Antral release of gastrin and somatostatin in duodenal ulcer and control subjects.

Organ culture was used to compare gastrin and somatostatin release from cultured antral mucosa obtained from duodenal ulcer and non-ulcer (control) subjects. In response to dibutyryl cyclic AMP (DBCAMP) cultured antral mucosal explants from patients with a history of duodenal ulcer released a greater proportion of antral gastrin into the medium than did antral mucosal explants from non-ulcer subjects. Somatostatin release from antral mucosa from duodenal ulcer patients was substantially less than somatostatin released by antral explants from non-ulcer subjects. In the non-ulcer subjects there was a direct positive correlation between the amounts of antral somatostatin and gastrin released into the culture medium (r = 0.64, less than p 0.01). In the duodenal ulcer patients, however, there was no correlation between gastrin release and somatostatin release from antral mucosa ( r = 0.09; p greater than 0.2). Results of these studies identify enhanced gastrin release in response to stimulation and decreased release of somatostatin from antral mucosa of duodenal ulcer patients. These alterations in paracrine relationships of antral somatostatin and gastrin in duodenal ulcer subjects may contribute, at least in part, to the pathogenesis of duodenal ulcer disease.     

Helicobacter pylori density and cagA status in cirrhotic patients: a case-control study

BACKGROUND AND AIM: Despite a similar Helicobacter pylori prevalence, peptic ulcer is more frequent in cirrhotic patients than in controls. We evaluated whether cirrhotic patients had an increased bacterial density and/or a higher prevalence of H. pylori cagA-positive strains than controls. METHODS: A total of 36 dyspeptic cirrhotic patients with H. pylori infection and 72 matched controls were enrolled. H. pylori infection was detected at histology on Giemsa staining, bacterial density was assessed using difference over baseline (DOB) values at 13C urea breath test, and cagA status was established at serology. RESULTS: Overall, both DOB values and prevalence of cagA did not significantly differ between cirrhotic patients and controls. However, peptic ulcer controls showed significantly higher DOB value (27.9 +/- 17.4 vs 19.4 +/- 9.3, respectively; P = 0.009) and cagA positive rate (85%vs 48%; P = 0.01) than non-ulcer dyspepsia patients. Although not statistically significant, a similar trend was observed in cirrhotic patients with peptic ulcer for DOB values (26.5 +/- 16.3 vs 18.3/1000 +/- 9.2, respectively; P = 0.07), whereas the cagA-positive rate was similar between peptic ulcer and non-ulcer dyspepsia patients (60%vs 50%; P = 0.30). CONCLUSIONS: The present data showed that both bacterial density and cagA prevalence did not differ between cirrhotic patients and controls.     

Effect of non-steroidal anti-inflammatory drugs on gastric and duodenal prostaglandin concentrations in patients with Helicobacter pylori infection.

BACKGROUND/AIMS: Both Helicobacter pylori and non-steroidal anti-inflammatory drugs are reported to affect gastroduodenal prostaglandin synthesis. However, their influence on gastric mucosal prostaglandins remains unclear. The aim of this study was to investigate the influence of nonsteroidal anti-inflammatory drugs on mucosal prostaglandin synthesis in patients with Helicobacter pylori infection. METHODOLOGY: We enrolled 87 Helicobacter pylori-infected patients in this study (gastric ulcer: 33, duodenal ulcer: 41, and non-ulcer dyspepsia: 13). Of them, 27 patients received non-steroidal anti-inflammatory drugs. Endoscopy was performed and biospy specimens from gastric body, antrum and duodenal bulb were assessed for Helicobacter pylori and prostaglandin concentration. RESULTS: A significantly lower mucosal prostaglandin E2 level at gastric body (142.2 +/- 28.1 ng/mg vs. 222.0 +/- 12.4 ng/mg, mean +/- SEM) and antrum (131.3 +/- 26.4 ng/mg vs. 226.0 +/- 19.0 ng/mg) was noted in Helicobacter pylori-infected gastric ulcer patients with non-steroidal anti-inflammatory drugs ingestion than in that of patients without non-steroidal anti-inflammatory drugs ingestion (p < 0.05). Using a multivariate analysis, we found that non-steroidal anti-inflammatory drug was an independent variable affecting gastric and duodenal mucosal prostaglandin E2 synthesis in patients with Helicobacter pylori-infected gastric ulcer. CONCLUSIONS: Non-steroidal anti-inflammatory drugs decrease gastroduodenal mucosal prostaglandin E2 synthesis in gastric ulcer patients with Helicobacter pylori infection.     

Are twelve days of omeprazole, amoxicillin and clarithromycin better than six days for treating H. pylori infection in peptic ulcer and in non-ulcer dyspepsia?

BACKGROUND/AIMS: To evaluate whether omeprazole, amoxicillin and clarithromycin for 12 days is more effective for Helicobacter pylori eradication than the same regimen for only 6 days; and to verify whether these eradication regimens are more effective in peptic ulcer disease than in non-ulcer dyspepsia. METHODOLOGY: We studied 411 patients in whom a gastroscopy was carried out due to symptoms related to the upper gastrointestinal tract and who were diagnosed with duodenal ulcer (175 patients, 43%), gastric ulcer (42 patients, 10%), or non-ulcer dyspepsia (194 patients, 47%), and concomitant infection by H. pylori. At endoscopy, biopsies were obtained for rapid urease test, and a 13C-urea breath test was carried out. Urea breath test was repeated four weeks after completing eradication treatment with 1) omeprazole (20 mg b.i.d.), amoxicillin (1 g b.i.d.) and clarithromycin (500 mg b.i.d.) for six days (239 patients), or 2) the same regimen for 12 days (172 patients). RESULTS: H. pylori eradication was achieved in 73.6% (95% CI, 68-79%) of the patients treated during 6 days, and in 84.3% (79-90%) of those receiving 12 days of therapy (P < 0.01). The overall eradication rate with both regimens (6 plus 12 days), respectively in patients with duodenal ulcer, gastric ulcer and non-ulcer dyspepsia, was 84.6% (79-90%), 75.6% (61-86%), and 72.8% (67-79%) (P < 0.01 when comparing duodenal ulcer vs. non-ulcer dyspepsia). Twelve-day regimen was more effective than 6-day regimen only in non-ulcer dyspepsia (62% vs. 83%, P < 0.01), but not in duodenal or gastric ulcer. In the multivariate analysis the duration (6 vs. 12 days) of eradication therapy (odds ratio: 2.2; 1.3-3.7) and the type of disease (duodenal ulcer vs. non-ulcer dyspepsia; odds ratio: 2.3; 1.3-3.8) were the only variables which influenced on H. pylori eradication efficacy (chi 2 model, 17; P < 0.001). CONCLUSIONS: Efficacy with omeprazole-amoxicillin-clarithromycin regimen in patients with duodenal ulcer is higher than in those patients with non-ulcer dyspepsia. The increase of H. pylori eradication rate by 21% in our non-ulcer dyspepsia patients justifies the prolongation from 6 to 12 days of omeprazole-amoxicillin-clarithromycin therapy, whilst the increase of cure rates in duodenal or gastric ulcer patients with a 12-day therapy would not be cost-effective.     

Somatostatin and gastrin content of gastric antral mucosa in ulcer disease

Gastrin and somatostatin containing cells are abundant in the gastric antral mucosa suggesting a role for these peptides in gastric physiology, presumably acid secretion. The concentration of these peptides in antral mucosa in ulcer disease is controversial, some finding normal levels, others decreased somatostatin levels. Biopsies of antral mucosa from patients with ulcer disease and non-ulcer dyspepsia were obtained at endoscopy, and somatostatin and gastrin concentration were measured by specific radioimmunoassay. Levels were similar in non-ulcer, duodenal and gastric ulcer patients but prior treatment with H₂-receptor antagonists in duodenal ulcer patients led to a fall in somatostatin and a rise in gastrin mucosal levels. It is thus unlikely that a lack of somatostatin or an increase in gastrin are factors in the pathogenesis of duodenal ulcer, but the cells may behave abnormally in ulcer disease.     

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients.

BACKGROUND: Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients. AIMS: To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status. PATIENTS AND METHODS: A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination. RESULTS: There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum. CONCLUSION: Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.     

Antibody response to Helicobacter pylori CagA and heat-shock proteins in determining the risk of gastric cancer development

OBJECTIVE: To investigate whether the systemic antibody response to Helicobacter pylori heat shock protein B can be considered, in addition to anti cytotoxin-associated protein [CagA) antibody determination, a further serological marker of increased risk of gastric cancer development. METHODS: A total of 98 Giemsa positive Helicobacter pylori patients (28 with gastric cancer, 30 with duodenal ulcer and 40 with nonulcer dyspepsia) were studied. Serum samples obtained from all patients were tested for IgG antibodies to CagA (116 kDa), VacA [89kDa) and heat skock protein B (54 kDa) antigens of Helicobacter pylori by the Western blot technique. RESULTS: 26/28 patients [(92.9% with gastric carcinoma, 29/30 patients [96.7%) with duodenal ulcer and 30/40 patients (75.0%) with non-ulcer dyspepsia were seropositive for CagA protein. The prevalence of serum IgG antibody to CagA in the cancer patients was not significantly higher than in duodenal ulcer and non-ulcer dyspepsia patients. The prevalence of antibodies to VacA was not significantly different between gastric carcinoma and non-ulcer dyspepsia patients. In contrast the prevalence of systemic antibodies to heat skock protein B was significantly higher in gastric cancer patients (78.6%) than in duodenal ulcer (36.7%, p=0.002) or nonulcer dyspepsia patients (52.5%, p=0.029). CONCLUSIONS: The detection of antibodies to heat shock protein B is proposed as an additional test which, in association with the determination of serum antibodies to CagA, could help in determining the risk of developing severe gastroduodenal disease, and gastric cancer, in particular.     

Prevalence of Helicobacter pylori infection and related gastroduodenal lesions in spouses of Helicobacter pylori positive patients with duodenal ulcer.

BACKGROUND: To date, very few studies have evaluated the risk of infection among spouses of Helicobacter pylori positive patients and their results are conflicting. AIM: To assess the seroprevalence of H pylori infection in spouse of H pylori positive patients with duodenal ulcer as compared with age and sex matched volunteer blood donors, as well as the frequency of endoscopic gastroduodenal lesions in these spouses, according to the presence or absence of gastrointestinal complaints. METHODS: Some 124 spouses (48% males) of patients with duodenal ulcer consecutively seen over a 10 month period were studied. They were all screened for serum IgG anti-H pylori antibodies and asked to complete a questionnaire with particular reference to the presence of chronic or recurrent dyspepsia. Upper gastrointestinal tract endoscopy with antral and corpus biopsy specimens taken for histological examination and urease rapid test was offered to all seropositive spouses. Volunteer blood donors (248), living in Milan and matched for age, sex, north-south origins, and socioeconomic status to the cases, were used as controls. RESULTS: Spouses of patients with duodenal ulcer had a significantly higher seroprevalence of H pylori infection than controls (71% v 58%, p < 0.05); 30 of 88 (34%) H pylori positive spouses complained of dyspeptic symptoms compared with only four of 34 (12%) seronegative spouses (p < 0.02). At endoscopy, H pylori infection was confirmed in 48 of 49 (98%) seropositive spouses. The endoscopic findings in those spouses showed active duodenal ulcer in eight (17%), duodenal scar and cap deformity in two (4%), active gastric ulcer in two (4%), erosive duodenitis in three (6%), antral erosions in two (4%), antral erosions plus duodenitis in one, and peptic oesophagitis in another patient. The prevalence of major endoscopic lesions was significantly higher in symptomatic spouses than in those who had never been symptomatic. CONCLUSIONS: These findings show that being the spouse of an H pylori positive patient with duodenal ulcer may increase the risk of H pylori colonisation and perhaps of peptic ulcer disease, and raises questions as to whether serological screening of cohabiting partners of H pylori positive patients with duodenal ulcer may be indicated.     

Helicobacter pylori and gastritis in patients with peptic ulcer and non-ulcer dyspepsia: ethnic differences in Singapore.

Peptic ulcer occurs with different frequencies in the three main racial groups in Singapore. This study aimed firstly to determine the prevalence of Helicobacter pylori in peptic ulcer and non-ulcer dyspepsia patients of the different races and secondly, to assess the relation between H pylori, histological gastritis, patient diagnosis, and race. Gastric antral biopsy specimens from 1502 patients undergoing gastroduodenoscopy were studied and 892 (59%) were positive for H pylori. H pylori was strongly associated with gastritis: 873 of 1197 (73%) patients with gastritis were positive compared with 19 of 305 (6%) without gastritis (p less than 0.0001). The prevalences of H pylori and gastritis were similar in peptic ulcer patients of different races. Malay patients with non-ulcer dyspepsia, however, were less likely to be positive for H pylori (10 of 46 (22%] or to have antral gastritis (17 of 46 (37%] than Chinese (292 of 605 (48%) were positive for H pylori and 421 of 605 (70%) had gastritis) and Indians (35 of 61 (57%) were H pylori positive and 42 of 61 (69%) had gastritis). Patients with duodenal ulcer were more likely to be positive for H pylori than those with non-ulcer dyspepsia, even when subjects with gastritis were considered separately. While our results do not help to explain the observed racial differences in peptic ulcer frequency it may be that the pathophysiology of non-ulcer dyspepsia is different in the different races in Singapore.     

Quantitative histological study of mucosal inflammatory cell densities in endoscopic duodenal biopsy specimens from dyspeptic patients using computer linked image analysis.

Inflammatory cell counting in endoscopic biopsy sections was carried out on duodenal mucosal samples from defined sites in patients with duodenal ulcer, duodenitis but no ulcer, non-ulcer dyspepsia, and asymptomatic controls using computer linked image analysis. The variables measured included polymorphonuclear and mononuclear cells per mm of superficial epithelium and per mm2 lamina propria. Duodenal ulcer crater margin and mucosal biopsy specimens from endoscopically inflamed mucosa in the group with duodenitis but no ulcer showed significantly higher inflammatory cell counts than endoscopically normal non-ulcer dyspepsia and control mucosa. Biopsy specimens from non-ulcer dyspepsia patients showed significantly higher lamina propria polymorphs than control group mucosa. Endoscopically normal duodenal ulcer and duodenitis but no ulcer mucosa also showed significantly higher acute and chronic inflammatory cell counts than controls. The prevalence of Helicobacter pylori in duodenal biopsy specimens was low (0-22%) and unrelated to local inflammatory response. Despite histological appearances, duodenal biopsy specimens from non-ulcer dyspepsia patients showed significantly higher inflammatory cell infiltration than control specimens, suggesting that at least some represent part of a spectrum of subclinical peptic disease.     

Gastrin and antral G cells in course of Helicobacter pylori eradication： Six months follow up study

ABM: To assess long-term effects of Helicobacter pylori (H pylori) eradication on antral G cell morphology and function in patients with and without duodenal ulcer (DU). METHODS: Consecutive dyspeptic patients referred to the endoscopy entered the study. Out of 39 H pylori positive patients, 8 had DU (Hpylori+DU) and 31 gastritis (Hpylori +G). Control groups consisted of 11 uninfected dyspeptic patients (CG1) and 7 healthy volunteers (CG2). Basal plasma gastrin (PGL), antral tissue gastrin concentrations (ATGC), immunohistochemical and electron microscopic characteristics of G cells were determined, prior to and 6 mo after therapy. RESULTS: We demonstrated elevated PGL in infected patients compared to uninfected controls prior to therapy. Elevated PGL were registered in all H pylori+patients (H pylori +DU: 106.78±22.72 pg/mL, H pylori+G: 74.95±15.63, CG1: 68.59±17.97, CG2: 39.24±5.59 pg/mL, P<0.01). Successful eradication (e) therapy in H pylori+patients lead to significant decrease in PGL (H pylori+DU:59.93±9.40 and H pylori+Ge: 42.36±10.28 pg/mL, P<0.001). ATGC at the beginning of the study were similar in infected and uninfected patients and eradication therapy lead to significant decrease in ATGC in H pylori+gastritis, but not in DU patients. In the H pylori+DU patients, the mean number of antral G cells was significantly lower in comparison with all other groups (P<0.01), but after successful eradication was close to normal values found in controls. By contrast, G cell number and volume density were significantly decreased (P<0.01) in H pylori+Ge group after successful eradication therapy (294±32 and 0.31±0.02, respectively), in comparison to values before eradication (416±40 and 0.48±0.09). No significant change of the G cell/total endocrine cell ratio was observed during the 6 mo of follow up in any of the groups. A reversible increase in G cell secretory function was seen in all infected individuals, demonstrated by a more prominent secretory apparatus. However, differences between DU and gastritis group were identified. CONCLUSION: H pylori infection induces antral G cell hyperfunction resulting in increased gastrin synthesis and secretion. After eradication therapy complete morphological and functional recovery is observed in patients with gastritis. In the DU patients some other factors unrelated to the H pylori infection influence antral G cell morphology and function.     

The systemic cellular immune response in the Helicobacter pylori-associated duodenal ulcer and chronic antral gastritis

BACKGROUND/AIMS: The exact pathogenesis of Helicobacter pylori infection is not fully understood. This study aims to evaluate the specific subset composition of peripheral blood lymphocytes in patients with H. pylori-positive duodenal ulcer n = 14), chronic antral gastritis n = 28), since reports so far have led to inconclusive and conflicting results. METHODOLOGY: 42 patients with dyspepsia and 50 controls underwent the following procedures: 1) gastroscopy and gastric biopsy (five specimens) 2) histology, 3) serologic test for anti-H. pylori antibodies IgG (Pyloriset EIA-G, Orion Diagnostica) and anticytotoxin associated gene A (cag A) IgG antibodies (VIVA Diagnositika by ELISA), 4) analysis of the peripheral blood lymphocytes using monoclonal antibodies reacting with lymphocyte cell surface antigens (anti-CD3, anti-CD19, anti-CD4, anti-CD8, anti-CD16 + CD56, anti-HLA DR) by flow-cytometry (Becton-Dickinson) to detect possible changes in the lymphocytes subpopulations in patients with duodenal ulcer and chronic antral gastritis. RESULTS: We found no alteration in total T and B lymphocytes and CD4+ T, CD8+ T lymphocytes and natural killer cells of both duodenal ulcer and chronic antral gastritis patients compared to normal persons. Although there was a slight increase in the proportion of active T lymphocytes in duodenal ulcer and chronic antral gastritis groups comparing to healthy subjects the difference was not statistically significant. CONCLUSIONS: These data indicate that there is no systemic alteration in the specific immune system in response to H. pylori in patients with duodenal ulcer and chronic antral gastritis.     

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients

Background. Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either, whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients.Aims. To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status.Patients and methods. A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination.Results. There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum.Conclusion. Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.     

Histological and clinical predictive value of determination of tissue CagA status by PCR in Helicobacter pylori infected patients; results of the large population based study in western Turkey

BACKGROUND/AIMS: Early experimental and epidemiological studies have suggested that the presence of cagA gene was a virulence factor for Helicobacter pylori. We aimed to investigate the clinical significance of tissue CagA status in Helicobacter pylori infected patients and to assess its association with histological changes in gastric mucosa. METHODOLOGY: Three hundred and forty-five patients with Helicobacter pylori infection established by both urease test and histological examination were included in the study. The symptoms of the patients were recorded according to the Glasgow dyspepsia scale. Biopsies (cardia, corpus, angulus and antrum) were evaluated histologically according to the Sidney system. The cagA status was determined by polymerase chain reaction method from an antral biopsy. Polymerase chain reaction studies were performed by Wizard genomic DNA purification system (promega). We also determined the serum levels of tumor necrosis factor-alpha, and gastrin. They were all prescribed lansoprazole (30 mg b.i.d.), clarithromycin (500 mg b.i.d.), and amoxycillin (1 g b.i.d.) for a week. At the 8th week a second endoscopy was performed and further biopsy specimens were obtained from the same sites. Mann-Whitney U and chi 2 tests were used for statistical analyses. RESULTS: Two hundred and thirty-five patients (68.1%) were infected with cagA-positive strains of Helicobacter pylori and the other 110 patients (31.8%) were infected with cagA-negative strains. We compared the parameters and measurements studied in this trial between the patients infected with cagA-positive and negative Helicobacter pylori strains. Helicobacter pylori density was greater in the cagA-positive group by 1.9 +/- 0.9 than in the cagA-negative group by 1.2 +/- 0.7 (P = 0.01). Helicobacter pylori activity and chronic inflammation also were significantly higher in the cagA-positive group with the values of 1.4 +/- 0.8 and 2.1 +/- 1.1 than in the cagA-negative group with 0.7 +/- 0.2 and 1.3 +/- 0.5, respectively (P = 0.001, P = 0.002). The presence of atrophy and lymphoid aggregate was not different between the two groups (P > 0.05). However intestinal metaplasia was shown to be significantly frequent in patients infected with cagA-positive Helicobacter pylori strains (0.001). Serum tumor necrosis factor-alpha and gastrin levels which were accepted as the markers of inflammation in Helicobacter pylori infection were increased in the cagA-positive group compared with the cagA-negative group. Serum tumor necrosis factor-alpha level was 11.3 +/- 7.0 pg/mL in the cagA-positive group and 4.9 +/- 2.7 pg/mL in the cagA-negative group (P = 0.001). Gastrin level also showed a significant difference between two groups by 66.8 +/- 31.1 pg/mL and 37.2 +/- 19.2 pg/mL, respectively, in the cagA-positive and negative groups (P = 0.001). The virulent strains seem to cause peptic ulcer more frequently. Peptic ulcer was determined in 17% of patients in the cagA-positive group but this ratio was 9% in the cagA-negative group (P = 0.608). Although, all these differences of the degree of inflammation, clinical spectrum and biochemical parameters were seen, interestingly there was no significant difference in the severity of the symptoms of the patients in both groups according to Glasgow dyspepsia severity score (P = 0.20). CONCLUSIONS: Our results confirm that cagA-positive strains of Helicobacter pylori cause greater histological changes. However this virulence is not associated with more severe symptoms. The histological changes can be predictable by determining the tissue cagA status.     

H pylori infection among 1000 southern Iranian dyspeptic patients

INTRODUCTION H pylori is a major cause of gastritis and peptic ulcer disease (PUD), and has been implicated in the development of gastric malignancy[1-3]. The prevalence of H pylori, a worldwide infection, varies greatly among countries and among populati…     

Seroprevalence of eight Helicobacter pylori antigens among 182 patients with peptic ulcer, MALT gastric lymphoma or non-ulcer dyspepsia. Higher rate of seroreactivity against CagA and 35-kDa antigens in patients with peptic ulcer originating from Europe and Africa.

BACKGROUND: It has been suggested that Helicobacter pylori may induce more or less severe gastroduodenal disease according to the strain virulence. DESIGN: We used Western blot to determine antigenic profiles associated with duodenal or gastric ulcer disease, MALT lymphoma and non-ulcer dyspepsia, and to identify geographical differences. METHODS: One hundred and eighty-two consecutive patients with H. pylori infection were studied. H. pylori infection was diagnosed by a rapid urease test or histological examination of gastric biopsy samples. Bacterial density and gastritis were assessed histologically by using the Sydney scoring system. Western blot was used to identify antibodies against eight antigens (CagA, VacA, urease A, heat shock protein B, and 19.5, 26.5, 30 and 35 kDa). Patients were questioned on their smoking habits and place of birth and childhood. RESULTS: There were 73 patients with duodenal ulcer, 30 with gastric ulcer, eight with erosive duodenitis, 17 with gastric MALT lymphoma and 54 with non-ulcer dyspepsia. Most (>85%) were seropositive for the heat shock protein B and 26.5-kDa antigens. The prevalence of the other antigens ranged from 45% (VacA) to 68% (urease B). The seroprevalence of CagA antigen was significantly higher (P < 0.01) in cases of gastroduodenal ulcer (84%) than non-ulcer dyspepsia (37%). Similarly, 35-kDa antigen reactivity was more frequent (P < 0.05) in duodenal ulcer patients (75%) than in those with non-ulcer dyspepsia (50%). The antigenic profiles associated with MALT gastric lymphoma and non-ulcer dyspepsia were similar. Multivariate analysis showed that only gastroduodenal ulcer was significantly associated with CagA. Gastroduodenal ulcer and a childhood spent in Africa were both associated with 35-kDa and combined CagA-35-kDa reactivity. CONCLUSIONS: This study confirms the strong seroprevalence of H. pylori CagA antigen and shows a high prevalence of the 35-kDa antigen in patients with gastroduodenal ulcer, especially those raised in Africa. There was no difference in the serological pattern between patients with non-ulcer dyspepsia and those with MALT lymphoma. Tests for antibodies to the CagA-35-kDa antigen combination might be used to select H. pylori-infected dyspeptic patients warranting treatment.     

Secretor status and Helicobacter pylori infection are independent risk factors for gastroduodenal disease.

The hypothesis that non-secretors of ABO blood group antigens, a group shown to be more susceptible to certain bacterial infections, may be at greater risk of gastroduodenal disease because of increased susceptibility to Helicobacter pylori infection was investigated. Of 101 patients with symptoms of dyspepsia who were undergoing endoscopy, 32% were non-secretors (determined from Lewis blood group phenotype), 36% had endoscopically visible gastroduodenal disease (antral gastritis, gastric ulcer, erosive duodenitis, duodenal ulcer or some combination), and 58% had H pylori detected in antral biopsy specimens. Non-secretors and patients with H pylori infection were significantly more likely to have gastroduodenal disease (p = 0.02 and p = 0.002 respectively). There was, however, no significant association between secretor status and H pylori infection, logistic regression analysis confirming that these were independently associated with gastroduodenal disease. Overall, the relative risk of gastroduodenal disease for non-secretors compared with secretors was 1.9 (95% confidence intervals 1.2, 3.2). Non-secretion of ABO blood group antigens is not related to H pylori infection but is independently and significantly associated with endoscopic gastroduodenal disease. The mechanism of this remains to be explained.     

Gastric electrical activity and gastrointestinal hormones in dyspeptic patients

AIMS: To explore the patterns of gastric electrical activity, gastric emptying and gastrointestinal hormones in dyspeptic patients and relate them to Helicobacter pylori status. METHODS: Twenty-two patients with functional dyspepsia and 29 healthy volunteers underwent cutaneous electrogastrography and dynamic ultrasound before and after a test meal. All dyspeptic patients underwent endoscopy and biopsy; all subjects were examined for the presence of antibodies to H. pylori, and the plasma levels of gastrin, neurotensin, cholecystokinin, and pancreatic polypeptide were measured. RESULTS: The area under the curve (AUC) of the normal slow wave percentage was lower in dyspeptic patients than controls (Kruskal-Wallis p = 0.016; Dunn's test: H. pylori-positive patients: 21,235.5 [19,101.0-22,688.8] vs. H. pylori-negative controls: 22,532.0 [20,133.0-23,755.0], p < 0.05). The AUC of the tachygastria percentage was higher in dyspeptic patients than controls (p = 0.0001; H. pylori-positive patients: 2,173.5 [325.8-3,055.3] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05; H. pylori-negative patients: 1,843.0 [1,107.0-4,277.0] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05). The AUC of gastrin was higher in H. pylori-positive than H. pylori-negative subjects (p = 0.0002; H. pylori-positive patients: 16,146.5 [11,368.8-33,141.7] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05; H. pylori-positive controls: 20,250.0 [12,070.0-64,430.0] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05). In the total group of dyspeptic patients and in the H. pylori-positive patients, a negative correlation was found between the AUC of neurotensin and the total score for postprandial fullness (dyspeptic patients r = -0.51, p = 0.01; H. pylori-positive patients r = -0.66, p = 0.02). CONCLUSIONS: In dyspeptic patients, alterations in gastric electrical activity were not related to H. pylori infection. Nevertheless, H. pylori infection induces higher gastrin levels in both patients and asymptomatic subjects.     

The influence of Helicobacter pylori infection on gastrin and somatostatin values present in serum

BACKGROUND/AIMS: Recent studies on the role of Helicobacter pylori in pathogenesis of duodenal ulcers have focused on the mechanism by which H. pylori infections causes exaggerated gastrin release. METHODOLOGY: We compared the gastrin and somatostatin serum values between two groups of patients; 37 H. pylori-positive ones and 29 H. pylori-negative ones. We applied radioimmunoassay technique to determine the gastrin and somatostatin values in serum. H. pylori was confirmed by urease test and by histopathological color according to Giemsa. RESULTS: The level of gastrin in the serum of Helicobacter pylori-positive patients with chronic gastritis were significantly higher in relation to H. pylori-negative patients. The somatostatin concentration in the sera of H. pylori-positive patients with duodenal ulcer (16.27 +/- 9.49 pg/mL) were less in comparison with those without duodenal ulcer (23.25 +/- 13.59 pg/mL). CONCLUSIONS: The results suggest that H. pylori infection suppresses the somatostatin secretion.