bacteriological culture. Gastric biopsy specimens were examined for detection of H. pylori (immunohistochemistry) and of non-H. pylori bacteria (modified Giemsa stain-positive and immunohistochemistry-negative at the same location). RESULTS: Non-H. pylori flora was detected in the gastric juice of 92 (41.8%) patients and in the gastric mucosa of 109 (49.6%) patients. In gastric juice, prevalence rate for non-H. pylori bacteria was higher in patients taking proton pump inhibitors than controls and those taking H(2)RAs (58.7% vs. 22.6% and vs. 30.6%, P < 0.0001 and P < 0.003, respectively), but did not differ statistically between H(2)RAs and controls. In gastric mucosa, prevalence rates for non-H. pylori bacteria were higher in patients taking proton pump inhibitors and H(2)RAs than in the controls (antrum: 46.9% and 48.6% vs. 25%, P < 0.05 for both; corpus: 52.2% and 56.8% vs. 23.7%, P < 0.001 for both), but did not differ between proton pump inhibitors and H(2)RAs. Both luminal and mucosal growth of non-H. pylori bacteria were significantly greater in H. pylori-positive than -negative patients taking proton pump inhibitors (P < 0.05 for both). Luminal growth of non-H. pylori flora increased with the intragastric pH level, whilst mucosal bacterial growth increased with the duration of acid inhibition. CONCLUSIONS: Non-H. pylori flora not only contaminates the gastric juice but also colonizes the gastric mucosa of a large proportion of patients treated long-term with acid inhibition. The relationship between H. pylori and non-H. pylori bacteria in the pathogenesis of atrophic gastritis and gastric cancer needs further elucidation.
Gastric juice samples from patients of a rural area of the Colombian Andes at high risk to gastric cancer were tested for mutagenesis with Salmonella typhimurium strains TA100 and TA1538. Direct mutagenic effect was found in samples with detectable amounts of nitrite. This effect was not accountable by nitrite alone. Nitrite-negative samples from the same area and samples from the low-risk area of Cali were negative using the same mutagenesis assay.
Gastric juice prostacyclin and thromboxane were radioimmunoassayed in patients with chronic gastritis and peptic ulcer and in normal subjects. Prostanoid secretion into the gastric lumen was found to reflect the degree of inflammatory changes in the gastric mucosa.
Gastric secretion was stimulated by insulin hypoglycaemia and the effect of increasing doses of anticholinergic drugs on the volume, acid, and electrolyte content of gastric juice was studied. The sodium and potassium output was depressed to a far less extent than the acid output and the drop in volume of secretion and acid output after anticholinergic drugs is almost entirely due to decreased acid secretion. With increasing anticholinergic suppression of the volume of secretion, there is a marked fall in potassium output and a lesser fall in sodium output. The potassium concentration showed a slight fall and there was a rise in sodium concentration.
The activity of lysozyme in the saliva, blood serum and gastric juice was studied in 51 patients operated upon for peptic ulcers. The activity of lysozyme in the acid gastric juice was found to be lower than that in the neutral and low-alkaline medium. Following vagotomy, the contents of lysozyme in the blood serum and gastric juice was higher than following the resection of the stomach. The investigation of factors of non-specific defense of the organism, lysozyme in particular, is thought to be necessary for the estimation of the postoperative period and healing of the ulcer.
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This study reports the electrophoretic pattern of the proteins in human gastric juice of control patients and patients with gastric ulcer and gastric carcinoma. Autodigestion was prevented by intragastric neutralization. The statistical limits of normal are defined and the changes found in the gastric juice of gastric ulcer and gastric patients with gastric carcinoma described.
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To investigate the pathology of gastric disorders, we compared the proteomic patterns of gastric juice from patients with various gastric disorders. In healthy subjects pepsin A, pepsin B and gastric lipase were the major proteins detected by two-dimensional gel electrophoresis. These digestive enzymes were not detected in 60% of gastric cancer cases (18 out of 30 analyzed cases). Interestingly, an extraordinary amount of alpha(1)-antitrypsin was observed in these cases. In contrast to gastric cancer cases, alpha(1)-antitrypsin was detected in only 5% of patients (three out of 56) with chronic atrophic gastritis, and the detection frequency went up as the disease developed (one of four intestinal metaplasia cases, two of seven tubular adenoma cases, a single examined case of hyperplastic polyp and 60% of gastric cancer). Zymography showed that a 60 kDa protease strongly associated with alpha(1)-antitrypsin and mass spectrometric analysis revealed that the gastric alpha(1)-antitrypsin was a protease-cleaved form. Our data suggest that alpha(1)-antitrypsin and 60 kDa protease may serve as good diagnostic and prognostic markers for conditions associated with gastric cancer.
Concentrations of free and total hydrogen ions, total protein and pepsin were measured in gastric juice fractions collected during basal secretion and upon stimulation by graded doses of pentagastrin administered intravenously. Undissociated hydrogen ion and non-pepsin protein concentrations were calculated as derived quantities. The studies were carried out in nine patients with duodenal ulcer both before and after truncal vagotomy. It was found that after vagotomy the undissociated hydrogen ion concentration was significantly lower and non-pepsin protein higher than before the operation. No correlation was found between the two quantities both before and after vagotomy. It was concluded that in duodenal ulcer patients either not all non-pepsin protein takes part in buffering of hydrogen ions secreted by parietal cells, or that non-protein buffers play a more important role.
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