Pylori IgG Titers Research Articles

Association of H. pylori IgG and CagA-IgG with some immunological and biochemical parameters in diabetic patients.

Helicobacter pylori a gram-negative, microaerophilic, spiral-shaped, and flagellated bacteria whose primary reservoir is the human stomach. It can cause gastric and extra-gastric diseases. So the study aimed to find the relationship between infection with H. pylori and progression of type II diabetes with other immunological markers. Method This study was conducted in Kirkuk City from Nov. 2022 to Apr. 2023 and included 106 individuals, 26 as a control group and 80 patients (34 males and 46 females) with mean age 57.61 suffering from DMII with H. pylori stool antigen positive results (immunochromatographic test cassette). Five ml of venous blood samples were taken for the HbA1c test (immunodetection technique), fast serum glucose (Hexokinase/G-6-PDH), serum H. pylori IgG, H. pylori CagA IgG, Interlukin-1?, and Interleukin-10 analysis (Sandwich-ELISA technique). Results There was a positive correlation between H. pylori IgG titer and HbA1c levels (0.0321, P = 0.004). In addition, there was a positive correlation between the levels of IL-1? and the H. pylori CagA IgG (r =0.579, P = 0.000). While a negative correlation was found between HbA1c level and IL-10 concentration, (r = -0.500, P = 0.000), there was also a negative association between IL-1? and IL-10 concentrations (r = -0.485, P = 0.000). Conclusion: Through the results of this correlation, we suggest a relationship between H. pylori infection and DMII.

High-Negative Anti-Helicobacter pylori IgG Antibody Titers and Long-Term Risk of Gastric Cancer: Results from a Large-Scale Population-Based Cohort Study in Japan.

Serologic testing of anti-Helicobacter pylori antibody, together with testing of pepsinogen I and II, is now widely used to stratify groups at high risk of gastric cancer in Japan. Those with a negative anti-H. pylori IgG titer, especially "high-negative" (3-<10 U/mL), are speculated to have higher risk of gastric cancer. We aimed to evaluate the association between a high-negative anti-H. pylori IgG titer and the long-term risk of gastric cancer in the Japan Public Health Center-based Prospective Study (JPHC Study) Cohort II. The study population consisted of 19,106 Japanese men and women who were followed from 1993 to 2013. A Cox proportional hazards model was used to assess the risk of gastric cancer for plasma anti-H. pylori IgG titers, together with the severity of atrophic gastritis by pepsinogen I and II levels. A total of 595 cases of gastric cancer occurred during an average of 18 years of follow-up. Compared with those with a low-negative anti-H. pylori IgG titer (≤3 U/mL), subjects with a high-negative titer (3-<10 U/mL) showed a significantly elevated risk of gastric cancer [HR = 2.81; 95% confidence interval (CI) = 1.62-4.89]. Among those with a high-negative titer, risk increase was observed under moderate or severe atrophic gastritis (HR = 18.73; 95% CI = 8.83-39.70). Our results suggest that those with a high-negative anti-H. pylori IgG titer and moderate and severe atrophic gastritis are at increased long-term risk of gastric cancer. Development of moderate or severe atrophic gastritis in subjects with high-negative anti-H. pylori IgG titer is suggested to increase risk of gastric cancer.

Incidence and association of genetic variations of IL-19 gene with H. pylori infection in the South Iranian population

Interleukin-19 (IL-19) is a pleiotropic cytokine with pro- as well as anti-inflammatory properties. It plays an important role in the pathogenesis of Helicobacter pylori (H. pylori) infection which in turn has been shown to be a major etiological factor in the development of gastric cancer and ulcers. Single Nucleotide Polymorphisms (SNPs) which alter the functioning of IL-19 could thus play a pivotal role in the pathogenesis as well as the outcome of these diseases. In this study, we explored the association of rs2243191 (Ser175Phe) and rs1028181 (−513 T/C) polymorphisms in IL-19 with the incidence of H. pylori infection in an Iranian population. 130 patients diagnosed with H. pylori infection (anti-H. pylori IgG titers > 90 ng/ml) and 130 healthy volunteers were genotyped for these two polymorphisms using Amplification-Refractory Mutation System (ARMS) PCR and Restriction Fragment Length Polymorphism (RFLP) PCR respectively. We analyzed the allelic frequencies of rs1028181 and rs2243191 polymorphisms in patients infected with H. pylori. The IL-19 gene polymorphism at rs1028181 was found to be significantly associated with the incidence of H. pylori infection (C vs. T, OR = 0.68; CI = 0.46 (1–0.01, P = 0.03)) suggesting a dominant role of rs1028181 mutation. However, no significant correlation between rs2243191 and H. pylori infection (C vs. T, OR = 0.65, CI = 0.35–(1-0.28, P = 0.22)) was observed. Furthermore, the serum levels of anti-H. pylori IgG were found elevated in the dominant allele. All these findings suggest a role of IL-19 in the pathogenesis of H. pylori infection, however, it may require further replication and validation.

Helicobacter pylori colonization and obesity \u2013 a Mendelian randomization study

Obesity is associated with substantial morbidity, costs, and decreased life expectancy, and continues to rise worldwide. While etiological understanding is needed for prevention, epidemiological studies indicated that colonization with Helicobacter pylori (H. pylori) may affect body mass index (BMI), but with inconsistent results. Here, we examine the relationship between H. pylori colonization and BMI/obesity. Cross-sectional analyses were performed in two independent population-based cohorts of elderly from the Netherlands and Germany (n = 13,044). Genetic risk scores were conducted based on genetic loci associated with either H. pylori colonization or BMI/obesity. We performed a bi-directional Mendelian randomization. Meta-analysis of cross-sectional data revealed no association between anti-H. pylori IgG titer and BMI, nor of H. pylori positivity and BMI. Anti-H. pylori IgG titer was negatively associated with obesity (OR 0.99972; 95% CI 0.99946-0.99997, p = 0.03) and with obesity classes (Beta −6.91 •10−5; 95% CI −1.38•10−4, −5.49•10−7, p = 0.048), but the magnitude of these effects was limited. Mendelian randomization showed no causal relation between H. pylori genetic risk score and BMI/obesity, nor between BMI or obesity genetic risk scores and H. pylori positivity. This study provides no evidence for a clinically relevant association between H. pylori and BMI/obesity.

Association of Helicobacter pylori specific IgG antibody with serum magnesium levels in peritoneal dialysis patients

Introduction: Few studies have reported the relationship between serum magnesium and Helicobacter pylori infection in chronic kidney disease (CKD) and patients receiving dialysis. Objectives: In this study, we aimed to test, the relationship between serum magnesium (Mg) level and H. pylori infection in CKD patients receiving peritoneal dialysis. Patients and methods: Around 40 patients were evaluated through the study. Serum magnesium levels and H. pylori specific IgG antibody levels were assessed. Results: The mean serum magnesium level was 3.00 ± 0.36 mg/dL. No significant difference was seen in serum Mg level between positive and negative groups of H. pylori. No correlations were reported between H. pylori IgG titers with age, serum Mg, Ca, P, parathyroid hormone (PTH), vitamin D, albumin, urea, creatinine (Cr) and plasma hemoglobin (P>0.05). Conclusion: In this study no correlation between serum magnesium levels and H. pylori specific IgG antibody was detected. We believe that this is the first study evaluating the relationship between serum magnesium level and H. pylori infection in peritoneal dialysis patients. More and larger clinical investigations are required to consider the conflicting results of studies regarding the association of serum magnesium and H. pylori in patients undergoing dialysis.

Correlation Between Expression of the Cancer/Testis Antigen KK-LC-1 and Helicobacter pylori Infection in Gastric Cancer.

Our previous study indicated that Kita-kyushu lung cancer antigen-1 (KK-LC-1) is a cancer/testis antigen (CTA) expressed in 82% of gastric cancer cases. Here, we investigated the relationship between KK-LC-1 expression and Helicobacter pylori infection in Japanese patients with gastric cancer. We examined CTA expression in 25 surgical gastric cancer specimens and anti-H. pylori IgGs in the serum of each patient. KK-LC-1 was expressed in 80% of tumor samples, markedly higher than melanoma antigen gene (MAGE)-A1, MAGE-A3, MAGE-A4, synovial sarcoma, X breakpoint 4 (SSX4) and New York esophageal squamous cell carcinoma-1 (NY-ESO-1). Anti-H. pylori IgG titers from the KK-LC-1-positive patients were significantly higher (67.5±7.6) than those from KK-LC-1-negative patients (15.8±7.5, p<0.01) although there were no significant differences between patients positive and negative for MAGE-A1, -A3 and-A4, SSX4 and NY-ESO-1. As far as we are aware, this is the first report of a correlation between a carcinogen and CTA expression in clinical samples. KK-LC-1 was frequently expressed in gastric cancer caused by H. pylori infection. The risk diagnosis for gastric cancer might be more accurate if KK-LC-1 expression status were also considered.

The Impact of Gastric Atrophy on the Incidence of Diabetes

Gastric atrophy results in lower plasma ghrelin, higher gastrin secretion, a change in gut microbiota, and altered dietary nutrient absorption, which may be associated with the incidence of diabetes. Helicobacter pylori (H. pylori) infection is a major cause of gastric atrophy and is associated with diabetes in some reports. Since there is no study which investigates the impact of gastric atrophy on diabetes, we conduct a prospective cohort study to examine the relationship between H. pylori infection, gastric atrophy, and incident diabetes. In this study, subjects with gastric atrophy had a lower risk of incident diabetes, compared to those without gastric atrophy. The extent of gastric atrophy, measured by serum pepsinogen (PG) I/II ratio, was correlated with age, H. pylori IgG titer, HOMA2-IR, and HOMA2%B. When gastric atrophy is more extensive, presented as a lower serum PG I/II ratio, the risk of incident diabetes is lower. On the other hand, there was no significant association between H. pylori infection and the incidence of diabetes. In conclusion, the presence and the extent of gastric atrophy, but not H. pylori infection, are associated with incident diabetes. Further studies are needed to investigate the detailed mechanisms and the potential applications of the findings to guide diabetes screening and treatment strategies.

An investigation into the relationship between anti-Helicobacter pylori and anti-Saccharomyces cerevisiae antibodies in patients with axial spondyloarthritis and Crohn disease.

Spondyloarthritis (SpA) is a musculoskeletal inflammatory disease linked with immune responses to intestinal microbiota, and subclinical intestinal ulcerations that are closely related to inflammatory bowel diseases. Helicobacter pylori is a common cause of gastroduodenal ulceration, and anti-Saccharomyces cerevisiae antibodies (ASCA) are associated with intestinal inflammation in both Crohn disease (CD) and SpA. We investigated the relationship between H. pylori and ASCA. Ninety-one patients with axial SpA and forty with CD were included. ASCA IgG/IgA and anti-H. pylori IgG titers were assessed by ELISA. The proportion of ASCA+ patients in the positive and negative anti-H. pylori IgG groups with SpA and CD were compared using Chi-square tests, and correlations were evaluated using the Spearman's coefficient. Anti-H. pylori IgG titers were significantly negatively correlated with the ASCA IgG (r = -0.563, p < 0.001) and IgA (r = -0.342, p = 0.019) titers in the axial SpA patients. The same pattern of negative correlation was also observed in the CD patients. Anti-H. pylori+ serology was significantly more frequent in axial SpA patients than in those with CD (52.4 vs. 18.4 %, p < 0.001), while ASCA+ serology was significantly more frequent in CD patients than in SpA patients. A negative correlation between the anti-H. pylori titers and ASCA was found for axial SpA and CD. Anti-H. pylori+ serology was more frequent in SpA than in CD, while ASCA positivity was more frequent in CD patients than in those with SpA. A possible influence of H. pylori on the development of ASCA needs further investigation.

Immune responses to Helicobacter pylori infection in children with intellectual disabilities

Infection with Helicobacter pylori was assessed through serum H. pylori IgG antibody in children with intellectual disabilities (ID). The sero-status of cytotoxin-associated gene A (CagA) was determined as a risk determinant for severe H. pylori-associated diseases. In total, 210 children with ID were included who were permanent resident of three institutes in Tehran. Medical history and demographic data were collected by reviewing the medical file records. The anti H. pylori IgG antibody was detected in serum of 74.8% of children using ELISA. Significant correlations were found between the rate of infection and age (P = 0.001) and duration of institutionalization (P = 0.018). The likelihood of H. pylori IgG positive response increased with age with the highest response in 15-18 years age group (OR = 6.66, 95% CI: 2.14-20.17; P = 0.001). Similarly, the average titers of H. pylori IgG antibody were increased with age. The institutionalization duration of more than 49 months affected the likelihood of H. pylori IgG positive response (OR = 2.437, 95% CI: 1.12-5.26; P = 0.023). Anti-CagA titers were higher than 5arbU/ml in 92 (58.6%) children, indicating a positive response against CagA protein. The titer of H. pylori IgG was significantly higher in CagA-positive (mean ± SE = 51.04 ± 3.41) than in CagA-negative children (38.07 ± 4.18; P = 0.017). In contrast to total H. pylori IgG titers, anti-CagA antibody had non-regular trend of alterations with age. The seropositivity rate of H. pylori infection in ID children was higher than other reports in healthy children from various regions of the country. The risk of H. pylori infection is increased with age and duration of institutionalization. The serostatus of CagA in children with IDs has not been reported so far. The regular monitoring of the CagA-positive carriers is recommended; since CagA positive cases carry the risk of progression of infection toward severe H. pylori associated sequels such as gastric cancer and duodenal ulcers.

Experimental study on prevention and treatment of Helicobacter pylori infection by Lactobacillus acidophilus in C57BL/6 mice

Objective To investigate the potential effects of Lactobacillus acidophilus strain L6 on prevention and treatment of Helicobacter pylori (H. pylori) infection in animal models. Methods A total of 200 hundred C57BL/6 mice were used in the study. ① Sixty mice were divided into control group (infected with H. pylori) and prevention group (previously treated with L6 and followed by infection with H. pylori) with 30 each. The incidence of H. pylori infection was compared between two groups.② Sixty mice were divided into control group (infected with H. pylori) and treatment group (infected with H. pylori for 4 weeks and followed by treatment with L6) with 30 each. The changes of H. pylori infection was compared between tow groups. ③ Eighty mice previously infected with H. pylori were orally administrated with L6 in the water supply over a period of 9 months. Of which, 40 H. pylori negative mice were either continuously or discontinuously treated with L6. The re-infection of H. pylori was compared between two groups. The H. pylori infection, gastric mucosal inflammatory and serum anti-H. pylori-lgG titer was measured by using urea breath test, histopathology and ELISA, respectively. Results The positive rate of H. pylori infection was 100% in control group and 20% in prevention group (pre-treated with L6 for 1 week). Whereas there was no H. pylori infection in the rest mice of prevention group pre-treated with L6 for 2 or 4 weeks. There was significant difference in H. pylori infection between two groups (P<0. 05). The serum anti-H. pylori IgG titer was lower in treatment group than in control group (P<0. 05). The reinfection of H. pylori in mice continuously treated with L6 was significantly lower than those discontiously treated with L6 (P<0. 05). Conclusions Preventively feeding L6 can significantly reduce the H. pylori infection in C57BL/6 mice, whereas the inhibition of H. pylori re-infection can also be achieved with long-term administration of L6. Key words: Lactobacillusacidophilus; Helicobacter pylori; Animal experimentation

Manganese Superoxide Dismutase Polymorphism and Risk of Gastric Lesions, and Its Effects on Chemoprevention in a Chinese Population

Manganese superoxide dismutase is the primary antioxidant enzyme in the mitochondria and is involved in carcinogenesis. To investigate the association between MnSOD Val(16)Ala polymorphism and risk of advanced gastric lesions, and its effects on chemoprevention, a population-based study was conducted in Linqu, a high-risk area of gastric cancer in China. Genotypes were determined by PCR-RFLP analysis in 3,355 subjects with the baseline histopathologic diagnosis in 1994, and 2,758 of these subjects received subsequent three interventions including vitamin supplementation for 7.3 years. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by unconditional logistic regression model. We found an increased risk of dysplasia in subjects with the Val/Ala+Ala/Ala genotype (OR, 1.31; 95% CI, 1.02-1.68) compared with the Val/Val genotype. Stratified analysis indicated that a significantly elevated risk of intestinal metaplasia (OR, 3.40; 95% CI, 2.64-4.38) or dysplasia (OR, 4.01; 95% CI, 2.79-5.74) was found in subjects carrying the Val/Ala+Ala/Ala genotype and Helicobacter pylori infection, and an interaction between this genotype and a high serum H. pylori IgG titer (>2.94) on the risk of dysplasia was observed (P(interaction) = 0.01). Furthermore, an elevated chance for regression of gastric lesions was observed in subjects with the Val/Ala+Ala/Ala genotype and high IgG titer in an intervention trial with vitamin supplementation (OR, 2.45; 95% CI, 1.37-4.38). These findings suggest that Val(16)Ala polymorphism may play an important role in development of advanced gastric lesions and modify the effect of vitamin supplementation on the evolution of gastric lesions. Val(16)Ala polymorphism is related to gastric cancer development.

Helicobacter pylori IgG Antibodies in Aqueous Humor and Serum of Subjects With Primary Open Angle and Pseudo-exfoliation Glaucoma in a South Indian Population

A prospective, nonrandomized, comparative study was carried out to investigate levels of anti-Helicobacter pylori-specific IgG antibodies in the aqueous humor and serum of patients with primary open angle glaucoma (POAG), exfoliation syndrome [pseudo-exfoliation glaucoma (PXFG)], and with normotensive cataract patients, who served as controls. Aqueous humor was aspirated at the beginning of glaucoma surgery from 50 eyes of 50 patients with POAG, with PXFG and at the beginning of phacoemulsification cataract surgery from controls. Serum samples were obtained. Anti-H. pylori IgG concentration in the aqueous humor and serum was measured by means of enzyme linked immunosorbent assay. Serum analysis of anti-H. pylori IgG antibodies revealed statistically significant difference between POAG and PXFG (52.26+/-52.51 vs. 25.22+/-35.27, P=0.01). Also, the difference between POAG and controls was statistically significant (54.05+/-55.04 vs. 33.83+/-41.73, P=0.04). However, on comparing PXFG with the control group, the difference was statistically insignificant (P=0.12). The mean concentration of anti-H. pylori IgG antibodies in aqueous humor of patients in POAG and controls were not statistically different (3.93+/-5.14 vs. 2.65+/-2.87, respectively, P=0.73). The mean concentration of anti-H. pylori IgG antibodies in aqueous humor of patients in PXFG and controls were not statistically different (8.87+/-30.25 vs. 2.65+/-2.87, respectively, P=0.83). There was also no statistical difference of IgG levels between POAG and PXFG (3.93+/-5.14 vs. 8.87+/-30.25, respectively, P=0.87). The levels of anti-H. pylori IgG titers in sera of individuals with POAG were significantly higher compared with PXFG and control groups. We support the hypothesis of the role of anti-H. pylori antibodies in causative mechanism for POAG. We could not find a significant link between the anti-H. pylori IgG antibodies and the PXFG.

Severity of gastritis determines glandular stomach carcinogenesis in Helicobacter pylori‐infected Mongolian gerbils

Helicobacter pylori (H. pylori) infection causes chronic gastritis and is also related to gastric carcinoma. The present study focused on severity of H. pylori-induced gastritis as a determinant of carcinogenesis. Seven-week-old male Mongolian gerbils were inoculated with H. pylori at experimental weeks 0, 12, or 18, then given N-methyl-N-nitorosourea (MNU) from weeks 20-40. At week 70, stomachs were then excised for histological examination 70, 58, or 52 weeks after H. pylori inoculation, respectively (Groups A, B, and C for long-, middle-, and short-term). The respective incidences of glandular stomach adenocarcinomas were 65.0% (13/20), 20.0% (2/10), and 23.0% (3/13) (P<0.05). Higher scores of infiltration of inflammatory cells, hyperplasia, intestinal metaplasia and mucosal bromodeoxyuridine (BrdU) labeling index in antrum and corpus mucosa, were seen in group A than B or C (P<0.05) and serum anti-H. pylori IgG titer and gastrin levels were also significantly higher, along with mRNA levels for mucosal interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). The results demonstrated the term and severity of H. pylori infection to play important roles in gastric carcinogenesis, with essential involvement of chronic inflammation, especially increased rates of cell proliferation, in H. pylori-associated carcinogenesis.

Host serological response to Helicobacter pylori after successful eradication: long‐term follow‐up in patients with cured and persistent infection

SummaryAimTo systematically determine the usefulness of Helicobacter pylori IgG antibody titer decline as a predictor of treatment success after H. pylori eradication in large patient samples.Patients and MethodsSerum samples from 258 H. pylori positive patients (52.8 yrs, 65% males) were retrospectively collected from five medical centers, and H. pylori titers were quantitatively determined by ELISA. Serial serum samples were collected at baseline and for up to 4.9 years after treatment. 169 patients underwent successful eradication while 89 remained infected. The median total observation period was 635 days (range, 51 to 1,800 days). Chronological changes in H. pylori titers were analyzed and compared between cured and infection persistent subjects.ResultsThe proportion of infection persistent patients who developed negative H. pylori IgG antibody titers was below 5%. A receiver operating characteristic (ROC) curve for the confirmation of successful eradication according to the percent decline over baseline at each time‐point showed that a 60% decline at 1 year or more after eradication treatment strongly correlated with successful eradication (sensitivity = 90% and specificity = 87%).ConclusionA 60% decline in H. pylori IgG titers (HEL‐p kit) from baseline to one year or greater is a reliable predictor of successful H. pylori eradication.

Host serological response to Helicobacter pylori after successful eradication: long‐term follow‐up in patients with cured and persistent infection

SummaryAimTo systematically determine the usefulness of Helicobacter pylori IgG antibody titer decline as a predictor of treatment success after H. pylori eradication in large patient samples.Patients and MethodsSerum samples from 258 H. pylori positive patients (52.8 yrs, 65% males) were retrospectively collected from five medical centers, and H. pylori titers were quantitatively determined by ELISA. Serial serum samples were collected at baseline and for up to 4.9 years after treatment. 169 patients underwent successful eradication while 89 remained infected. The median total observation period was 635 days (range, 51 to 1,800 days). Chronological changes in H. pylori titers were analyzed and compared between cured and infection persistent subjects.ResultsThe proportion of infection persistent patients who developed negative H. pylori IgG antibody titers was below 5%. A receiver operating characteristic (ROC) curve for the confirmation of successful eradication according to the percent decline over baseline at each time‐point showed that a 60% decline at 1 year or more after eradication treatment strongly correlated with successful eradication (sensitivity = 90% and specificity = 87%).ConclusionA 60% decline in H. pylori IgG titers (HEL‐p kit) from baseline to one year or greater is a reliable predictor of successful H. pylori eradication.

Helicobacter pylori and Schistosoma japonicum co-infection in a Chinese population: helminth infection alters humoral responses to H. pylori and serum pepsinogen I/II ratio

The effects of helminth infection on humoral IgG responses and clinical outcome of gastric Helicobacter pylori infection are unknown. IgG and IgG subclass responses to H. pylori and serum pepsinogen I/II ratio, a marker of gastric atrophy, were investigated in a Schistosoma japonicum prevalent Chinese population. H. pylori, CagA and IgG subclass responses were assayed by ELISA. Serum pepsinogen I and pepsinogen II were assayed by ELISA and the pepsinogen I/II ratio determined. In 150 subjects, infection with S. japonicum and H. pylori was 55.3% and 51.3%, respectively. H. pylori IgG titres and CagA seropositivity were significantly lower ( P < 0.05) in co-infected subjects, and differences in H. pylori IgG isotype responses were evident. In H. pylori positives, a significantly higher ( P < 0.05) pepsinogen I/II ratio was observed in co-infected subjects. The difference between S. japonicum positive and negative subjects was only evident in H. pylori CagA seronegative subjects. In conclusion, S. japonicum co-infection with H. pylori is associated with alterations in IgG responses to H. pylori and less gastric atrophy.

The association between tumour necrosis factor-alpha gene polymorphism and the susceptibility to rugal hyperplastic gastritis and gastric carcinoma.

Some subjects infected by Helicobacter pylori have enlarged folds in the gastric body, the precise mechanism of which remains obscure. The aim of this study was to clarify the association of tumour necrosis factor-alpha (TNFA) gene polymorphism with susceptibility to hyper-rugosity. We also examined the association of TNFA polymorphism with gastric carcinoma. Four hundred and seventy-two subjects (male/female = 351/121, aged 26-81 years) without gastric carcinoma (control group), and 300 patients (male/female = 218/82, aged 32-91 years) with gastric carcinoma. Barium meal roentgenograms were performed in 396 subjects in the control group and fold width was measured at the greater curvature of the middle portion of the gastric body. Fasting plasma anti-H. pylori IgG titres, pepsinogens (PGs) I and II were analysed, and TNFA -857 promoter polymorphism was distinguished by the 5' nuclease polymerase chain reaction assay and polymerase chain reaction restriction fragment length polymorphism using HincII in both groups. Adjusted odds ratios of TNFA -857 T/T genotype and H. pylori seropositivity for hyper-rugosity (fold width = 6.0 mm) were 6.7 (95% confidence interval (CI) 1.5-28, P < 0.01) and 18.2 (95% CI 4.2-78, P < 0.0001), respectively. There were no significant differences in any genotype or allele frequencies between the control and total gastric carcinoma group. In a subgroup of gastric carcinoma patients who were negative for the PG assay, however, the odds ratio of the T allele was 1.4 (95% CI 1.0-2.0, P < 0.05). The TNFA -857 T/T genotype and H. pylori infection were strongly associated with rugal hyperplastic gastritis. The TNFA -857 T allele may promote gastric carcinoma without severe atrophy.

Long-term effects of Helicobacter pylori eradication in Mongolian gerbils.

In this study, to clarify whether Helicobacter pylori eradication alters the course of the development of gastric mucosal changes in the stomach, we examined the long-term effects of H. pylori eradication on H. pylori-inoculated gerbils. A total of 40 H. pylori-inoculated gerbils were randomized and subjected, at 22 months after inoculation, to eradication treatment with dual therapy of omeprazole plus clarithromycin, or with therapy with a novel quinolone compound, Y-34867, alone. The animals were killed at the start of administration (control group) or at 8 months after the completion of therapy (vehicle or eradication-treatment groups). Severe histopathological changes in the gastric mucosa were observed in all H. pylori-inoculated gerbils at the start of administration. At 8 months after completion of therapy, the frequency of gastritis, erosion, intestinal metaplasia, and gastric carcinoid in the eradication therapy groups was markedly reduced compared with that in the control and vehicle groups. Values for anti- H. pylori IgG titer, bacterial counts, and gastrin also decreased significantly. These results suggest that H. pylori eradication may have had a therapeutic effect not only on gastritis, erosion, and gastric ulcer but also on glandular atrophy, intestinal metaplasia, and gastric carcinoid.

Helicobacter pylori infection in recurrent abdominal pain in children--a prospective study.

A total of 40 children was recruited to assess the role of Helicobacter pylori infection in children with recurrent abdominal pain syndrome. Among 40 children, seven (17.5%) cases were confirmed to have H. pylori infection. All H. pylori-positive patients had active chronic gastritis histologic findings (p < 0.0001); however, the majority of the H. pylori-negative patients had minimal to mild gastritis histologic findings (p = 0.001). Grossly, chronic gastritis picture was present in all children infected with H. pylori and antral nodular gastropathy present in 43%. 71% of H. pylori-positive patients had elevated anti-H. pylori IgG titer; however, 15% in H. pylori-negative patients (p = 0.006). Serum H. pylori assay had a sensitivity of 71% and specificity of 85%; however, sensitivity and specificity of rapid urease test were 86% and 100% respectively. Antral nodularity is a specific, peculiar endoscopic finding of children infected with H. pylori (p = 0.004). Although the present study suggests that H. pylori-related chronic gastritis may play an etiological role in a subgroup of children with RAP syndrome, but the routine screening of H. pylori infection in children with RAP is not recommended, since no compelling data support the significant association between H. pylori infection and RAP syndrome.

Liver disease and Helicobacter.

Liver disease and Helicobacter.