CagA antibodies in Japanese children with nodular gastritis or peptic ulcer disease

cagA(+) Helicobacter pylori strains have been linked to more severe gastric inflammation, peptic ulcer disease, and gastric cancer in adults, but there have been few studies of cagA in children. We examined the relationship between H. pylori cagA status and clinical status in Japanese children. Forty H. pylori-positive children were studied: 15 with nodular gastritis, 5 with gastric ulcers, and 20 with duodenal ulcers. H. pylori status was confirmed by biopsy-based tests and serum anti-H. pylori immunoglobulin G (IgG) antibody. As controls, 77 asymptomatic children with sera positive for anti-H. pylori IgG were enrolled. Levels of IgG antibodies to CagA in serum were measured by an antigen-specific enzyme-linked immunosorbent assay. In 16 patients with successful H. pylori eradication, posttreatment levels of CagA and H. pylori IgG antibodies also were studied. The CagA antibody seropositivities of asymptomatic controls (81.8%) and patients with nodular gastritis, gastric ulcers, and duodenal ulcers (80.0 to 95.0%) were not significantly different. Compared with pretreatment levels of CagA antibodies, posttreatment levels decreased progressively and significantly. We conclude that, as in Japanese adults, a high prevalence of cagA(+) H. pylori strains was found in Japanese children, and that there was no association with nodular gastritis or peptic ulcer disease. In the assessment of eradicative therapies, monitoring of serum anti-CagA antibodies does not appear to offer any direct benefit over monitoring of anti-H. pylori antibodies.     

IgG subclass response to Helicobacter pylori and CagA antigens in children

Specific serum IgG subclass antibodies against Helicobacter pylori antigens and recombinant CagA were analysed in 75 symptomatic children with histologically confirmed H. pylori infection. H. pylori stimulated an IgG1 predominant response, and IgG3 titres showed a positive association with peptic ulcer disease, chronicity of antral inflammation and density of H. pylori colonization. Two methods used for assessing serum IgG CagA antibody status, i.e. Western blotting and enzyme-linked immunosorbent assay (ELISA), were concordant. CagA stimulated an IgG1 and IgG3 predominant humoral response. Total CagA IgG titres were higher in children with active and more severe chronic antral inflammation. These findings suggest that in children the systemic humoral immune response to H. pylori infection may reflect gastroduodenal pathology.     

Importance of IgG anti-CagA antibodies of Helicobacter pylori in Venezuelan patients with gastric diseases

Helicobacter pylori is one of the most common bacterial infections worldwide. It is associated with chronic gastritis, peptic ulcer disease and constitutes a major risk factor for gastric adenocarcinoma and lymphoma. The aim of this study was to evaluate the specific serologic immunoglobulin G (IgG) response to whole cells proteins, CagA and urease antigens of Helicobacter pylori in a Venezuelan population. We evaluated 66 patients from the Hospital Universitario de Caracas, attending in the gastroscopy service. H. pylori infection was detected by culture and rapid urease test. IgG antibodies against, CagA and ureases were tested by enzyme-linked immunosorbent assay method using highly purified recombinant antigens. We demonstrated the presence of H. pylori in 48/66 (72.7%), by culture and rapid urease test. We found a seroprevalence of 45 (68%) to whole cells, 34/66 (51%) to CagA and 18/66 (27%) to urease. The positive rates of CagA antibodies in patients with gastric ulcer, gastric cancer and chronic gastritis were 87.8%, 77.7% y 40.8% respectively. The serum antibodies anti-CagA were similar between peptic ulcer disease and gastric cancer patients.     

幽门螺杆菌感染对消化性溃疡患者胃肠动力及胃肠激素的影响

为探讨幽门螺杆菌（Hp)感染对消化性溃疡患者胃肠动力及胃肠激素的影响，对85例消化性溃疡患者进行了胃肠测压和血浆胃动素（MTL）及血浆生长抑素（SS）的测定，结果显示消化性溃疡患者与正常对照组相比消化间期胃肠动力明显减低，主要表现为消化间期移行性复合运动（MMC）Ⅲ期缺失和收缩波振幅减低，血中SS水平也明显低于正常对照组；在Hp阳性和Hp阴性的两组之间胃肠动力和SS水平均无显著差异，在血中MTL水平，Hp阳性组明显高于Hp阴性组，也高于正常对照组，结果表明消化性溃疡患者存在胃肠动力障碍和胃肠激素的异常改变。Hp感染对胃肠动力和SS水平无明显影响，但可促进MTL的分泌或释放。     

Evaluation of western blot CagA seropositivity in Helicobacter pylori-seropositive and -seronegative subjects

CagA seropositivity is an important risk factor for gastric adenocarcinoma and duodenal ulcer. However, CagA seropositivity is also found in Helicobacter pylori-seronegative subjects. Is CagA seropositivity in these subjects a sign of a past H. pylori infection, or does it represent a false-positive reaction? This study investigates the intensity of the CagA immune reaction and the variation in CagA seroprevalence with year of birth for 650 subjects belonging to the Malmo Preventive Medicine cohort. CagA and H. pylori seroprevalences were determined by Western blot analysis (Helicoblot 2.1) and enzyme-linked immunosorbent assay. The peak intensity of the CagA band was significantly lower in H. pylori-seronegative subjects than in those with concomitant H. pylori seropositivity. In H. pylori-seropositive subjects, peak CagA intensity had a bimodal distribution. The prevalence of CagA-seropositive but H. pylori-seronegative subjects increased successively and significantly with year of birth, in contrast to the prevalence of CagA-seropositive and H. pylori-seropositive subjects, which decreased significantly. However, within H. pylori-seropositive and -seronegative subgroups, CagA seroprevalences were constant for different birth cohorts. If CagA seropositivity in H. pylori-seronegative subjects represents a past H. pylori infection, there must have been some mechanisms of eradication that were more common in younger subjects and that were of more importance than the presence of gastric atrophy and the longer duration and higher prevalence of H. pylori infection found in older subjects. Antibiotic treatment of H. pylori was not common practice at the time of enrollment. On the other hand, a false-positive reaction would be constant and independent of birth cohorts, as with the H. pylori-seronegative subgroup of our study. Peak CagA intensity in H. pylori-seronegative subjects corresponded to the lower part of the bimodal distribution of peak CagA intensity in H. pylori-seropositive subjects. We conclude that a major proportion of CagA seropositivity in H. pylori-seronegative subjects represents a false-positive reaction. Peak CagA intensity has a bimodal distribution in H. pylori-seropositive subjects. Low-intensity CagA seropositivity in H. pylori-seropositive subjects is indeterminate, representing both false-positive and true-positive reactions.     

Association of Helicobacter pylori with gastritis and peptic ulcer diseases

The occurrence of Helicobacter pylori(H.pylori) and its relationship with gastric mucosa were studied by light and electron microscopy and culture of biopsy specimens from gastric mucosa of 160 patients with upper gastrointestinal symptoms. H. pylori were present in 96.6% of patients with active chronic gastritis, 100% of patients with duodenal ulcer and 76.9% of patients with gastric ulcer, while present in only 6.3% of individuals with histologically normal gastric mucosa. The bacteria colonized the antral mucosa more frequently than the body or than the duodenal cap mucosa. The bacteria were rarely seen in the intestinalized epithelium per se, but there was no significant difference in prevalence of H. pylori between gastritis with intestinal metaplasia and gastritis without intestinal metaplasia. H. pylori could be seen in close association with the surface of gastric epithelial cells below the mucus layer without evidence of intracellular parasitism, All of the strains tested were susceptible to penicillin, erythromycin, and most of them susceptible to tinidazole and bismuth salts. It is concluded that H. pylori are highly associated with gastritis and peptic ulcer diseases and its prevalence rates in patients with those diseases is higher than in developed countries. This strong association of H. pylori infection with gastritis and peptic ulcer diseases suggest a possible etiologic role for the bacterium in those diseases.     

Detection of serum antibodies to CagA and VacA and of serum neutralizing activity for vacuolating cytotoxin in patients with Helicobacter pylori-induced gastritis.

Thirty patients with dyspepsia, with histological diagnosis of gastritis, and with endoscopic diagnosis of peptic ulcer disease (PUD) (n = 13) or nonulcer dyspepsia (NUD) (n = 17) were admitted to the study. Helicobacter pylori vacuolating cytotoxin-producing strains (Tox+) were isolated from 14 (46.7%) patients, whereas non-cytotoxin-producing (Tox-) H. pylori strains were isolated from the remaining patients. Of 30 patients studied, 20 (66.7%) had serum cytotoxin neutralizing activity in vitro. Fourteen patients with Tox+ H. pylori strains showed serum cytotoxin neutralizing activity and serum immunoglobulin G (IgG) and IgA antibodies reactive with both 87-kDa H. pylori vacuolating cytotoxin (VacA) and 128-kDa cytotoxin-associated gene product (CagA) by immunoblotting using native enriched preparations of VacA and CagA proteins from H. pylori culture supernatants as the antigens. A 94-kDa antigen cross-reacting with the 87-kDa VacA protein could be demonstrated in culture supernatant with immune sera from humans and animals. All patients (n = 10) lacking serum neutralizing activity were also negative for IgG or IgA against VacA antigen, whereas 6 of the 10 patients showed IgG serum antibody responses against CagA antigen. The prevalence of antibodies to VacA and CagA antigens was significantly (P < 0.001) higher in patients with gastritis (20 and 26 patients for VacA and CagA, respectively, of 30 patients) than in H. pylori culture-negative controls (0 of 27 for both VacA and CagA) and in randomly selected blood donors (17 and 21 for VacA and CagA, respectively, of 120 subjects). All patients with PUD had antibodies to CagA, whereas 13 of 17 (76.5%) patients with NUD had anti-CagA antibodies. Serum IgG antibodies to VacA were present in 9 (69.2%) patients with PUD of 13 patients and in 11 (64.7%) patients with NUD of 17 patients. Anti-CagA antibodies seemed to correlate better with PUD than anti-VacA antibodies.     

Antral histopathological changes in acid peptic disease associated with Helicobacter pylori

The histopathology of the antral mucosa of patients with acid peptic disease was studied in relation to Helicobacter pylori infection. Three hundred and fifty-five patients underwent gastroscopy and biopsy on 443 occasions. During each gastroscopy, two antral samples were taken for Rapid Urease Test (RUT) for H. pylori and two antral samples for histopathology. Haematoxylin and Eosin and modified Giemsa stained sections were studied. Histopathological changes in the antrum and the density of H. pylori were graded according to the Sydney System criteria. There was a significant association between the RUT and histology results for detection of H. pylori. The overall prevalence of H. pylori was 61.4% with a maximum incidence in the third and fourth decades of life, and an equal sex distribution. H. pylori colonisation was seen in 90.7% of patients with duodenal ulcer, 66.7% with gastric ulcer and 44.3% with non-ulcer dyspepsia. H. pylori colonisation was associated with more severe antral chronic active gastritis, lymphoid follicles, intestinal metaplasia and dysplasia. Elimination of H. pylori by treatment with anti-H. pylori regimens resulted in regression of the changes.     

Functional analysis of the cag pathogenicity island in Helicobacter pylori isolates from patients with gastritis, peptic ulcer, and gastric cancer

Helicobacter pylori is the causative agent of a variety of gastric diseases, but the clinical relevance of bacterial virulence factors is still controversial. Virulent strains carrying the cag pathogenicity island (cagPAI) are thought to be key players in disease development. Here, we have compared cagPAI-dependent in vitro responses in H. pylori isolates obtained from 75 patients with gastritis, peptic ulcer, and gastric cancer (n = 25 in each group). AGS gastric epithelial cells were infected with each strain and assayed for (i) CagA expression, (ii) translocation and tyrosine phosphorylation of CagA, (iii) c-Src inactivation, (iv) cortactin dephosphorylation, (v) induction of actin cytoskeletal rearrangements associated with cell elongation, (vi) induction of cellular motility, and (vii) secretion of interleukin-8. Interestingly, we found high but similar prevalences of all of these cagPAI-dependent host cell responses (ranging from 56 to 80%) among the various groups of patients. This study revealed CagA proteins with unique features, CagA subspecies of various sizes, and new functional properties for the phenotypic outcomes. We further showed that induction of AGS cell motility and elongation are two independent processes. Our data corroborate epidemiological studies, which indicate a significant association of cagPAI presence and functionality with histopathological findings in gastritis, peptic ulcer, and gastric cancer patients, thus emphasizing the importance of the cagPAI for the pathogenicity of H. pylori. Nevertheless, we found no significant association of the specific H. pylori-induced responses with any particular patient group. This may indicate that the determination of disease development is highly complex and involves multiple bacterial and/or host factors.     

Immune response to Helicobacter pylori and its association with the dynamics of chronic gastritis in the antrum and corpus

The aim of the study was to establish possible factors which play a role in progression of gastritis to atrophic gastritis in long-term follow-up among the Estonian population, to assess the association between the host immune response and different Helicobacter pylori antigens and autoantigens in relation to the histological parameters of gastritis in the antrum and corpus. ELISA and immunoblot were used for detection of IgG to H. pylori acid glycine-extracted cell surface proteins, CagA protein, and H. pylori HSP60. Anticanalicular autoantibodies (ACAB) in the serum were evaluated according to Faller et al. (1996). Apoptosis was evaluated using the TUNEL method. Study subjects were 1958 persons from an unselected Estonian population, and 70 persons from a sample from Saaremaa Island, who had been investigated over a period of 18 years. Seropositivity for CagA was a sign of gastritis activity [OR=14.8 (4.5-50.3)] and atrophy [OR=7.0 (2.1-23.1)] and might predict development of atrophy, particularly in the corpus [OR=7.1 (1.8-27.7)]. The prevalence of ACAB increased significantly with duration of H. pylori gastritis from 22% in 1985 to 46% in 1997 (p=0.004). Immune response to H. pylori HSP60 indicates chronic inflammation in the antrum (p=0.003). Apoptosis of gastric epithelial cells is largely dependent on grade of activity of gastritis, and, particularly in the antrum, on grade of H. pylori colonization (p=0.01; p=0.02), but is not associated with development of atrophy. Seropositivity for different H. pylori antigens (CagA, HSP 60) serves as a marker of different histological manifestations in the antrum and corpus mucosa.     

CagA和机体免疫反应在幽门螺杆菌致病中的作用及相互关系

目的　探讨幽门螺杆菌 (Helicobacterpylori,Hp)菌型差异和机体免疫反应在Hp致病中的作用及其相互关系。方法　采用间接ELISA法检测了 175例患者血清抗HpCagA IgG和抗HpIgE。结果　①Hp感染者抗HpCagA IgG的阳性率 (80 % )明显高于抗HpIgE(5 8 2 9% ,P <0 0 1)。②血清抗HpCagA IgG在慢性活动性胃炎 (ACG)和十二指肠球部溃疡 (DU)患者显著高于胃溃疡 (GU)、胃癌(GCa)、慢性非活动性胃炎 (NACG)和对照组 (P <0 0 1) ,而后 4组之间差异无显著性。③血清抗HpIgE在ACG显著高于DU、GU、GCa、NACG和对照组 (P <0 0 1) ,并且在中重度胃炎显著高于轻度胃炎(P <0 0 0 1)。④血清抗HpCagA IgG和抗HpIgE无明显相关性 (r=0 2 45 9,P >0 0 5 )。结论　CagA和血清抗HpIgE参与了Hp的致病过程 ,但是两者之间无明显相关性 ,并且它们在疾病中的含量也有一定差异 ,这说明二者在Hp的致病过程中是相互独立的因素 ,Hp感染引起疾病是多因素的综合作用。     

Helicobacter pylori genotypes, host factors, and gastric mucosal histopathology in peptic ulcer disease

From 183 patients undergoing upper gastrointestinal endoscopy, we used antral and corpus gastric biopsies for bacterial culture and histopathologic examination, blood samples to detect immunoglobulin G antibodies against Helicobacter pylori, and H pylori genomic DNA to analyze cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) genotypes. As expected, among H pylori biopsy-positive patients, those with duodenal ulcer (DU) (n = 34) had significantly more severe chronic and acute inflammation (P <.001) and epithelial degeneration (P =.004) in the gastric antrum than in the gastric corpus. Each of those 3 parameters and H pylori density were significantly higher in the antrum of patients with DU than in patients with gastric ulcer (GU) or no ulcer. Colonization with vacA s1/cagA-positive strains of H pylori was associated with inflammation and epithelial degeneration in gastric mucosa and increased risk for peptic ulcer disease (PUD), whereas colonization with vacA s2m2/cagA-negative strains was associated with mild gastric histopathology and was not associated with any significant risk for PUD. The predominant H pylori strains in African Americans were vacA s1bm1/cagA-positive, whereas all genotypes were well represented in non-Hispanic-Caucasians. By multivariate analysis, H pylori colonization was significantly associated with DU (Adjusted odds ratio [AdjOR] = 3.2 [1.4-7.2]) and nonsteroidal anti-inflammatory drugs (NSAID) use was inversely associated (AdjOR = 0.3 [0.2-0.7]). NSAID use (AdjOR = 4.3 [1.02-18.5]) and African-American ethnicity (AdjOR = 10.9 [2.6-50]) were significantly associated with GU. Smoking and age were not significantly associated with either DU or GU. These data indicate that DU is associated with an antral-dominant gastritis, and H pylori genotype and NSAID use independently contribute to the pathogenesis of PUD. HUM PATHOL 32:264-273. This is a US Government work. There are no restrictions on its use.     

Response of IgG1 and IgG2 subclasses to Helicobacter pylori in subjects with chronic inflammation of the gastric mucosa, atrophy and gastric cancer in a country with high Helicobacter pylori infection prevalence

Polarized immune response to Helicobacter pylori and induction of chronic inflammation may increase the risk of gastric atrophy and adenocarcinoma. We studied the association of the response of IgG1 and IgG2 antibodies to H. pylori with grade of gastric chronic inflammation and atrophy in a population with a high prevalence of H. pylori, and compared these data with the data obtained from the study of gastric cancer patients, as well as with the data for CagA positivity. Altogether, 114 persons from two adult population samples from Estonia and 45 consecutive gastric cancer patients were studied. All patients were positive for the H. pylori antibody determined by ELISA. Adenocarcinoma was classified histologically according to the Laurén's system. The response of the IgG subclasses to H. pylori (acid glycine-extracted whole cell proteins) was determined by ELISA and the results were compared with the ELISA results for the recombinant fragment of the CagA protein. Helicobacter pylori IgG level was lower in atrophic gastritis compared with nonatrophic gastritis (chronic inflammation) (p=0.001). In the group of cancer patients, the response of IgG and IgG1 was lower compared with both gastritis groups (p=0.01 and p=0.0002 for IgG, and p=0.001 and p=0.0005 for IgG1). IgG2 was lower for gastric cancer localized in the corpus (p=0.03). In conclusion, atrophic gastritis and gastric cancer were associated with a significant decline in IgG and IgG1 response to H. pylori compared with nonatrophic gastritis. Higher value of CagA antibodies was seen in gastric cancer and in gastric atrophy compared with nonatrophic gastritis; in gastric cancer patients, IgG1 response to H. pylori was correlated with CagA status.     

Relevance of CagA positivity to clinical course of Helicobacter pylori infection in children

A potential virulence determinant of Helicobacter pylori is the cagA gene product. To determine the relevance of the expression of CagA to the clinical picture and outcome of H. pylori infection in children, we examined 104 consecutive children diagnosed with H. pylori infection. Serum samples were collected to test for the presence of immunoglobulin G (IgG) anti-CagA antibodies. Forty-five patients (43%) had antibodies to the CagA protein (group I), and 59 did not (group II). Seropositive patients had a longer prediagnostic history of abdominal pain (P = 0.02), more severe abdominal pain (defined as ulcer pain) (P = 0.05), a higher prevalence of duodenal ulcer (38 versus 7%; P<0.01), more active chronic gastritis (82 versus 32%; P<0.001), and a higher titer of serum IgG anti-H. pylori antibodies (P<0.001). Ninety percent of the patients were monitored for 27+/-18 months. On multivariate analysis, CagA-negative patients had a 3.8-fold-higher chance of achieving a disease-free state than CagA-positive patients (95% confidence interval, 1.5- to 9.5-fold). We conclude that infection with CagA-producing strains of H. pylori is a risk factor for severe clinical disease and ongoing infection.     

Distinct diversity of vacA, cagA, and cagE genes of Helicobacter pylori associated with peptic ulcer in Japan

Colonization of the stomach mucosa by Helicobacter pylori is a major cause of acute and chronic gastric pathologies in humans. Several H. pylori virulence genes that may play a role in its pathogenicity have been identified. The most important determinants are vacA and cagA in the cag pathogenicity island (cagPAI) genes. In the present study, to consider the association of molecular genetics between vacA and the cagPAI regarding clinical outcome, we selected H. pylori strains with various genotypes of vacA in Japan and sequenced full-length vacA, cagA, and cagE genes. Sequencing of vacA and cagA genes revealed variable size, whereas the cagE gene was well conserved among strains. Each of the phylogenetic trees based on the deduced amino acid sequences of VacA, CagA, and CagE indicated that all three proteins were divided into two major groups, a Western group and an East Asian group, and the distributions of isolates exhibited similar patterns among the three proteins. The strains with s2 and s1a/m1a vacA genotypes and the Western-type 3' region cagA genotype were classified into the Western group, and the strains with the s1c/m1b vacA genotype and the East Asian-type 3' cagA genotype were included in the East Asian group. In addition, the prevalence of infection with the Western group strain was significantly higher in patients with peptic ulcer (90.0%, 9/10) than in patients with chronic gastritis (22.7%, 5/22) (chi2 = 12.64, P = 0.00057). These data suggest that the molecular genetics of vacA and cagPAI are associated and that the Western group with vacA and cagPAI genes is associated with peptic ulcer disease.     

Efficacy of sonicated and acid-extractable antigens in the serodiagnosis of H. pylori infection in peptic ulcer patients

Helicobacter pylori is implicated in causation of peptic ulcers and gastric cancer and plays a pivotal role in gastric pathophysiology. In the present study we evaluated the relative efficacy of sonicated and acid-extractable antigens in the serodiagnosis of H. pylori infection in peptic ulcer patients by ELISA. In the present study we evaluated the relative efficacy of sonicated and acid-extractable antigens in the serodiagnosis of H. pylori infection in peptic ulcer patients by ELISA. The two types of antigens mentioned above were prepared from H. pylori subcultures following appropriate procedures. Sera were collected from 13 subjects of whom eight were diagnosed to be suffering from duodenal ulcer (DU) and five from non-ulcer dyspepsia (NUD) and screened for the presence of anti H. pylori antibodies by ELISA. A case was considered seropositive, if the OD value was more than or equivalent to twice the mean OD value of blank. Analysis of our results showed that, with acid extractable antigen at a concentration of 2 mg/mL, 12 cases were seropositive. Contrastingly, with sonicated antigen, at a concentration of 2 mg/mL only eight cases were positive. It is concluded from this study, that the use of relatively purified antigens like acid extractable antigens enhances the sensitivity and specificity of this serodiagnostic test, indicative of its relatively higher efficacy over sonicated lysate containing multiple antigens.     

The prevalence of anti-Helicobacter (Campylobacter) pylori antibodies in patients and healthy blood donors

An enzyme linked immunosorbent assay (ELISA) with a sonicated suspension of Helicobacter (Campylobacter) pylori as antigen was used to detect anti-H. pylori antibodies in 517 patients without dyspepsia or peptic ulcer symptoms and 401 healthy blood donors. The criterion of seropositivity was determined from a receiver operating curve computed with the values of optical densities of 48 sera from dyspeptic patients with proven helicobacter-associated gastritis and 16 sera from dyspeptic patients with normal antral mucosa and no microbiological or histological evidence of H. pylori infection. The 227 (44%) seropositive persons amongst the patient group appeared to be significantly higher than the 142 (35%) sera with antibodies in the blood donors tested (p less than 0.03), even when adjustment was made for increasing age. We conclude that the prevalence of antibodies against H. pylori increases with age and that although antibodies are more prevalent in patients attending a hospital than in healthy blood donors, seropositivity suggestive of current or past infection can be found in one third of a randomly chosen population of blood donors.     

Serum antibody positivity for distinct Helicobacter pylori antigens in benign and malignant gastroduodenal disease

Infection with Helicobacter pylori may be associated with a variety of gastroduodenal diseases. Although H. pylori infection is common, peptic ulcer disease and gastric cancer occur in only a small minority of infected persons. This work was intended to correlate the pathological findings with the serological response to certain H. pylori antigens. Serum samples were taken from 285 patients who underwent gastroscopy. H. pylori infection was diagnosed by histology, culture or rapid urease test (RUT). Serum IgG reactivity against H. pylori-specific antigens was studied by Western blot. There was a significant association between the diagnosis of gastric cancer and the presence of IgG antibodies against the 19.5, 33 and 136 kDa (CagA) antigens. Comparing all H. pylori-positive patients with the gastric cancer group for the presence of the 19.5, 33 and 136 kDa (CagA) antigens, the results were as follows: chi2: 17.482, p < 0.001, power P = 0.994, odds ratio (OR) for the presence of gastric cancer: 19.5 (95% confidence interval (CI): 4.11-92.56). Antibodies against CagA alone or other bands (except 33 and 19.5 kDa antigens), as well as the age of patients were not related to a diagnosis of gastric cancer. Male patients were more likely to develop duodenal ulcer. IgG antibodies against the 19.5, 33 and 136 kDa (CagA) antigens could be helpful to identify patients at enhanced risk for the development of gastric cancer.     

Presence of Helicobacter pylori Antibodies in Haemodialysis Patients

Aim:  Renal dysfunction may influence the colonization of gastric mucosa by urea-splitting bacteria such as Helicobacter pylori , by increasing urea concentrations in the gastric juice. Our aim was to investigate the prevalence of H. pylori in patients with end-stage renal disease (ESRD), receiving long-term haemodialysis treatment.
Methods:  This study included 40 sera from patients with ESRD (29 male and 11 female) undergoing periodic haemodialysis; mean time of treatment was 42.6 months. Using ELISA technique, we investigated the presence of IgG and IgA antibodies against H. pylori as well as IgG CagA (antibodies specific for CagA(+) strains of H. pylori ). Sera from 40 healthy blood donors were used as a control group.
Results:  H. pylori IgG antibodies were detected in 32 out of 40 (80%) patients in the dialysis group, while 31/40 (77.5%) tested positive for IgA. IgG CagA antibodies were present in 13 out of 40 (32.5%). Prevalence of H. pylori IgG, IgA and CagA IgG antibodies in the control group was 33, 7 and 15%, respectively.
Conclusions:  Although international data suggest that prevalence of H. pylori infection is the same in ESRD patients as in healthy individuals, in our study that seems not to be the case. The higher blood and gastric juice urea levels may be a risk factor (among many others), but more studies are required in order to understand the relation of H. pylori infection in this group of patients.