Genotypic and clinical differences of seropositive Helicobacter pylori children and adults in the Polish population.

Helicobacter pylori (H. pylori) plays an important role in the pathogenesis of the upper gastrointestinal tract diseases in both children and adults. The aim of this paper was to assess the differences between the clinical course of the disease in children and adults. This paper also presents an analysis of clinical symptoms, endoscopic and histopathological findings, H. Pylori cagA and vacA genotypes rates and analysis of the sensitivity of these strains to antibiotics in the Polish population, with possible practical and therapeutic implications. The multicenter study on the frequency of H. pylori infections assessed by the presence of antibodies in IgG class against H. pylori in serum was conducted in the years 2002 and 2003. The study group included 6565 children and adults, in 3827 of whom antibodies levels were above 24 U/mL. The authors analyzed clinical and endoscopic symptoms and in some patients with H. pylori seropositivity also histopathological changes, and cagA and vacA genes. Sensitivity of H. pylori strains to antibiotics were also analyzed. Differences between the frequency of infection between children and adults were determined. Endoscopic examination in adults revealed more frequent cases of gastropathy (P=0.003) and erosive gastritis (P=0.001), and in children-thick mucosal folds (P<0.0001). Histopathological examinations carried out in adults have revealed atrophic gastritis and intestinal metaplasia. In children, cagA(+) s1m1 was observed more frequently than in adults (34.0% versus 23.1%; P=0.02) contrary to cagA(-)s2m2 which occurred more frequently in adults (27.1% versus 14.0%; P=0.003). No effect of the infection on nausea, regurgitation, vomiting, heartburn, and abdominal pain in children was detected. However, adults infected with H. pylori suffered from more frequent episodes of heartburn and abdominal pain. The H. pylori strain exhibited a high resistance to metronidazole (higher in adults: 41.7% versus 27.4%; P=0.002), and to clarithromycin (higher in children: 20.2% versus 15.4%; P>0.05), and dual resistance to metronidazole and clarithromycin (higher in children: 9.9% versus 8.4%; P>0.05). Resistance of the H. pylori to amoxicillin and tetracycline was not detected. The conducted study indicated clinical differences in the H. pylori infection in children and adults. Among the differences in children, especially the more frequent infections by the cagA(+)s1m1/m2 strain could have an influence on further consequences of the infection. The obtained results could be useful in therapeutic decisions.

Complications of endoscopic retrograde cholangiopancreatography (ERCP) and their risk factors.

PURPOSE: Determination of the type and frequency of complications developing after diagnostic and therapeutic endoscopic retrograde cholangiopancreatography (ERCP) as well as the risk factors predisposing to them. MATERIAL/METHODS: The retrospective study, including 734 ERCP performed in 550 patients, with 404 (55%) ES (endoscopic sphincterotomy) during a 4-year period. RESULTS: Among 734 ERCP procedures, 76.4% (561) had both diagnostic and therapeutic purpose, 15.2% (112) were only diagnostic. Complications developed after 26 procedures (3.5%): acute pancreatitis (AP) in 8 patients (1.09%), cholangitis in 7 (0.95%) and delayed bleeding in 11 (1.5%) patients. After 49 (6.7%) ES immediate bleeding was observed. The risk factors for AP were: unintentional pancreatic duct contrasting, mechanical lithotripsy, the use of the "pre-cut" technique and bile duct dilatation. Cholangitis was more common in cases with difficult cannulation at older age and with lower baseline bilirubin level. The risk factors for delayed bleeding were: location of the ampulla of Vater in the diverticulum and the use of the "precut" technique. Immediate bleeding was more frequent after revision of bile ducts with Dormia's basket or with balloon, after introduction of contrast medium to the pancreatic duct or in ductal cholelithiasis. CONCLUSIONS: ERCP performed in the endoscopy unit of a specialist hospital department is a relatively safe procedure, with a low burden of complications as compared to the benefits it provides to appropriately qualified patients.

Exocrine pancreatic function in biliary tract pathology treated with the endoscopic methods.

PURPOSE: Incidence of pancreatic exocrine insufficiency in biliary pathology is estimated for about 30%. The objective was to assess pancreatic exocrine function in biliary tract pathology (cholelithiasis, strictures) before and after endoscopic treatment. PATIENTS AND METHODS: Twenty-eight patients with choledocholithiasis and its complications (19F/9M; aging 31-90 years, median: 69 years) were evaluated. Fecal elastase 1 concentration was measured using ELISA, before, early, and 6-8 weeks after endoscopic treatment. The inflammatory response of pancreas to the treatment was also assessed. RESULTS: Initial fecal elastase 1 concentration in patients (median 454 microg/g) was not significantly different as compared to the control (median 357 microg/g). Nine patients (32%) had low fecal elastase 1 concentration (below 250 microg/g) and out of them 6 had the concentration below 200 microg/g, suggesting impairment of exocrine pancreatic function. Endoscopic treatment was successful in 82% of patients. Pancreatic inflammatory response was noted only in one patient. After 6-8 weeks fecal elastase 1 concentration in the whole group of patients did not significantly change in comparison to the initial level. However, out of 9 patients with initially low fecal elastase 1 concentration (median 191 microg/g) at least in 6 pancreatic function improved (median 310 microg/g), P < 0.001. CONCLUSION: One third of the patients with biliary pathology had a low fecal elastase 1 concentrations, suggesting pancreatic dysfunction. In at least 2/3 of these patients successful endoscopic treatment of biliary pathology resulted in the significant increase of fecal elastase 1 concentration. Therefore, an additional positive effect of such treatment in some patients, could be an improvement of the exocrine pancreatic dysfunction.

Serum profiles of E-selectin, interleukin-10, and interleukin-6 and oxidative stress parameters in patients with acute pancreatitis and nonpancreatic acute abdominal pain.

INTRODUCTION: Excessive inflammatory response is one of the major causes of early mortality in acute pancreatitis (AP). AIM: To evaluate the serum profiles of E-selectin, interleukin (IL)-6, and IL-10 along with their correlation to the markers of oxidative stress and neutrophil activation in patients with AP and patients with nonpancreatic acute abdominal pain (NPAAP). METHODOLOGY: This prospective clinical study included 56 patients with AP (28 with mild AP and 28 with severe AP) as well as 15 patients with NPAAP. RESULTS: Serum concentrations of E-selectin, IL-10, and IL-6 and plasma concentrations of polymorphonuclear leukocyte elastase (determined on days 1-3, 5, and 10 after admission) were the highest in severe AP during the first 3 days and then declined. At day 10, the E-selectin level in severe AP was still higher than that in mild AP, and the IL-10 concentration increased again. There was no elevation in the E-selectin concentration in NPAAP patients, and IL-10 levels remained unchanged in mild AP. Oxidative stress, measured by serum malondialdehyde and 4-hydroxyalkenals levels, was the most pronounced in severe AP. CONCLUSIONS: The serum E-selectin concentration is markedly elevated in severe AP and is less in mild AP but not in NPAAP. It may result from stimulation with different inflammatory mediators or indicate vascular endothelium injury mediated by oxidative stress, especially in the severe form of AP.

Effect of Helicobacter pylori infection on the activity of class I, III and IV alcohol dehydrogenase in the human stomach.

BACKGROUND/AIMS: In the human stomach various alcohol dehydrogenase (ADH) isoenzymes exist. The gastric ADH activity is affected by a number of factors including also the infection of Helicobacter pylori. The objective was to investigate the activity of alcohol dehydrogenase isoenzymes of class I, III and IV in endoscopic specimens of gastric mucosa from the different parts of the stomach of men and women, considering the H. pylori infection. METHOD: Biopsy samples of gastric mucosa were taken from the corpus and antrum of 68 patients (42 of men and 26 of women) suspected for gastric ulcer. The colonization of H. pylori was present in 22 samples of men and 13 samples of women. The activity of class I isoenzyme was measured by the fluorimetric method with a specific substrate (4-methoxy-1-naphthaldehyde) and the activity of class III and IV by the photometric method with n-octanol and m-nitrobenzaldehyde as a substrates, respectively. RESULTS: In infected samples from the antrum and corpus of men's and women's stomachs the activity of class IV isoenzyme was decreased as compared to non-infected specimens. The activity of class III isoenzyme was decreased in the infected samples from the corpus of male patients, but the activity of class I does not significantly differ between infected and noninfected specimens from both sexes. CONCLUSION: H. pylori infection leads to significant decrease in the activity of class IV ADH in the stomach of men and women.

Helicobacter pylori infection and gastric secretion in duodenal and gastric ulcer patients--the effect of eradication after one year.

The mechanism by which Helicobacter pylori (Hp) predisposes to duodenal and gastric ulcers remains still unclear. It is possible that Hp infection impaires gastric secretion. Evaluation of gastric acid and mucus secretion before and after Hp eradication would let to estimate the influence of Hp infection on gastric secretion. To evaluate the effect of Hp infection on gastric acid and gastric mucous secretion before and one year after Hp eradication. We examined 28 Hp positive peptic ulcer disease patients (10-gastric ulcer GU, 18-duodenal ulcer DU) before and one year after antibacterial treatment. Gastric acid output was examined basely (BAO) and in response to pentagastrin (6 micrograms/kg) (MAO) using Kay's standard method. Some components of gastric mucus as fucose, galactose, hexosamines and sialic acid were measured using calorimetric methods basaly and after pentagastrin stimulation. Plasma gastrin concentration was measured in 20 patients (6-GU, 14-DU) by radioimmunoassay before and one year after eradication. Hp status was determined by rapid urease test (CLO) and histology (Giemsa stain). One year after Hp successful eradication gastric acid secretion was significantly reduced-BAO: 3,31 vs 1,474 mmol/h; MAO: 19,63 vs 14,85 mmol/h, p < 0.05. Plasma gastrin concentration decreased significantly from 9,783 to 6,017 pmol/I, p < 0.05. In patients with ineffective eradication we did not observe any significant changes in gastric acid secretion. An evident, but not statistically significant, decrease of sialic acid output in eradicated patients was noted. The study has shown the significant influence of Hp infection on gastric acid secretion. Those results support the hypothesis that increased gastric acid secretion may be one of the pathogenic mechanism of Hp infection inducing mucosal damage.

Multicenter evaluation of dual-therapy (omeprazol and amoxycillin) for Helicobacter pylori-associated duodenal and gastric ulcer (two years of the observation).

Treatment with the proton pump inhibitor (omeprazole) and single antibiotic (amoxycillin), two synergistic compounds, can cure Helicobacter pylori (H. pylori) infection, but this therapy is not as effective as had been expected. However, some studies show promising results. The aim of our study was to evaluate the effect of two weeks dual-therapy with omeprazole (O) and amoxycillin (A) on gastric (GU) and duodenal ulcer (DU) patients: ulcer healing, eradication of the H. pylori and recurrence rate of the ulcer. We studied 216 patients (aged 18-70) endoscopically proven GU (58 patients) and DU (158 patients). Rapid urease test from the two antrum biopses and two antral and two corporeal biopses using Giemsa stain method for confirmation of the H. pylori infection were used. The patients were treated with omeprazole 20 mg BID and amoxycillin 1.0 g BID for 2 weeks and investigated every 4 months during 2 years. Clearance effect of Hp infection was achieved in 65.1% GU and 66.4% DU patients. Eradication ("check point" after 4 months) in 43% DU and 56.6% GU patients was confirmed. Reinfection rate was found in 16% during 2 years. We conclude--dual-therapy (O and A) is not sufficiently effective to be recommended as an anti-H. pylori treatment. H. pylori eradication prevents recurrence of peptic ulcer and is an important issue in attempts to achieve permanent ulcer healing.

Mucolytic effects of Helicobacter pylori.

The mechanisms associated with colonization of human gastroduodenal mucosa by Helicobacter pylori remain unclear. To colonize gastric-type epithelium H. pylori must enter the gastric lumen, resist damage by all bactericidal factors operating within the acidic gastric milieu, penetrate the mucus gel despite highly viscous and hydrophobic properties of the mucus layer, and, finally, secure optimal conditions for its further multiplication. Since the H. pylori microorganism has been seen freely spread throughout the entire mucus layer thickness as well as in intimate contact with surface epithelium, the interrelationship between this spiral microorganism and the mucus seems to be of paramount importance. H. pylori has been shown to affect adversely the chemical and physical properties of the mucus layer. Therefore, the mucus layer compromised by the presence of this microorganism may become an easy target for acid and peptic damage, which ultimately leads to mucosal pathology, inflammation and/or peptic ulcer disease.

Peptic ulcer and chronic gastritis: their relation to age and sex, and to location of ulcer and gastritis.

The progression, age-behaviour and profiles of chronic gastritis were studied in 460 patients with active gastric or duodenal ulcer, and in 226 patients with ulcer scar. The results were compared with those obtained from a sample of subjects representing the general population. In patients with ulcer or ulcer scar, the progression of chronic gastritis was more rapid in antrum than in body mucosa, and was more rapid in patients with proximal ulcer in those with distal ulcer or in controls. In the body the progression of gastritis was significantly slower in patients with duodenal or juxtapyloric ulcer than in patients with proximal ulcer or in nonulcer controls: body gastritis tended to remain on the same level at all ages whereas it showed a steady progression with age in the nonulcer controls. The degree of gastritis showed a tendency to increase along the shift of ulcer to more proximal in the stomach; the prevalence of gastritis of pure B type (moderate or severe atrophy in antrum, but no atrophy in body mucosa) correspondingly increased along this shift. Severe antral atrophic gastritis was found in 7 per cent of proximal active gastric ulcers and in 20 per cent of proximal ulcer scars. The progression of antral and body gastritis was on the whole more rapid in males than in females irrespectively of the location of ulcer. We conclude that gastritis in different types of ulcers shows characteristic patterns of distribution, dynamics and progression with age. The high prevalence of severe grades of atrophic antral gastritis may also be of significance in regard to the pathogenesis of gastric cancer.

Gastric ulcer and gastritis: results of short-term follow-up examinations.

A hundred and one cases of gastric ulcer were examined in Poland by direct-vision endoscopic biopsy obtained from the antrum, angulus and body far outside the ulcer area, and from the edge of the ulcer. A simple mean score of gastritic changes and of intestinal metaplasia (IM) was calculated for each area, as also a mean score of IM for the mucosa around the ulcer. Two re-examinations were performed, one on average 2 months and the other on average 4.5 years, after the first examination. On the whole, gastritic changes and IM behaved as expected from earlier studies. The most striking finding was the high mean score of the angular mucosa in the case of more proximally situated ulcers. This angular peak was present at all examinations and both in patients healed during the follow-up and those in whom the disease remained active. A corresponding peak of gastritic changes and IM at the angulus was not found in more comprehensive Finnish control material, but was present in another smaller outpatient series, although the differences between the angulus and surrounding tissues were insignificant. At the first examination the mean scores of gastritis and of IM outside and around the ulcer were higher in patients with proximal ulcers in whom the ulcer healed during the observation period than in those, in whom it remained active. This difference was found at the first and at all subsequent examinations, and some of the differences were statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Lysolecithin affects the viscosity, permeability, and peptic susceptibility of gastric mucin.

The effect of lysolecithin and lecithin on gastric mucin viscosity, permeability to hydrogen ion, and degradation by pepsin was investigated. Preincubation with lysolecithin produced a marked decrease in the glycoprotein viscosity. This decrease was concentration-dependent and at 10 mM lysolecithin reached a value of 74%. A 25% increase in mucin viscosity was obtained with 10 mM lecithin. Permeability measurements showed that 10 mM lecithin increased the retardation ability of the glycoprotein to hydrogen ion by 11%, whereas a 12% decrease in the retardation capacity of the glycoprotein was obtained with 10 mM lysolecithin. The results of peptic activity assay indicated that whereas lecithin had no effect on the rate of mucin proteolysis, the lysolecithin exerted significant (75%) stimulatory effect. The results suggest that lysolecithin in the stomach weakens the integrity of the protective mucus layer by promoting peptic degradation, reducing the ability to resist acid penetration, and decreasing viscosity of its mucin component.

Effect of sucralfate on the viscosity of gastric mucus and the permeability to hydrogen ion.

The effect of sucralfate on the viscosity of pig gastric mucus and on its ability to retard the diffusion of hydrogen ion was investigated. Using a cone/plate viscometer at shear rates between 1.15 and 230 s-1, it was found that preincubation of mucus with increasing concentrations of sucralfate led to a gradual enhancement of the mucus viscosity. This enhancement in viscosity was proportional to the sucralfate concentration up to 1.0 X 10(-4) M and increased about 18% for each 10-fold increment in its concentration. The permeability measurements, conducted in a specially designed two compartment chamber, revealed that addition of sucralfate to gastric mucus had a profound beneficiary effect on its ability to retard the diffusion of hydrogen ion. In the presence of 1.0 X 10(-6) M sucralfate the permeability of mucus to hydrogen ion decreased by 35%, while the 1.0 X 10(-3) M sucralfate reduced the mucus permeability by 68%. The results show that sucralfate increases the viscosity of gastric mucus and improves its ability to impede the hydrogen ion penetration.

In vitro inhibition of peptic degradation of porcine gastric mucus glycoprotein by sucralfate.

The effect of sucralfate on the proteolytic activity of pepsin towards gastric mucus glycoprotein was investigated. Mucus glycoprotein isolated from pig stomach was incubated with pepsin with and without sucralfate, and the released alpha-amino residues were quantitated. In the absence of sulcralfate the rate of proteolysis was proportional to mucus glycoprotein concentration up to 450 micrograms and remained constant with time of incubation for up to 1 h. The apparent Km value of pepsin towards mucus glycoprotein was 8.7 X 10(-7) M. Introduction of sucralfate to the reaction mixtures resulted in reduction of the rate of glycoprotein proteolysis. The rate of inhibition was proportional to the sucralfate concentration up to 1 microM and was of the competitive type, with an apparent Ki value of 2.0 X 10(-6)M. The results suggest that among the beneficial effects of sucralfate on ulcer healing, one may be attributed to its ability to interfere with peptic digestion of gastric mucus glycoprotein.

Effect of sucralfate on the viscosity and retardation of hydrogen ion diffusion by gastric mucus glycoprotein.

The effect of an antiulcer drug (sucralfate) on the viscosity and the ability of pig gastric mucus glycoprotein to retard the diffusion of hydrogen ions was investigated. Preincubation with sucralfate produced a marked enhancement in the glycoprotein viscosity. This enhancement was concentration-dependent and at 1.0 X 10(-3) M sucralfate a 60% increase in viscosity was attained. Permeability measurements revealed that sucralfate caused a substantial improvement in the ability of the glycoprotein to retard the diffusion of hydrogen ions. At 1.0 X 10(-3) M sucralfate, permeability decreased by 25% and a 43% reduction was obtained with 1.0 X 10(-3) M sucralfate. It is suggested that sucralfate, by increasing the viscosity of the glycoprotein and by improving its ability to retard the diffusion of hydrogen ions, strengthens the integrity of gastric mucus.