Atrophic Corpus Gastritis and Helicobacter pylori Infection in Primary Biliary Cirrhosis

Chronic atrophic corpus gastritis, termed as autoimmune corpus gastritis or type A gastritis, and primary biliary cirrhosis (PBC) are characterized by a common immunological process against the exocrine glandular structures of both the stomach and bile duct. However, there has been controversy over whether atrophic corpus gastritis is associated with PBC. Recently, it has been suggested that Helicobacter pylori plays an important role in the early stage of atrophic corpus gastritis due to the induction of autoantibodies that are reactive with a protein in the gastric parietal cells. One hypothesis is that molecular mimicry, possibly resulting from H. pylori infection, might be responsible for initiating an autoimmune response in a predisposed host due to cross-reactivity among gastric mucosal, bile ductular, and bacterial antigens. The aim of this study is to assess whether atrophic changes of the gastric corpus could affect patients with PBC, and to determine the correlation with H. pylori infection. Sixteen patients with PBC were enrolled in this study. All patients were examined by serological studies of anti-pyruvate dehydrogenase (PDH) antibody, anti-H. pylori antibody, gastrin and vitamin B₁₂. Gastroscopy was performed on all patients in order to verify the histological findings and to microscopically identify H. pylori. Atrophic corpus gastritis was found in 2 of 16 patients with PBC (12.5%), one of whom was confirmed to have pernicious anemia, a developed stage of atrophic corpus gastritis. H. pylori infection in the gastric corpus and the anti-H. pylori antibody were found in 7 (43.8%) and 11 (68.8%) of 16 patients, respectively. Anti-H. pylori antibody was confirmed to be positive in both of the patients with atrophic corpus gastritis, although H. pylori was absent in the gastric biopsy specimen. There was a positive correlation between anti-PDH antibodies and anti-H. pylori antibodies in sera from patients with PBC. Atrophic corpus gastritis is not frequently involved in PBC. However, H. pylori is a possible pathogenic factor in atrophic corpus gastritis in PBC patients because of the presence of anti-H. pylori antibody. A positive correlation between the titer of anti-PDH antibodies and the titer of anti-H. pylori antibodies was confirmed. Consequently, H. pylori infection could induce autoimmune responses in the development of both PBC and atrophic corpus gastritis. H. pylori infection associated with PBC requires further study.     

Association Between Gastric Atrophy and Helicobacter pylori Infection in Japanese Children: A Retrospective Multicenter Study

The purpose of this study was to determine whether Helicobacter pylori infection and mucosal inflammation result in gastric atrophy in Japanese children. A total of 196 patients ages 1–16 years were retrospectively studied: 131 patients were infected with H. pylori and 65 patients were uninfected. Antral (n = 196) and corpus biopsy specimens (n = 70) were investigated based on the Updated Sydney system. In both the antrum and corpus, H. pylori-infected patients showed significantly higher degrees of inflammation and activity of gastritis, compared with noninfected patients. The prevalence of grade 2 or 3 atrophy in the antrum was 10.7% in H. pylori-infected patients and 0% in the noninfected patients (P < .01) and in corpus 4.3% and 0%, respectively (P = .20). The frequency of intestinal metaplasia in the 2 study groups was 4.6% and 4.6% in the antrum and 0% and 4.2% in the corpus, respectively. Among H. pylori-infected patients, the antrum showed significantly higher degrees of H. pylori density, inflammation and activity of gastritis, and atrophy than the corpus. In the antrum, atrophy was significantly correlated with activity, whereas in the corpus, atrophy correlated with H. pylori density, inflammation, and activity. H. pylori-induced gastric inflammation can cause atrophy in Japanese children, predominantly in the antrum. It remains to be determined whether H. pylori-infected children with gastric atrophy are at increased risk for gastric cancer.     

Circadian Gastric Acidity and Helicobacter pylori Infection in Patients with Chronic Pancreatitis

A high prevalence of duodenal ulcer has been reported in patients with chronic pancreatitis. Data from previous studies on gastric acid secretion in these patients have provided conflicting results, and the potential role of H. pylori infection has been poorly investigated. The aim of this study was to assess the circadian pattern of gastric acidity and the prevalence of H. pylori infection in a group of patients suffering from this disease. Thirty-five patients with chronic pancreatitis ascertained by means of pancreatic calcifications or ductal alterations revealed by ERCP were recruited for this prospective study. They underwent 24-hr gastric pH-metry with glass minielectrodes positioned in the gastric corpus, and their profile of gastric acidity was compared with that of 35 healthy subjects, matched for age and sex. H. pylori infection was diagnosed by means of serology. There was no statistical difference (P = NS) in gastric pH of circadian, nocturnal, daytime, and postprandial periods between healthy subjects and patients with chronic pancreatitis. The prevalence of H. pylori infection was rather low (31%) in our patients and similar to that of a comparable control population (37%) in our geographical area. In conclusion, our study shows that patients with chronic pancreatitis have a circadian pattern of gastric acidity similar to that of normal subjects. Moreover, the prevalence of H. pylori infection is low in this population. These findings greatly differentiate the ulcer diathesis in chronic pancreatitis from that of patients with ordinary duodenal ulcer and suggest that other factors are implicated in the ulcerogenic process.     

Helicobacter pylori Seroprevalence in Patients with Autoimmune Hepatitis

Autoimmune hepatitis is characterized by a continuing hepatocyte necrosis that usually progresses to liver cirrhosis. Autoimmunity is also a feature of chronic infection by Helicobacter pylori, a gram-negative bacterium involved in the pathogenesis of peptic ulcer and upper gastrointestinal bleeding, with both events frequently occurring in patients with chronic liver disease. A newly described pathogenetic mechanism for chronic hepatitis and hepatocellular carcinoma in the mouse is linked to Helicobacter spp. infection. A high prevalence of H. pylori infection was demonstrated in patients with viral-related cirrhosis but never studied in cases of autoimmune hepatitis. In a case-control study, we examined 31 consecutive patients (25 women and 6 men, age range 20–66, mean age 46 ± 4.3 years) suffering from autoimmune hepatitis and 62 sex- and age-matched blood donors (50 women, 12 men, age range 20–65, mean age 46 ± 5.4 years) resident in the same area. Antibodies to H. pylori were present in 20 of 31 (64.5%) autoimmune patients compared to 33 of 62 (53.2%) controls (P = 0.3, odds ratio 1.60, 95% CI 0.60–4.28). The difference was not statistically significant either in female or male patients. In conclusion, the prevalence of H. pylori infection in patients and controls was similar in our study of patients with chronic autoimmune hepatitis.     

Progression of Atrophic Gastritis and Intestinal Metaplasia Drives Helicobacter pylori Out of the Gastric Mucosa

This study was performed to evaluate the implication of anti-H. pylori IgG positivity when CLOtest, histological test, and culture in the antrum and body are all negative, and to find out the specific disease category that is more affected by the hostile relationship of atrophic gastritis and intestinal metaplasia (IM) with H. pylori. Four hundred thirty-six patients (84 controls, 69 with duodenal ulcer, 96 with benign gastric ulcer, 43 with dysplasia, 144 with gastric cancer), who had not received any eradication therapy, were divided into three groups according to H. pylori test: CLOtest or histological H. pylori-positive group (group A; 294 cases), only anti-H. pylori IgG-positive group (group B; 62 cases), and anti-H. pylori IgG-negative group (group C; 80 cases). The grade of neutrophil and monocyte infiltration, atrophic gastritis, and IM was compared according to the updated Sydney system classification. Neutrophil and monocyte infiltrations were significantly severe in the group A. In contrast, the grade of atrophic gastritis and IM in the antrum was significantly higher in group B than the other two groups, A or C. When patients were divided according to the disease outcome in each group, the grade of IM in the body was statistically higher only in the patients with cancer or dysplasia in group B. These results suggest that anti-H. pylori IgG positivity with all negative invasive H. pylori tests represents past infection with H. pylori rather than a false negative, especially in the case of dysplasia and gastric cancer.     

Long-Term Rebamipide Therapy Improves Helicobacter pylori-Associated Chronic Gastritis

We investigated an antiinflammatory effect of rebamipide {2-{4-chlorobenzoylamino}-3-[2(1H)-quinolinon-4-yl] propionic acid}, a gastroprotective agent, in H. pylori-associated gastritis. Eighty-six patients with H. pylori-positive chronic gastritis were enrolled: 53 were treated with rebamipide (300 mg daily for 12 months) and 33 served as controls. Significant decreases in mononuclear cell infiltration into the antrum and corpus were noted in the rebamipide treatment group (before vs after, 1.42 ± 0.15 vs 1.02 ± 0.15; P < 0.01 and 1.60 ± 0.15 vs 1.21 ± 0.14; P < 0.05, respectively). Levels of infiltrating neutrophil were also decreased in the antrum (before vs after, 0.98 ± 0.14 vs 0.70 ± 0.13; P < 0.05) and were associated with a decrease in iNOS production. Sera from patients treated with rebamipide showed a significant decrease in gastrin (276.3 ± 58.3 pg/ml vs 173.0 ± 34.2 pg/ml; P < 0.05), whereas no change was observed in the control group. These suggest that long-term rebamipide treatment improved histologic gastritis and decreased serum gastrin levels in H. pylori-associated gastritis.     

Helicobacter pylori infection and food-cobalamin malabsorption

Two entities of considerable recent interest,Helicobacter pylori infection of the stomach and food-cobalamin malabsorption, are each intimately associated with gastric abnormalities. A possible connection between the two entities thus suggested itself and prompted us to study 98 subjects with low serum cobalamin levels but normal Schilling test results and 17 controls with normal cobalamin levels. Food-cobalamin absorption was measured with the egg yolk-cobalamin absorption test (EYCAT) and was abnormal in 56 of the 115 subjects. IgG antibody toH. pylori was found in 78% of the 27 patients with severe food-cobalamin malabsorption (EYCAT <1.0% excretion), compared with only 45% of 29 subjects with mild malabsorption (EYCAT 1.0–1.99%) and 42% of 59 subjects with normal absorption (EYCAT 2.0%) (x²=9.52,P<0.01). Antibody-positive patients had lower EYCAT excretion values than those without antibody (2.03±1.83% vs 3.11±2.13%,t=2.913,P=0.005). While Hispanic patients tended to malabsorb food cobalamin more frequently than did white or black patients, and men were more often antibody-positive than women, race, sex, or age characteristics were not responsible for the significant association between serologic evidence ofH. pylori infection and severe malabsorption of food cobalamin. The association that we describe suggests that gastritis induced byH. pylori predisposes to a more severe form of food-cobalamin malabsorption, among its other effects on gastric status.This study was supported by grant DK-32640 from the National Institutes of Health, by the NIH National Center for Research Resources of the General Clinical Research Centers grant MO1 RR-43, by the Medical Research Service of the Department of Veterans Affairs, and by the Procter & Gamble Company.     

Influence of Smoking and Helicobacter pylori on Gastric Phospholipids

Smokers show higher rates of peptic ulcer disease (PUD) than nonsmokers, probably due to detrimental effects on the gastric mucosa. Surface-active phospholipids (SPL) are believed to play a key part in gastric cytoprotection. The aim of this study was to determine the chronic effects of smoking on the gastric SPL and to relate them to H. pylori (Hp) -induced effects. Gastric juice was aspirated in 52 patients, with normal findings at planned upper gastrointestinal endoscopy, and concentrations of seven phospholipid subclasses were analyzed. Concentrations of lysophosphatidylethanolamine (l-PE) were increased (P = 0.006) in smokers compared to nonsmokers in non-Hp-infected samples. Nonsmokers infected with Hp showed increased levels of l-PE (P = 0.01) and phosphatidylinositol (PI) (P = 0.02) compared to subjects not infected. In human gastric juice PI seems to be the dominating PL subclass, in contrast to the composition in biopsy specimens. We also found both Hp-infected and smoking subjects to have higher concentrations of more polar phospholipid subclasses, ie, l-PE, making the mucosa more vulnerable to acid attack as the gastric surfactant becomes less hydrophobic.     

Helicobacter pylori Reduces Intracellular Glutathione in Gastric Epithelial Cells

Helicobacter pylori infection has been associated with stimulation of gastric mucosal reactive oxygen species (ROS) production, and it was postulated that ROS production is due to neutrophil infiltration and activation. The aim of this study was to investigate the direct effect of H. pylori on ROS formation in gastric epithelial cells in vitro. The human gastric cancer cell line HM02 was incubated with H. pylori for 24 hr, and the effects on cell number and the intracellular radical scavenger reduced glutathione (GSH) were assessed. H. pylori caused a concentration-dependent reduction of cellular GSH concentrations over a broad bacteria-to-cell ratio (1.4–42) in the absence of cell necrosis. The radical scavengers MnTBAP (a cell permeable superoxide dismutase) and ebselen provided protection against H. pylori-induced decrease in cellular GSH concentrations. We conclude that H. pylori directly decreases cellular GSH concentrations in gastric epithelial cells. We suggest that this effect is caused by the release of ROS by H. pylori.     

Helicobacter pylori Infection Is the Major Risk Factor for Gastric Inflammation in the Cardia

We attempted to clarify the pathogenesis of gastric inflammation in the cardia. Eighty Japanese participated in this study. Biopsy specimens of the gastric antrum, corpus, and cardia (1 cm from the squamocolumnar junction) were obtained, and histological gastritis was evaluated. Cardiac inflammation was also evaluated using magnifying gastroscopy. We examined Helicobacter pylori infection, gastric juice pH/bile acid (BA), serum pepsinogen and gastrin levels, gastroesophageal reflux disease (GERD), and habitual smoking and assessed the relations between these factors and cardiac inflammation. The prevalence of H. pylori infection was statistically higher in patients with cardiac inflammation than in those without inflammation (P < 0.05). The relationship was also demonstrated by magnifying gastroscopy. Cardiac inflammation was linked to low acid output but not linked to the BA concentration or habitual smoking. Cardiac inflammation was more pronounced in patients without GERD. These results suggest that H. pylori is a major risk factor for cardiac inflammation in the Japanese.     

Helicobacter pylori infection and gastric juice vitamin C levels

H. pylori has recently been recognized as a novel risk factor of gastric cancer, but its precise role in gastric carcinogenesis is as yet unknown. The aim of the present study was to assess the relationship betweenH. pylori infection and vitamin C levels in gastric juice and also to examine whether eradication ofH. pylori could have any impact on these levels. Gastric juice and plasma vitamin C levels were measured in 88 dyspeptic patients who had an upper gastrointestinal endoscopy. In the subgroup ofH. pylori-positive patients, eradication was attempted with triple therapy. This subgroup was studied on two occasions, ie, before and after treatment. There were 58H. pylori-positive and 30 -negative patients. Gastric juice vitamin C levels inH. pylori-positive patients were statistically lower (P<0.001) than the levels in theH. pylori-negative patients. Triple therapy achieved eradication in 45 patients (77.6%) of the 58H. pylori-positive patients. BeforeH. pylori was eradicated in these 45 patients gastric juice vitamin C levels were significantly (P<0.001) lower than those after eradication, the latter being no different than the group of 30H. pylori-negative patients. There was a significant (P<0.001) improvement of gastritis after eradication, which paralleled the elevation of gastric juice vitamin C levels. No difference was noted in plasma vitamin C levels betweenH. pylori-negative and -positive patients or in the latter before and afterH. pylori treatment. In 13 of the 58H. pylori-positive patients where eradication was not successful there was no difference in gastric juice vitamin C levels before and after eradication and the same was observed for the degree of gastritis. It is concluded thatH. pylori-infected patients have lower gastric juice vitamin C levels in comparison toH. pylori-negative patients.H. pylori eradication restores gastric juice vitamin C levels, which may prove potentially important in the prevention of gastric cancer.This work was presented in part during the V Workshop on Gastroduodenal Pathology andHelicobacter pylori; Dublin, July 5–7, 1992, and published as an abstract (Irish Journal of Medical Sciences 161(suppl 10):25, 1992) and during the American Gastroenterological Association meeting in Boston, Massachusetts, May 15–21, 1993, and published as an abstract (Gastroenterology 104(suppl) A181, 1993).     

Role of Helicobacter pylori infection and nonsteroidal anti-inflammatory drug use in bleeding peptic ulcers in Japan

Background Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) are well-known major causes of peptic ulcers. This study aimed to characterize the features of bleeding peptic ulcers in Japan. Methods This prospective study evaluated 116 patients revealed to have bleeding peptic ulcers from January 2000 to December 2002. Results Eighty-eight of the 116 patients (75.9%) had H. pylori infection. Seventy (60.3%) patients were positive for H. pylori with no history of NSAID use (group A), and 18 (15.5%) were positive for H. pylori with a history of NSAID use (group B). Among the H. pylori-negative patients, 15 (12.9%) were associated with NSAID use (group C). Thirteen (11.2%) patients had no H. pylori infection or history of NSAID use (group D). Among the 33 patients with a history of NSAID use, 11 were on-demand NSAID users and 14 took daily low-dose aspirin. The patients in groups B and C were significantly older that those in groups A and D, and they more frequently had coexisting diseases compared with group A. In group D, 11 patients had atrophic changes revealed by endoscopic examination, suggesting a past H. pylori infection, and these atrophic changes remained at the time of bleeding. Many of the patients in group D had serious comorbidity. Compared with healthy control subjects, the concentrations of both phosphatidylcholine and phosphatidylethanolamine were significantly decreased in the antral gastric mucosa in all patient groups. Conclusions NSAID use contributed to bleeding ulcers in 28.4% of patients; thus, low-dose aspirin or on-demand NSAID use may cause bleeding ulcers. There were only two (1.7%) confirmed cases of H. pylori-negative, non-NSAID ulcers.     

Infection with Helicobacter pylori Affects All Major Secretory Cell Populations in the Human Antrum

We have investigated how gastric H. pylori infection affects antrum secretory cell types by studying the expression of secretory proteins in antrum epithelium. Antrum biopsy specimens were prospectively collected from 102 individuals (49 H. pylori-infected). Immunohistochemistry was performed for secretory mucins (MUC5AC, MUC5B, MUC6), Trefoil factor family (TFF)-peptides (TFF1, TFF2), endocrine peptides (gastrin, chromogranin A), and proliferating cells (Ki-67). Protein expression was quantified morphometrically. H. pylori infection was significantly correlated to mucosal inflammation and to epithelial atrophy and proliferation. In H. pylori-infected patients the number of proliferating cells increased significantly, and the zone of proliferating cells shifted toward the surface epithelium of the antral glands. Infection was correlated with decreased MUC5AC, TFF1, and TFF2 expression and increased MUC6 and MUC5B expression. Endocrine cells expressing chromagranin A and gastrin shifted toward the surface epithelium of the antral glands in H. pylori-infected patients. H. pylori infection and concomitant inflammation induced increased epithelial proliferation and triggered coordinate deregulation of secretory cell populations in the antrum. In particular, infection led to a coordinated increase in cells expressing MUC6 and MUC5B at the expense of MUC5AC-producing cells.     

Helicobacter pylori Infection is Associated with a High Incidence of Intestinal Metaplasia in the Gastric Mucosa of Patients at Inner-City Hospitals in New York

Gastric carcinogenesis is a multistep process progressing from chronic gastritis, through glandular atrophy (GA), intestinal metaplasia (IM) and dysplasia. Infection of the stomach with H. pylori increases the risk of developing gastric cancer. Few studies have examined the degree to which Hp-induced changes occur in specific populations. In the present study, we examined the association between Hp infection and histological changes in the gastric mucosa of patients at two inner-city hospitals in New York. Patients enrolled in this study were undergoing endoscopy for gastrointestinal complaints. One antral biopsy was taken for detecting and genotyping Hp by PCR. Additional biopsies were taken from the antrum and fundic region for histological analysis and were scored with respect to acute and chronic inflammation, GA, IM and Hp infestation according to the Sydney classification. Hp strains infecting these patients were genotyped with respect to the expression of Hp virulence factors including VacA, CagA, and BabA2. Samples were collected from 126 patients at Kings County Hospital in Brooklyn and St. John’s Episcopal Hospital in Queens. Hp infection rates were highest in Blacks (41.6%) and Hispanics (29.4%) and lowest in Caucasians (18.8%). Scores for acute and chronic inflammation and IM were higher in Hp-infected individuals in both the antrum and fundic regions, whereas Hp infection did not affect the incidence or intensity of GA. In Hp-infected individuals, the incidence of IM was greater in the antrum (Hp-infected 37.8% vs. non-infected 9.2%, p < 0.05) and fundic region (Hp-infected 15.1% vs. non-infected 1.8%, p < 0.05). Genotyping of the Hp strains infecting these patients revealed that the predominant VacA allele was s1bm1 and that the CagA gene was present in 69.8% of Hp-infected samples. Interestingly, the BabA2 gene was detected in only four samples (9.3%). The incidence of IM in the antrum was higher in CagA+ samples when compared with CagA- samples (52.2% vs. 15.4%, respectively). Our findings indicate that the virulent Hp strain infecting minority patients treated at inner-city hospitals in New York City is associated with a high incidence of IM and that these patients may be at greater risk for developing gastric cancer than the general population. Support: This work was supported by grants from the Rosalyn S. Yalow Foundation for Medical Research and the Cancer Research and Prevention Foundation.     

Intracellular VacA Is a Valuable Marker to Predict Whether Helicobacter pylori Induces Progressive Atrophic Gastritis That Is Associated with the Development of Gastric Cancer

VacA was histochemically stained in biopsy specimen and was intracellularly and mainly located in fundic gland area. It is recognized gastric atrophy was observed in the H. pylori-positive patients with intracellular VacA compared with others. The aim of study is to understand the relationship between intracellular VacA and the progression of gastric atrophy that is associated with gastric cancer. Biopsy specimens and sera were obtained from 364 people in their 50s and 60s without gastric cancer diagnosed at first endoscopy undergoing diagnostic endoscopy, for H. pylori infection, histology, and the histochemical status of intracellular VacA using anti-VacA Ab during the follow-up period (mean, 7.3 years). Three hundred eleven of 364 enrolled patients were H. pylori positive and 53 patients were H. pylori negative at first endoscopy. VacA was intracellularly stained with vacuolation and cell destruction in the fundic gland in 98 of 311 H. pylori-positive patients and not stained in another 213 H. pylori-positive patients plus 53 H. pylori-negative patients at first endoscopy. Gastric atrophy has significantly progressed in the H. pylori-positive patints with intracellular VacA with gastric ulcers compared with the others and six gastric cancers have developed in this group during the follow-up period (mean, 7.3 years). Intracellular VacA is a valuable marker to predict whether Helicobacter pylori induces progressive atrophic gastritis that is associated with the development of gastric cancer.     

Effect of Helicobacter pylori Eradication on 24-Hour Gastric pH and Duodenal Gastric Metaplasia

Published data on the regression of the extent of duodenal gastric metaplasia (DGM) after the eradication of Helicobacter pylori infection and the normalization of the organism-induced alterations in gastric physiology are scanty and controversial. Therefore, we decided to assess the circadian pattern of gastric acidity and the degree of DGM before and one year after H. pylori eradication in a group of duodenal ulcer patients. Fifteen consecutive H. pylori-positive patients with endoscopically proven duodenal ulcer were recruited for this study. The diagnosis of H. pylori infection was based on CLO-test and histology, and DGM was assessed on four bulb biopsies taken before and one year after H. pylori eradication. At the same time, gastric pH was measured by 24-hr continuous intraluminal recording. H. pylori eradication was ascertained by means of concomitant negative CLO-test and histology performed both four weeks after the end of the eradicating treatment and at the one-year endoscopic control. After successful cure, all patients discontinued any antiulcer medication. The mean 24-hr gastric pH was 1.7 ± 0.4 before and 1.6 ± 0.4 after one year of H. pylori eradication (P = 0.75). DGM improved in three cases, worsened in four cases, and was unchanged in eight cases at the one-year control (P = 0.87). No correlation was found between 24-hr gastric pH and DGM (P = NS) both at baseline and one year after eradication. Our results show that neither circadian gastric acidity nor DGM change significantly one year after H. pylori eradication in duodenal ulcer patients. Thus, the disappearance of H. pylori infection does not determine any increase in gastric pH and any reversal of gastric-type epithelium in the duodenum.     

The Effect of Intragastric Ammonia Production on Titratable Gastric Acid Output in Helicobacter pylori-Infected Patients with Chronic Gastritis

The purpose of this study was to assess whether intragastric neutralization of HCl by ammonia in Helicobacter pylori-infected patients could meaningfully affect the titratable acid output as a measure of gastric acid secretion in a relation to the severity of infection. In 79 patients with different degrees of Helicobacter pylori infection and chronic gastritis, the basal acid output (BAO) and maximal acid output (MAO) after pentagastrin (6 μg/kg s.c.) was estimated. Cl⁻ and NH₄⁺ contents in these fractions were also assayed. H⁺/Cl⁻ ratio in the MAO fraction was diminished in markedly infected patients (68.1 ± 3.9%, vs 84.1 ± 3.3% in noninfected patients; P < 0.005). Ammonium content was maximal in patients with marked infection (0.912 ± 0.086 vs 0.149 ± 0.034 mmol/hr in MAO [P < 0.001] and 0.475 ± 0.063 vs 0.105 ± 0.016 mmol/hr in BAO of noninfected patients [P < 0.001]), with intermediate values in mild and moderate infection. The NH₄⁺/(H⁺ + NH₄⁺) ratio reached 27.01 ± 7.34% in the BAO of moderately infected patients, vs 10.22 ± 3.81% in noninfected patients (P = 0.05), and 7.25 ± 1.06% in the MAO of markedly infected patients, vs 1.14 ± 0.33% in noninfected patients (P < 0.001). The intragastric ammonia production affects the titratable acid output in Helicobacter pylori-infected patients dependent on the severity of infection. Therefore this factor should be taken into consideration in the evaluation of gastric secretory function in Helicobacter pylori-infected patients. This study was supported by Medical University of Bialystok Grant 514 928.     

Serum and Tissue Beta-2 Microglobulin Levels in Patients with Helicobacter pylori Infection

Background and aim Beta-2 microglobulin (β₂-m) is a minor plasma protein, secreted from the plasma membranes as a result of the continuous regeneration of membrane proteins in the cell surface of all nucleated cells. The relationship between Helicobacter pylori and β₂-m has not been adequately established in studies. In this study, we aimed to compare the levels of serum and tissue β₂-m in patients with and without H. pylori infection, and to examine the relationship between levels of serum and tissue β₂-m. Material and methods About 30 patients with H. pylori gastritis and 22 healthy persons were enrolled in this study. Gastric biopsies were histologically analyzed and compared according to tissue and serum β₂-m levels. Results Serum β₂-m levels were comparable in H. pylori and control groups. There was no significant link between tissue H. pylori grade and serum β₂-m levels. Subendothelial β₂-m was detected in 19 (63.3%) cases with H. pylori and none of the control group with immunohistochemical staining (P < 0.001). There was no correlation between serum and tissue levels of β₂-m. Conclusion β₂-m accumulates in the majority of gastric tissues of patients with active chronic gastritis who were H. pylori (+), whereas no accumulation was found in H. pylori (−) control subjects.     

Clinical Relevance of cagE Gene from Helicobacter pylori Strains in Japan

It has been reported that H. pylori-containing cagE was associated with duodenal ulcer. The aims of the present study were to clarify the association between the cagE gene and clinical outcome and to analyze the relationship between the cagE gene and two other virulence factors—cagA and vacA—in two areas in Japan (Fukui and Okinawa) where the prevalence of duodenal ulcer and gastric cancer risk are quite different. Eighty of 81 isolates possessed the cagE gene, and all isolates possessed the cagA gene. The vacA genotype s1c/m1 was a major genotype in both areas in Japan. There was no significant association between cagE, cagA status, or vacA genotype and clinical outcome. Phylogenetic analysis of the cagE gene indicated that most Japanese isolates formed a different cluster from strains isolated in the West with an association with the vacA genotype. In conclusion, the strains with cagE, cagA, and the s1c/m1 genotype of vacA are predominant in Japan regardless of clinical outcome and construct a different phylogenetic cluster from those in the West.     

Effects of Chronic Administration of Helicobacter pylori Extracts on Rat Gastric Mucosal Microcirculation In Vivo

The mechanisms by which Helicobacter pylori contributes to gastroduodenal injury are unclear. We have previously described platelet aggregation within rat gastric mucosal microcirculation following acute administration of H. pylori extracts. However, leukocyte activation was not observed. This study aimed to determine whether chronic administration of H. pylori could induce leukocyte activation. Rats were gavaged with either H. pylori or E. coli extracts or with distilled water three times daily at three-day intervals. Acridine red was used to quantitate gastric mucosal leukocyte/platelet activity using fluorescent in vivo microscopy. Further animals received additional acute H. pylori after 1 hr and recordings were made for a further 1 hr. Significant numbers of flyers, rollers, and adherent leukocytes were observed throughout the study in H. pylori animals. Only adherent leukocytes were observed following E. coli. Acute H. pylori induced a further significant increase in adherent leukocytes. Significant platelet thrombi were also present in H. pylori-treated animals. In conclusion, earlier studies demonstrated platelet aggregation but no leukocyte activation, which is in contrast to the current chronic studies. Platelet activation may be the initial response to H. pylori and involved in recruitment of leukocytes. These activated cells may contribute to the development of gastric mucosal damage.