Functional Dyspepsia is Associated with cagA-positive Helicobacter pylori Strains

Background: The antigen CagA can be used as a marker for virulence of Helicobacter pylori. It is tempting to assume that H. pylori strains positive for cytotoxin-associated gene A (cagA) could be responsible for functional dyspepsia. A cross-sectional study was performed in patients presenting with functional dyspepsia to correlate the clinical presentation with the presence of cagA-positive and -negative H. pylori strains. Methods: Consecutive patients referred for endoscopy were studied. An inclusion criterion was the absence of any endoscopic abnormality. Biopsy specimens were obtained from the gastric antrum for HE and immunoperoxidase stain, rapid urease test, and culture. A serum sample was taken for detection of IgG antibodies against H. pylori as well as CagA. A validated questionnaire of 14 questions regarding the upper gastrointestinal tract was used for assessment of the clinical presentation. Nine questions were scored on a 5-point Likert scale. Results: 422 patients were included, 222 were H. pylori-positive, the remaining 200 were H. pylori-negative. Mean symptom score in patients with cagA-positive strains was significantly higher than in patients with cagA-negative strains. No difference was present if cagA-negative patients were compared with H. pylori-negative dyspeptics. Four different complaints were more prevalent in the cagA-positive patients compared with cagA-negatives. When cagA-positive patients were compared with H. pylori-negative dyspeptics, seven complaints were significantly more prevalent in cagA-positives; when cagA-negatives were compared this number was only two. Conclusions: Functional dyspeptics with cagA-positive H. pylori strains have more dyspeptic symptoms and higher symptom scores than patients with cagA-negative H. pylori strains as well as H. pylori-negative functional dyspeptics.     

Helicobacter pylori Endemic and Gastric Disease

H. pylori infection of the stomach is widespread among human populations including Iranians and is considered to play a major role in the pathogenesis of gastric diseases such as peptic ulcer, adenocarcinoma, and MALT lymphoma. The association between H. pylorivirulence markers and disease has been studied in other populations around the world. The aim of this study was to investigate the distribution of H. pylori vacA and cagA genotypes and their association with clinical outcomes in Iran. H. pylori was cultured from gastric biopsy specimens obtained from 137 Iranian patients (58 with duodenal ulcer, 61 with nonulcer dyspeptic [NUD], and 18 with gastric adenocarcinoma). The vacA alleles and cagA genotypes were determined by PCR. The vacA sl allele was present in 107 of the 137 subjects (78%). Multiple strains (m1 and m2) were detected in H. pylori isolates from the patients. VacA s1 genotypes were more frequent in patients with peptic ulcer (46/58; 79%) than in NUD patients (47/61; 77%). CagA was present in 44% of the patients. NUD patients had a frequency of cagA positivity similar to that of the overall population (46%). CagA was present more frequently more than cagA-negative (20% vs. 8%, respectively) in patients with gastric carcinoma (20%) than cagA-negative in patients with gastric carcinoma (8%). This is the first comprehensive study to demonstrate the frequency of colonization with mixed strain, vacA s1, m1 and m2 as the dominant genotype in these Iranian patients, where a high rate of H. pylori infection exists and is similar to the region with a low rate of H. pylori infection. Therefore, host genetics, environmental factors, and the substantial genetic heterogeneity among different H. pylori strains may contribute to the different clinical outcomes.     

Helicobacter pylori cagA Status and Peptic Ulcer Disease in Iran

Helicobacter pylori contributes to the development of peptic ulcers and atrophic gastritis. Furthermore, H. pylori strains carrying the cagA gene are more virulent than cagA -negative strains and are associated with the development of gastric adenocarcinoma. The cagA gene is a putative H. pylori virulence factor of unknown function. The aim of this study was to determine the prevalence of the cagA gene among H. pylori isolates and its relationship with peptic ulcer disease in 128 Iranian patients. A total of 107 (83.6%) samples were positive, including 40 (95%) of the 42 patients with duodenal ulcer, 43 (86%) of the 50 patients with gastric ulcer, and 24 (66.6%) of the 36 patients with gastritis. cagA was present in 32 (80%) of 40 strains from duodenal ulcer patients, 33 (77%) of 43 strains from gastric ulcer patients, and 11 (46%) of 24 from gastritis patients. We also attempted to investigate the subtypes of 3′ region of cagA gene in H. pylori strains isolated from Iranian patients and their relation to H. pylori-associated gastroduodenal diseases. The PCR product of cagA positive strains obtained with primer set CAG1/CAG2 differed in size, varying from 642 to 651 bp (subtype A) in 33 isolates to 756 bp (subtype B/D) in 13 isolates. This does not support the view that subtypes of the 3′ region of cagA gene in H. pylori isolated from Iran correlate with the clinical outcomes of H. pylori, but colonization with cagA positive strains was significantly higher among duodenal ulcer than gastritis patients in Iran.     

Gastric mucosal cytokine levels in relation to host interleukin-1 polymorphisms and Helicobacter pylori cagA genotype

Objective The outcome of a Helicobacter pylori infection is related in part to interrelationships among H. pylori virulence factors and the H. pylori-induced mucosal response. The host inflammatory response is partly governed by polymorphisms in pro-inflammatory genes.

Material and methods Cytokine levels (interleukin (IL)-1β, IL-6 and IL-8) were examined in H. pylori-infected and uninfected normal-appearing mucosa from patients with non-ulcer dyspepsia (NUD), margins of gastric ulcers and cancer tissues. Cytokine levels were compared with cagA genotypes and host interleukin (IL)-1 polymorphisms.

Results The study comprised 168 Thai patients. All infected patients possessed anti-CagA antibody. Gastric mucosal IL-8 levels were significantly higher in H. pylori-positive cases than in -negative cases in all three tissue types (e.g. 1115 versus 217?pg/mg protein for NUD) (p<0.001). Normal-appearing but H. pylori-infected antral mucosa of patients with cagA type 1a strains had higher IL-8 levels than those with type 2a strains (2632 versus 1036 pg/mg protein) (p<0.005). IL-1B-511T/T carriers had higher antral mucosal IL-1β levels versus non-carriers (pg/mg protein) (T/T=221, T/C=178, C/C=70) (p=0.005). IL-1B-511T/T carriers also had higher IL-1β levels versus non-carriers in H. pylori-negative patients.

Conclusions It was found that both the host factors (IL-1 polymorphisms) and bacterial factors (cagA type 1a versus type 2a) influenced gastric mucosal cytokine levels. Future studies should concentrate on interactions among host factors (e.g. genetics and tissue responses) and bacterial and environmental factors.     

Bile acid reflux and possible inhibition of Helicobacter pylori infection in subjects without gastric surgery

Bile acids are generally known to inhibit growth of Helicobacter pylori in vitro, but whether they do so in humans with no gastric surgery has been uncertain. The present study addresses this issue. Among healthy control subjects with preserved acid secretion, H. pylori-positive subjects were older and had lower gastric bile acid concentrations than H. pylori-negative subjects (P < 0.05). Among gastric ulcer patients with preserved acid secretion, H. pylori-positive patients had a higher basal acid output than H. pylori-negative patients (P < 0.05). Among H. pylori-positive subjects with preserved acid secretion, duodenal ulcer patients had a higher basal and maximum acid output than healthy control subjects (P < 0.01). In conclusion, gastric bile acids may suppress initial stages of H. pylori infection in subjects without gastric surgery. However gastric bile acids may have little effect on peptic ulcer disease, once H. pylori infection is established.     

Correlation between expression of MMP-9 and MMP-3 in Helicobacter pylori infected patients with different gastroduodenal diseases

Background and study aims

Helicobacter pylori (H. pylori) has been implicated in the pathogenesis of most important gastro-duodenal diseases, such as gastritis, peptic ulcer disease (PUD) and gastric cancer. H. pylori upregulates the expression and activity of several matrix metalloproteinases (MMPs) in the gastric mucosa, but the role of MMP-3 and MMP-9 in infected patients with H. pylori have not been clearly defined yet. We examined mucosal MMP-3 and MMP-9 mRNA levels in gastric mucosa of H. pylori infected patients and evaluated the effects of virulence factors cagA and vacA allelic variants on these levels. We also determined correlation between mucosal MMP-3 and MMP-9 mRNA levels and types of disease.

Influence ofHelicobacter pylori on gastric mucosal adaptation to naproxen in man

Our objective was to determine whetherH. pylori influences gastric mucosal injury and adaptation caused by naproxen. Twenty-four healthy volunteers, 12H. pylori-positive and 12H. pylori-negative, were given a 28-day course of naproxen 500 mg twice a day. They were each gastroscoped to assess gastric mucosal damage and mucosal blood flow before and at 1, 7, and 28 days during treatment. Maximal gastric mucosal damage (median grade+IQR) occurred during the first 24 hr in both groups and was of similar magnitude (H. pylori-positive: 2.5, 2.0–3.0P<0.01;H. pylori-negative: 2.0, 1.0–3.0P<0.01). This damage was associated with a fall in antral but not corpus mucosal blood flow. With continued NSAID administration, gastric damage resolved confirming adaptation (H. pylori-positive 1.0, 0–2.0,H. pylori-negative: 1.0, 0–1.0) and antral mucosal blood flow returned to baseline in both groups by day 28. These observations suggest that initial gastric mucosal injury is not influenced byH. pylori colonization and adaptation occurs regardless of its presence.     

Relationship between gastric disease and deletion of cag pathogenicity island genes of Helicobacter pylori in gastric juice

The cag pathogenicity island genes of Helicobacter pylori (ie, cag1, cag5, cagT, cagE, and cagA) were detected by PCR in DNA extracted from endoscopically collected gastric juice, and the relationship between these genes and gastric disease was studied in 25 patients with early gastric cancer, 9 patients with gastric ulcer, and 15 patients with chronic active gastritis. In three patients with early gastric cancer and one patient with gastric ulcer, cag pathogenicity island genes were amplified although H. pylori was not detected by conventional methods. Compared with conventional methods, the sensitivity of detection of cag genes was 92.3% (36/39) and the specificity was 60% (6/10). Among the patients with cagA amplification, only cagE was not amplified in one case each with early cancer and chronic active gastritis. In addition, none of cag1, cag5, cagT, and cagE were amplified in spite of cagA amplification in one patient with gastric ulcer. This method is a simple procedure, has a high sensitivity, and appears to be useful for accurate assessment of infection with cagA-positive strains. Because deletion of cag PAI genes was found in the patients with all three gastric diseases that we studied, it was suggested that the pathogenicity of H. pylori might not be determined by cag PAI genes in those cases.     

No Protective Role of Helicobacter pylori in the Pathogenesis of Reflux Esophagitis in Patients with Duodenal or Benign Gastric Ulcer in Korea

Little is known about the relationship between H. pylori infection and reflux esophagitis. To evaluate whether or not H. pylori plays a protective role in the pathogenesis of reflux esophagitis, the prevalence rates of reflux esophagitis depending on H. pylori status in consecutively diagnosed duodenal ulcer or benign gastric ulcer patients were evaluated. In addition, the incidence rates of reflux esophagitis depending on H. pylori status were evaluated for those patients who received follow-up endoscopy at least 6 months after eradication treatment. The prevalence rates of reflux esophagitis were 8.0% (2 patients) in the 25 H. pylori-negative duodenal ulcer group patients and 6.5% (36 patients) in the 555 H. pylori-positive duodenal ulcer group patients, and there was no statistical difference. Similarly, that of gastric ulcer patients was 9.4% (32 patients) in the 340 H. pylori-positive group patients, slightly higher than that in the 41 H. pylori-negative group patients 4.9% (2 patients), but without statistical significance. After eradication treatment the reflux esophagitis incidence rates were 2.5% (2 patients) in the 81 H. pylori-eradicated duodenal ulcer group patients and 7.7% (3 patients) in the 39 noneradicated duodenal ulcer group patients, and there was no statistical difference. Similarly, those of gastric ulcer patients were 6.8% (3 patients) in the 44 H. pylori-eradicated and 8.7% (2 patients) in the 23 noneradicated group patients again without statistical difference. These results suggest that H. pylori does not play a protective role in the pathogenesis of reflux esophagitis in patients with duodenal or gastric ulcer in Korea.     

Relationship between the diversity of the cagA gene of Helicobacter pylori and gastric cancer in Okinawa, Japan

Background Helicobacter pylori CagA protein is considered to be one of the virulence factors associated with gastric cancer. CagA is injected into gastric epithelial cells, undergoes tyrosine phosphorylation, and binds to Src homology 2 domain-containing protein-tyrosine phosphatase (SHP-2). Two major subtypes of CagA have been observed in the SHP-2-binding site, the Western and East Asian types. The East Asian-type CagA binds to SHP-2 more strongly than the Western-type CagA. The diversity of CagA, which collectively determines the binding affinity of CagA to SHP-2, may be an important variable in determining the clinical outcome of infection by different H. pylori strains. Methods We investigated the relationship between the diversity of CagA and clinical outcome in Okinawa, Japan. A total 24 strains, 13 gastric cancer strains and 11 duodenal ulcer strains, were studied. We sequenced full-length cagA genes and analyzed the phylogenetic relationships between Okinawa isolates and previously characterized Western H. pylori strains. Results All isolates examined were cagA positive. The prevalence of East Asian CagA-positive strains was significantly higher in patients with gastric cancer (84.6%) than in patients with duodenal ulcer (27.3%) (χ-squared = 8.06, P = 0.011). The phylogenetic analysis showed that all gastric cancer strains with East Asian-type CagA were in the East Asian cluster, and that most duodenal ulcer strains were in the Western cluster. Conclusions The origins of H. pylori isolates are different between gastric cancer strains and duodenal ulcer strains, and East Asian CagA-positive H. pylori infection is associated with gastric cancer. The strain diversity observed in Okinawa may affect the difference in the prevalence of disease associated with H. pylori infection in Japan.     

Helicobacter pylori Infection Reduces Intraluminal Nitric Oxide

Background: Nitric oxide (NO) plays an important role in gastrointestinal mucosal protection. We have previously shown that Helicobacter pylori infection is associated with a lower concentration of NO in the human stomach. The aim of this study is to explore the pathogenesis of this finding using an animal model. Methods: Mongolian gerbils were divided into four groups: H. pylori-negative and -positive, each with and without the intraperitoneal addition of superoxide dismutase (SOD). Intraluminal NO and serum nitrate were measured by using a chemiluminescence system. Inducible nitric oxide synthase (iNOS) levels in gastric mucosa were measured by using the NOSdetect Assay Kit. Results: iNOS levels in H. pylori-positive gerbils were significantly greater than in those without infection. Intraluminal NO levels in H. pylori-positive gerbils were significantly lower than those in H. pylori-negative ones and increased after SOD administration. Serum nitrate levels in H. pylori-positive gerbils were significantly greater than those in H. pylori negative ones and decreased after SOD administration. Conclusions: The low level of NO in the gastric lumen in H. pylori infection is likely a result of superoxide production related to H. pylori-induced inflammation.     

Low frequency of cagA-positive Helicobacter pylori strains isolated from Iranian patients with MALT lymphoma

Helicobacter pylori is predominantly involved in the etiology of digestive diseases. The aim of our study is to determine the relationship of cagA frequency with less investigated gastroduodenal disorders such as MALT (mucosal associated lymphoid tissue) lymphoma and gastric cancer. One hundred-twenty eight H. pylori-positive patients including: gastritis (n = 74), gastric cancer (n = 26) and MALT lymphoma (n = 28) were entered in our study. Antral biopsy specimen transport, bacterial culture and cagA detection were performed based on standard protocols. In brief, biopsies from positive H. pylori patients were investigated for presence of cagA gene by polymerase chain reactions (PCR) method. Of 128 consecutive Iranian patients with gastroduodenal disorders examined in our study, we identified 84 (65.6%) cagA-positive strains. However, six patients were excluded because of negative culture for identification of H. pylori. Prevalence of cagA in each categorized groups are following: 63/74 (85.1%) of gastritis patients, 16/28 (57.1%) and 5/26 gastric cancer (19.2%) of MALT lymphoma, respectively. Current findings reveal that the presence of cagA is not a reliable marker for prediction of digestive disorders caused by H. pylori infection. All our patients with gastric cancer were diagnosed as adenocarcinoma. The low rate of cagA among gastric cancer and MALT lymphoma groups was not statistically significant, possibly due to the small number of patients enrolled in the study. We suggest that a study with a high number of patients is needed for making more definitive assessment of the correlation between cagA-positive H. pylori and gastric cancer and MALT lymphoma.     

Effects of Helicobacter pylori infection on Zollinger-Ellison syndrome

Both Zollinger-Ellison syndrome (ZES) and Helicobacter pylori infection are major etiologic factors for peptic ulcer. The aim of this study was to investigate the effect of H. pylori infection on ZES with special reference to acid secretion. Sixteen patients with ZES were selected (median age, 59 years; range, 39–66 years; M/F, 9/7), and H. pylori status, ulcer location, gastric acid secretion, serum pepsinogen (PG) I and II concentrations, and PG I/II ratio were determined. The seroprevalence of H. pylori infection was 50%, whereas active H. pylori infection was seen in only 25% of the patients. Thirteen patients had duodenal ulcer (DU), 1 had gastric ulcer (GU), and 2 had both GU and DU. DU was seen in both H. pylori-positive and H. pylori-negative patients, whereas GU was found only in H. pylori-positive patients. Both basal and maximal acid outputs were significantly lower in H. pylori-positive patients than in H. pylori-negative patients (P < 0.05). Moreover, both serum PG I and the PG I/II ratio were significantly lower in H. pylori-positive patients than in H. pylori-negative patients. These results indicate that ZES is an independent risk factor for DU, but H. pylori infection may play some role in the development of GU in ZES. In patients with ZES, H. pylori infection may reduce both hypersecretion from parietal cells and PG I secretion from chief cells, and hyperacidity of the stomach in ZES may have eradicated H. pylori in some patients. Received: March 30, 2000 / Accepted: May 26, 2000     

Enhanced levels of C-X-C chemokine,human GROα, in Helicobacter pylori-associated gastric disease*

C-X-C Chemokines play an important role for neutrophil extravasation through microvessels. Although the level of interleukin (IL)-8 is known to increase in the Helicobacter pylori-infected gastric mucosa, another C-X-C chemokine, GROα, has not been evaluated in the H. pylori-associated gastric mucosal injury. The present study was designed to investigate gastric contents of GROα in relation to those of IL-8 in the gastric mucosa of H. pylori-infected peptic ulcer patients. Thirty-eight patients with gastric ulcer and 41 with gastritis underwent endoscopy with informed consent and 49 were found to be H. pylori positive and 30 H. pylori negative. Biopsies from the gastric corpus were performed in each patient to examine the H. pylori colonization by bacterial culture, the rapid urease test and histological specimens as well as measurement of the contents of human GROα and IL-8. Helicobacter pylori infection was eradicated in 21 patients by triple therapy (lansoprazole 30mg, amoxycillin 2.0g, clarithromycin 600 mg; 2 weeks). The samples for GROα and IL-8 assay were homogenized in 0.02% aprotinin containing phosphate-buffered solution and the mucosal contents of GROα and IL-8 in the supernatants were quantified by sandwich enzyme immunoassay methods. The levels of GROα and IL-8 in H. pylori-positive gastric mucosa were significantly higher than those in the H. pylori-negative mucosa. There was a significant linear correlation between the levels of GROα and IL-8 (r= 0.798, P < 0.01). After the eradication of H. pylori by the triple therapy, the levels of GROα and IL-8 were significantly decreased. The GROα showed an increase in the H. pylori-positive gastric mucosa in a similar fashion as IL-8 contents, suggesting a pathogenetic role for GROα in H. pylori-associated gastric mucosal injury.     

Helicobacter pylori Infection Influences Tumor Growth of Human Gastric Carcinomas

Background: Helicobacter pylori infection is considered a risk factor for gastric carcinoma. However, the effect of eradication therapy in gastric carcinoma patients is not well known. The aim of this study was to investigate the relationship between H. pylori infection and tumor growth of gastric carcinoma. Methods: Fifty-one patients with gastric carcinoma participated in the study. Thirty-three were H. pylori-positive, 6 were H. pylori-negative, and 12 were diagnosed with gastric carcinoma after eradication of H. pylori. To investigate tumor growth of gastric carcinoma, cell proliferation and angiogenesis of the tumors were evaluated by immunohistochemical techniques using Ki-67 and CD34. Results: The Ki-67 labeling index was 47.9?±?2.6 (mean?±?s) in the H. pylori-positive group, 38.1?±?3.6 in the H. pylori-eradicated group, and 22.2?±?5.5 in the H. pylori-negative group. It was significantly lower in the H. pylori-eradicated and H. pylori-negative groups than in the H. pylori-positive one, and a significant difference was also found between the H. pylori-positive and H. pylori-eradicated groups. The microvessel counts were 62.5?±?3.0, 50.2?±?4.0, and 66.0?±?9.8 in the positive, eradicated, and negative groups, respectively. A significant difference was found between the H. pylori-positive and H. pylori-eradicated groups. Conclusion: Our results suggest that H. pylori infection is associated with cell proliferation, and its eradication may influence tumor vascularity of gastric carcinoma. Therefore, H. pylori eradication therapy may contribute to the suppression of tumor growth.     

Helicobacter pylori-negative gastric and duodenal ulcers

It is unclear whether Helicobacter pylori infection is essential to the development of peptic ulcers. In this study, we examined the rates of H. pylori-negativity among patients with peptic ulcers. We also attempted to clarify the characteristics of H. pylori-negative peptic ulcers to throw light on the pathogenesis of peptic ulcers. The study included 215 consecutive patients with gastric ulcers (GUs) and 120 consecutive patients with duodenal ulcers (DUs). After routine endoscopic examination and phenol red dye endoscopy, forceps biopsies were performed for culture, histology, and the rapid urease test. A patient was considered H. pylori-negative when the serum anti-H. pylori IgG and the three tests on biopsied specimens were all negative. H. pylori-negative rates were 3.2% in the patients with GUs and 1.7% in the patients with DUs. Lack of atrophy of the gastric mucosa was significantly more common in the H. pylori-negative patients with GUs. A history of ulcer disease was less common and antral ulcers were more common in H. pylori-negative GU patients, but not significantly so. As the urea breath test had not been performed, the possibility of a false-negative result cannot be completely ruled out, but we believe that the H. pylori-negative rate in our study is more reliable than these rates in previous reports, because we visualized H. pylori distribution by phenol red dye endoscopy to avoid false-negative results in biopsies, and we used both biopsy and serum anti-H. pylori IgG findings to establish an H. pylori-negative diagnosis. Since H. pylori-negative peptic ulcers certainly exist, H. pylori infection is thought not to be essential to the development of peptic ulcers. There were few differences between the characteristics of H. pylori-negative and H. pylori-positive peptic ulcers in our study. A large-scale study is required to clarify the characteristics of H. pylori-negative peptic ulcers. Received: September 25, 1998 / Accepted: February 26, 1999     

Analysis of the 3′ Variable Region of the <Emphasis Type="Italic">cagA</Emphasis> Gene of <Emphasis Type="Italic">Helicobacter pylori</Emphasis> Isolated in Koreans

CagA protein of Helicobacter pylori is injected into epithelial cells, and it undergoes tyrosine phosphorylation, resulting in inducing cytoskeletal rearrangements. A few studies have suggested that the number of CagA tyrosine phosphorylation motifs (EPIYA) and subtypes of CagA were associated with gastric cancer. This study was performed to characterize the 3' variable regions of the cagA gene of H. pylori and to investigate whether or not there is any relationship between the diversities of cagA and the disease outcome in Korea. Seventy-nine patients (chronic gastritis, 15; duodenal ulcer, 27; benign gastric ulcer, 18; gastric cancer, 19) were enrolled. Biopsy specimens were taken from the antrum for H. pylori culture, and genomic DNA was extracted. PCR and DNA sequence analysis was carried out for the 3′ variable region of the cagA gene. Seventy-eight strains (98.8%) contained three EPIYA motifs and one strain (1.2%) isolated from a patient with duodenal ulcer contained four EPIYA motifs. Seventy-six strains (96.2%) were the East Asian type. In conclusion, there was no significant difference between the number of EPIYA motifs or CagA subtypes and various gastroduodenal diseases in Korea.     

<Emphasis Type="Italic">cagA</Emphasis> Gene and Protein Status Among Iranian <Emphasis Type="Italic">Helicobacter pylori</Emphasis> Strains

The wide geographic genetic diversity of Helicobacter pylori (Hp) and, in particular, the varying prevalence of cagA in different countries has been documented repeatedly. This study was designed to determine the frequency of cagA in Iranian Hp strains by means of genotyping and assessment of host antibodies. Helicobacter pylori strains from 235 patients, including 174 non-ulcer dyspepsia, 25 peptic ulcer and 36 gastric cancer patients, were studied. The frequencies of the 5′, middle and 3′ terminal regions of the cagA gene were 90.6, 57.6, 89%, respectively, with no correlation to the clinical outcomes. Antibodies against the CagA protein were present in 90.7% of patients. Multiple biopsy sampling in 97 cases revealed multiple infection in 16.5% of the patients. Sequencing of the seven variants of the 3′ end of the cagA gene revealed no clustering and the distribution of the Iranian strains among those of other countries. Our results from the genotyping and serology analyses confirm that the majority of Iranian Hp strains are cagA-positive.     

Does Antral Distension Inhibit Gastric Acid Secretion or Stimulate Bicarbonate Secretion in ‘Healthy’ Subjects?

The effects of a 150-ml antral balloon distension on pentagastrin-stimulated gastric acid secretion and bicarbonate secretion were studied in nine healthy subjects and eight duodenal ulcer (DU) patients. The gastric secretions were simultaneously measured, using a luminal perfusion and pH/PCO₂ measurements. Two of the healthy subjects and six of the DU patients were positive for Helicobacter pylori. When H. pylori-positive and -negative subjects were compared, basal gastric acid and bicarbonate outputs did not differ significantly. In H. pylori-infected subjects the bicarbonate transport increased by about 70% on pentagastrin stimulation. In the H. pylori-negat'we group pentagastrin had no effect on the bicarbonate secretion. Antral distension elicited a 30-35% inhibition of pentagastrin-stimulated gastric acid secretion in the group of H. pylori-negative subjects, whereas the acid secretory level remained essentially unchanged in the positive group. Bicarbonate secretion decreased transiently by the distension in the negative subjects, whereas a slight increase was observed in the infected group. We conclude that antral distension inhibits pentagastrin-stimulated gastric acid output in healthy H. pylori-negative subjects. Our results strongly suggest that the underlying mechanism is a direct inhibition of gastric parietal cell function and not an increased gastric bicarbonate secretion. Furthermore, the results indicate that this defective distension-induced acid inhibition may be correlated to H. pylori infection rather than to duodenal ulcer disease.