Association of erosive esophagitis with Helicobacter pylori eradication: a role of salivary bicarbonate and glycoprotein secretion.

In some populations, Helicobacter pylori eradication is associated with development of erosive esophagitis. The aim of this study was to evaluate the contribution of salivary bicarbonate and glycoprotein secretion to the pathogenesis of erosive esophagitis developing after H. pylori eradication. Gastroscopy and saliva collection were performed at recruitment and 12 months after completion of eradication therapy. Eighty-eight patients with duodenal ulcer were recruited to the study. Erosive esophagitis was found in 13 patients (grade A, 8 patients; grade B, 4 patients; grade C, 1 patient). Among the 74 subjects who completed the study, erosive esophagitis was detected in 21 patients (grade A, 15 patients; grade B, 6 patients); they all were successfully eradicated. Bicarbonate and glycoprotein secretion was not found to differ significantly between the subjects with and without erosive esophagitis both before and 1 year after H. pylori eradication. However, it was lower in H. pylori-infected (baseline) than in H. pylori-noninfected erosive esophagitis subjects (1 year after successful eradication) (bicarbonate 2.34 [1.29-3.40)]vs. 3.64 [2.70-4.58]micromol/min and glycoprotein 0.23 [0.15-0.31]vs. 0.35 [0.28-0.43] mg/min, P= 0.04 and P= 0.04, respectively). We conclude that changes in salivary bicarbonate and glycoprotein secretion related to H. pylori eradication do not promote the development of erosive esophagitis in duodenal ulcer patients.

MUC 1 mucin content in gastric juice of duodenal ulcer patients: effect of Helicobacter pylori eradication therapy.

It has been suggested that Helicobacter pylori can interact via carbohydrate structures with gastric mucins. Particularly, the Lewis b structures of the secretory MUC 5AC mucin are considered to be putative receptors for bacterial adhesins. Also the epithelial MUC 1 mucin is implicated by some authors to have a major role in the mechanism of infection. The main objective of our study was to evaluate MUC 1 mucin levels in human gastric juice before and at the end of eradication therapy. Any possible changes could suggest the participation of MUC 1 in H. pylori infection. We assume that the amount of the soluble form of MUC 1 exfoliated to the juice correlates with MUC 1 expressed on epithelial cells. Gastric juice samples of 14 duodenal ulcer patients infected with H. pylori were assayed before and at the end of eradication. In all samples, DNA content was determined. Mucin fractions were isolated by gel exclusion chromatography. High molecular mass material containing MUC 1 was subjected to 4%-12% polyacrylamide gradient gels, electrotransfer to Immobilon P and immunodetection. In 12 infected patients (86%), the initial low level of MUC 1 mucin in gastric juice increased at the end of eradication. In comparison to the infected patients, neutral carbohydrate and DNA content in gastric juice diminished after treatment. Our results indicate that the bacterium affects the soluble form of MUC 1 mucin, thus suggesting a likely role of this mucin in the course of H. pylori infection.

Adenosine deaminase activity in patients with the intestinal type of gastric carcinoma.

Adenosine deaminase activity was studied in tissue slices taken endoscopically from gastric mucosa of patients with the intestinal type of gastric carcinoma. The enzyme activity was measured in mucosal homogenates by determination of ammonia liberated from substrate during 10-min incubation. It was found that: (1) the enzyme activity of de novo gastric cancer was significantly lower than that of recurrent cancer of the gastric remnant; and (2) the enzyme activity of uninvaded gastric mucosa surrounding the neoplastic lesion of non-operated stomach was significantly lower than of the gastric mucosa of partially resected stomach due to malignancy. Since the enzyme activity in gastric cancer and surrounding uninvaded gastric mucosa correlated well with the advance of neoplastic disease estimated by ultrasonography examination, we speculate that some systemic factors associated with tumor progression might be implicated in the regulation of adenosine deaminase activity.

Adenosine deaminase activity in gastric cancer.

Adenosine deaminase activity, the key enzyme of adenosine inactivation, was studied in slices taken endoscopically from gastric cancer and macroscopically unchanged gastric mucosa surrounding the cancer. The activity of the enzyme was measured in mucosa homogenates by determination of ammonia liberated from substrate. It was found that adenosine deaminase activity in neoplastic lesions did not differ significantly from normal mucosa and that the gastric region studied (antrum, corpus) did not have an impact. A significant difference in enzyme activity was noticed between intestinal and diffuse-type gastric carcinoma (according to Lauren's classification); the intestinal type was characterized by lower adenosine deaminase activity than was the diffuse type. Since the activity of adenosine deaminase in gastric cancer did not exhibit significant differences from normal mucosa the diagnostic value of its determination is of less importance.

Glycogen content in the gastric mucosa of partially resected stomach; a possible relationship with the development of cancer.

Since gastric carcinoma, unlike uninvaded mucosa, has a relatively high glycogen content and the risk of gastric carcinoma is especially high in patients with a partially resected stomach, the aim of this study was to follow glycogen storage in both uninvaded gastric stump mucosa and carcinoma developing in the stump postsurgery performed for benign and malignant conditions. One hundred patients were recruited, including controls with non-operated stomachs (duodenal ulcer or gastric cancer patients). In endoscopically taken biopsies glycogen was determined by the anthrone method. It was found that the glycogen content in the gastric remnants was higher than in non-operated stomachs and increased with the time after surgery. It is possible that the risk of gastric cancer, which increases with the time from surgery, may be related to glycogen storage.

Adenosine deaminase activity in the gastric mucosa in patients with gastric ulcer. Effects of ranitidine and sucralfate.

Adenosine deaminase activity was studied in the gastric mucosa of patients with peptic ulcer in relation to ulcer localisation and treatment with ranitidine or sucralfate. Enzyme activities observed in the corpus mucosa were higher at a distance of over 2 cm from the ulcer margin than that recorded close to the ulcer. A significant decrease in adenosine deaminase activity was found after treatment with ranitidine but not with sucralfate. In the antral mucosa, enzyme activity was constant in all the groups observed. The evaluation of adenosine deaminase activity in gastric mucosa can be useful for studies of pathologic changes in the stomach.

Mucosal adenosine deaminase activity and gastric ulcer healing.

Adenosine deaminase activity was studied in gastric corpus mucosa close to an ulcer crater. It was found that 6 weeks of therapy with ranitidine was accompanied by a decrease in enzyme activity in the mucosa around healed ulcers and an increase around those which failed to heal. The different activities of adenosine deaminase in the vicinity of healed and unhealed ulcers may indicate its possible role in peptic ulcer healing.

Adenosine deaminase activity in the human duodenal mucosa in relation to gastric acid secretion.

Adenosine deaminase (ADA) activity was estimated in mucosal specimens obtained endoscopically from the duodenal bulb. Three groups of subjects were studied: 1. 9 patients with achlorhydria, 2. 12 subjects with normal gastric acid secretion, 3. 5 patients with hypersecretion. Enzyme activity was measured by determination of ammonia liberated from the substrate according to the Chaney and Marbach method. In patients with hypersecretion the ADA activity was lower than in those with achlorhydria (p less than 0.001) and normal acid secretion (p less than 0.02). A significant negative correlation between ADA activity in the duodenal bulb mucosa and basal and maximal gastric acid outputs was found. The present study seems to indicate a possible relationship between gastric acid secretion and duodenal ADA activity.

Mucosal adenosine deaminase activity and stump ulcer healing.

Adenosine deaminase activity was studied in endoscopically taken slices from gastric mucosa in patient after partial gastric resection performed due to complicated duodenal ulcer, and currently with peptic ulcer in the stump. The samples of gastric mucosa were taken before and after 6 weeks of treatment with ranitidine, 150 mg twice daily, at a distance within 2 cm and greater than 2 cm from the ulcer crater. Adenosine deaminase activity was measured in mucosa homogenates by determination of ammonia liberated from substrate. It was found that therapy with ranitidine was accompanied by an increase in enzyme activity in the mucosa surrounding unhealed stump ulcers, while no changes were noted in mucosa around healed stump ulcers. A possible role of mucosal adenosine deaminase activity in stump ulcer healing is postulated.

Modulatory effect of esophageal intraluminal mechanical and chemical stressors on salivary prostaglandin E2 in humans.

As has been demonstrated, infusion of hydrochloric acid (HCl) and pepsin into the human esophageal lumen, which mimics the natural gastroesophageal reflux, results in a significant increase in salivary volume, salivary bicarbonate and epidermal growth factor. However, the impact of intraluminal acid/pepsin solution on salivary prostaglandin E2 (sPGE2), the major protective factor of the upper alimentary tract, has never been explored. Therefore, using the newly developed esophageal perfusion model, the impact of both mechanical and chemical stimuli of the esophagus on sPGE2 secretion in humans was studied. Salivary PGE2 was assessed in saliva collected during basal conditions, chewing of parafilm, placement of intraesophageal tubing, inflation of intraesophageal balloons, and perfusion with sodium chloride, HCl, or HCl/pepsin solutions. The concentration of sPGE2 was measured using the RIA kit from Amersham (Arlington Heights, IL) after the solid-phase extraction and derivatization. The concentration of sPGE2 in the basal saliva was (mean +/- standard error of mean) 186 +/- 31 pg/mL and was similar during the chewing of parafilm (171 +/- 32 pg/mL). The placement of intraesophageal tubing, however, resulted in a significant decline of sPGE2 concentration to the value of 91 +/- 22 pg/mL (P < 0.01). This decline was maintained when intraesophageal balloons, which compartmentalized a 7.5 cm perfused segment of the esophagus, were inflated (86 +/- 17 pg/mL; P < 0.01). This decline was potentiated further when subsequent perfusion with saline was implemented to reach the lowest value of 46 +/- 17 pg/mL (P < 0.001 versus basal and P < 0.05 versus tubing and balloon evoked values) at the end of the perfusing procedure. Esophageal perfusion with acid and acid/pepsin solution, however, partly restored the significant decline in sPGE2 concentration observed during prolonged perfusion with saline. The sPGE2 output during basal conditions was 89 +/- 13 pg/min and increased dramatically during stimulation by placement of intraesophageal tubing (241 +/- 48 pg/min; P < 0.01) and inflation of intraesophageal balloons (244 +/- 48 pg/min; P < 0.01). Subsequent esophageal perfusion with saline resulted in a gradual decline of sPGE2 output evoked by mechanical stimuli that reached the final value of 178 +/- 39, which was not significantly different from that observed in the basal condition (P < 0.1 versus basal value). Introduction of HCl and pepsin into the perfusing solution significantly prevented the decline of sPGE2 output observed during perfusion with saline (252 +/- 36 pg/min; P < 0.01 versus basal). The modulatory impact of mechanical and chemical stimulation on sPGE2, demonstrated for the first time in humans, may suggest the potential contribution of salivary prostanoids to the maintenance of the integrity of the esophageal mucosa.

The effect of esophageal mechanical and chemical stimuli on salivary mucin secretion in healthy individuals.

Because of a newly developed model of esophageal perfusion in humans, the authors could study the role of esophago-salivary reflex in salivary neutral and acidic mucin output. The basal rate of neutral mucin output was 0.24 +/- 0.06 mg per minute. Placement of intraesophageal tubing and inflation of balloons resulted in a highly significant increase in salivary mucin output (2.10 +/- 0.22 mg per minute; p < 0.00001). However, implementation of esophageal perfusion with saline resulted in a significant decline of salivary mucin output (1.28 +/- 0.10 mg/mL NaCl4 versus 2.08 +/- 0.24 mg/mL NaCl1; p < 0.001). Esophageal perfusion with hydrochloric acid prevented the decline of salivary mucin output observed during perfusion with saline, whereas infusion of hydrochloric acid/pepsin resulted in a significant enhancement of salivary mucin output (2.89 +/- 0.31 mg per minute; p < 0.01). Therefore, mechanical and chemical stimulations resulted in an overall 9-fold and 12-fold increase in the rate of salivary mucin output over the basal value, respectively. The basal rate of acidic mucin secretion was 0.26 +/- 0.06 mg per minute. After placement of intraesophageal tubing, inflation of balloons, perfusion hydrochloric acid, or hydrochloric acid-pepsin solution, a significant enhancement in the rate of salivary acidic mucin output, similar to that observed during measurement of neutral mucin, was observed. Therefore, during mechanical and chemical stimulation, the rate of salivary acidic mucin output increased 7.3-fold and 11.1-fold over the basal value, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Gastric cancer with special references to WHO and Laurén's classifications: glycogen and triacylglycerol concentrations in the tumor.

In eighty patients with histologically verified gastric carcinoma the concentrations of glycogen and triacylglycerols were evaluated in specimens taken endoscopically from the tumor and the surrounding unchanged gastric mucosa. The results were analyzed in relation to the histological type of carcinoma according to WHO's and Laurén's classifications. The control group consisted of sixteen patients with superficial chronic gastritis. An elevated glycogen concentration was found in tumors of all types of gastric carcinoma; its level in the neoplasm was significantly higher also in relation to unchanged gastric mucosa surrounding the tumor. A particularly high glycogen level was present in the slow growing well-differentiated cancers, e.g. papillary and tubular adenocarcinomas or intestinal-type carcinoma. Reversely, in the fast growing and poorly differentiated cancers, e.g. undifferentiated or diffuse-type carcinoma, the glycogen contents were lower. Also triacylglycerol concentrations in the tumors as well as in the surrounding unchanged gastric mucosa were significantly higher than those in the control gastric mucosa specimens; no significant difference in triacylglycerol concentrations was observed between groups of patients with various types of carcinoma. It was concluded that (1) glycogen concentrations in the neoplastic tissue are cancer-growth related and characteristic for each kind of carcinoma, (2) an elevated triacylglycerol content in the tumor is probably a result of general lipid changes in the host.

Treatment of the gastric stump ulcer: an open study with five drugs.

BACKGROUND/AIMS: Despite a great progress in the treatment of peptic ulcer disease, the management of gastric stump ulcers still remains to be established. METHODOLOGY: Eighty-one patients with peptic ulcer developed postoperatively in the gastric remnant were treated in an open trial with 5 antiulcer drugs (cimetidine, omeprazole, sucralfate, colloidal bismuth and misoprostol) characterized by different mechanisms of action. The ulcer healing rate was evaluated endoscopically after 2, 4 and 6 weeks. RESULTS: It was found that after 2 weeks the most rapid ulcer healing was in the omeprazole and cimetidine treated groups, 67 and 43% of healing, respectively. Also after 4 weeks the antisecretors were more effective than gastroprotective drugs; ulcer healing rate for omeprazole was 87% and cimetidine 68%, while for sucralfate, colloidal bismuth and misoprostol 50%, 52%, and 33%, respectively. After 6 weeks all drugs represented very close ulcer healing rates. CONCLUSIONS: Both antisecretory and gastroprotective drugs may be useful in the management of stump ulcers, however, to initiate and accelerate the stump ulcer healing omeprazole appears to be the drug of choice.

Study of salivary response to continuous infusion of cerulein and secretin in healthy subjects.

OBJECTIVE: The effects of intravenous infusion of cerulein and secretin on the secretion and biochemical composition of whole saliva in humans were studied. STUDY DESIGN: A total of 33 subjects were divided into 3 groups, which underwent intravenous infusion with saline solution (NaCl 0.15 mol/L(-1)); saline solution, cerulein (1.25 x 10(-3) microg kg(-1) min(-1)), and cerulein supplemented with secretin (2.5 x 10(-2) clinical units kg(-1) min(-1)); and saline solution, secretin (2.5 x 10(-2) clinical units kg(-1) min(-1)), and secretin supplemented with cerulein (1.25 x 10(-3) microg kg(-1) min(-1)). RESULTS: Cerulein reduced salivary flow rate, bicarbonate concentration and output, and protein output and increased amylase activity. The inhibitory effect of cerulein on salivary flow rate and bicarbonate concentration and output prevailed when an infusion of cerulein was supplemented with secretin. Cerulein and secretin acting together increased protein concentration. Secretin alone decreased salivary flow rate and bicarbonate concentration, whereas secretin supplemented with cerulein not only decreased salivary flow rate, bicarbonate concentration, and bicarbonate output but also increased protein concentration. CONCLUSION: The effect of secretin and cerulein on salivary secretion and its composition is quite different from that observed in the pancreas.

The occurrence of Helicobacter pylori antigens in dental plaque; an association with oral health status and oral hygiene practices.

PURPOSE: Helicobacter pylori present in the oral cavity can be a source of gastric infection. Since in the oral cavity H. pylori is mostly found in dental plaque, the aim of the study was to determine whether the oral health status and oral hygiene practices affect the incidence of H. pylori antigens in dental plaque. MATERIALS AND METHODS: The study was performed in 155 patients aged 19-78 years. Patients who had taken antibiotics within 4 weeks preceding the study and those with a past history of H. pylori eradication were excluded. Each patient filled out a questionnaire on the procedures of dental plaque removal from natural teeth and dentures, and underwent oral examination. H. pylori antigens in supragingival plaque were determined by the immunological method with the use of a kit for detection of H. pylori antigens in stool samples. RESULTS: The presence of H. pylori antigens in dental plaque was found in 65.6% of the study subjects. The oral health status, frequency of dentist visits as well as the number and technique of dental plaque removal from natural teeth and dentures did not differ significantly between patients with infected and non-infected dental plaque. CONCLUSIONS: The occurrence of H. pylori antigens in dental plaque of natural teeth is not associated with oral health status or dental plaque removal practices from both natural teeth and removable dentures.

Patient factors affecting culture of Helicobacter pylori isolated from gastric mucosal specimens.

PURPOSE: Culture is one of the methods used for detecting Helicobacter pylori in the stomach. However, since it is costly, labor-consuming, and in a number of infected subjects gives a false negative result, the procedure is not routinely used. The aim of the study was to analyze some of the factors that may affect the outcome of H. pylori culture from endoscopic gastric mucosal specimens. MATERIAL AND METHODS: The study was conducted in a group of 265 subjects. The culture of gastric mucosal specimens was verified by urease test and histological examination. If the culture result was not consistent with one or two verifying tests, an additional two tests were used, i.e. H. pylori antigens in stool samples and anti-H. pylori antibodies in blood serum. RESULTS: In patients infected with H. pylori (at least two positive diagnostic tests), the analysis of factors that may affect the culture outcome revealed that neither age, gender, smoking, history of eradication, endoscopic diagnosis, use of proton pump inhibitors, ultrasonography of the abdomen or chest radiology performed the day before or on the day of gastroscopy, nor preparation for colonoscopy using osmotic fluids 1-2 days prior to gastroscopy had an effect on the culture outcome. Only high activity of gastritis (neutrophil infiltration) and low bacterial load in gastric mucosal specimens as well as drinking alcohol and the use of histamine H2 receptor blockers reduced culture efficacy in infected subjects. CONCLUSIONS: High activity of gastritis, low bacterial load, drinking alcohol and the use of histamine H2 receptor blockers can be the cause of failed H. pylori culture from gastric mucosa in the infected subjects. These factors should be taken into consideration when qualifying patients for the test and interpreting the results.