Background. Helicobacter pylori infection is a major cause of peptic ulcer disease and gastric cancer. This study postulated that cranberry juice would be effective in the suppression of H. pylori in an endemically infected population at high risk for gastric cancer. Materials and methods. A prospective, randomized, double‐blind, placebo‐controlled trial was conducted in Linqu County of Shandong Province, China, where 189 adults aged 48.9 ± 11.2 years (mean ± SD) with H. pylori infection were randomly divided into two groups: cranberry juice (n = 97) and placebo (n = 92). Participants were assigned to orally receive two 250‐ml juice boxes of cranberry juice or matching placebo beverage daily for 90 days. The degree of H. pylori infection was determined using the 13 C‐urea breath test before randomization at 35 and 90 days of intervention to assess the efficacy of cranberry juice in alleviating infection. Results. A total of 189 subjects with positive 13 C‐urea breath test results prior to randomization completed the study. At day 35 of intervention, 14 of the 97 (14.43%) from the the cranberry juice treatment group and 5 of the 92 (5.44%) of the placebo recipients had negative 13 C‐urea breath test results. After 90 days, the study concluded that 14 of the 97 subjects in the cranberry juice treatment group versus 5 of the 92 in the placebo group yielded negative test results. Eleven individuals from the cranberry juice treatment group and only two from the placebo group were negative at 35 and 90 days of experiment. These results are significant ( p < .05). Conclusions. Regular consumption of cranberry juice can suppress H. pylori infection in endemically afflicted populations.
Background. Gastric atrophy induced by Helicobacter pylori is thought to predispose patients to noncardiac gastric cancer development. However, the host genetic factors that influence the progression of gastric atrophy have not been elucidated. In this study, we examined the effects of cytokine polymorphisms on H. pylori ‐induced gastric atrophy. Methods. Blood samples were taken from 454 Japanese subjects. The interleukin‐2 (IL‐2; T‐330G), IL‐4 (C‐33T), and IL‐13 (C‐1111T) polymorphisms were genotyped by polymerase chain reaction with confronting two‐pair primers (PCR‐CTPP). Anti‐ H. pylori IgG antibody and pepsinogen I and II were measured to diagnose H. pylori infection and atrophic gastritis. Results. The odds ratios (ORs) for the association between IL‐2 polymorphism [OR = 2.78, 95% CI (confidence interval) = 1.26–6.17 (T/T to G/G)] or IL‐4 polymorphism [OR = 2.22, 95% CI = 1.01–4.89 (T/C to C/C)] were increased significantly with gastric atrophy, whereas the corresponding OR of IL‐13 polymorphism was decreased with gastric atrophy [OR = 0.61, 95% CI = 0.39–0.96 (C/T and T/T to C/C)]. There were no significant H. pylori seropositivity‐related differences between these polymorphisms. We examined the relationship between these polymorphisms and gastric atrophy separately in H. pylori ‐seropositive and ‐seronegative groups. In the H. pylori ‐seropositive group, the IL‐2 T/T (OR = 2.78, 95% CI = 1.12–6.93) had a significant association with gastric atrophy. Conclusions. These results reveal that the IL‐2 gene polymorphism is associated with an increased risk of gastric atrophy induced by H. pylori infection and might predispose to gastric cancer.
Background. Ghrelin stimulates growth hormone and has orexigenic and adipogenic effects. Plasma ghrelin levels are reduced in obesity and possibly in Helicobacter pylori infection. Aim. To investigate whether there was a relation between H. pylori infection, body mass index (BMI) and serum ghrelin or leptin levels. Methods. University students undergoing an annual health check‐up were invited to participate. H. pylori status was based on the presence of specific IgG H. pylori antibodies in urine. Fasting serum ghrelin, leptin levels, and pepsinogen I and II levels were measured by enzyme immunoassay (EIA). Results. Eight hundred and one students volunteered. There was no significant difference in the height and BMI between those with and without H. pylori infection. The population of ghrelin study consisted of 132 (66 H. pylori ‐positive and 66 H. pylori ‐negative) students matched for age, sex, and BMI. The ghrelin level in the H. pylori ‐positive group was significantly lower (median 55 pmol/l) compared to the H. pylori‐ negative group (103 pmol/l) ( p < .00001). Leptin, triglyceride, total cholesterol, and HDL‐cholesterol were not different between the two groups, whereas LDL‐cholesterol levels were significantly higher (106 versus 100 mg/dl) ( p = .03) in the H. pylori ‐positive group. Leptin levels correlated with the BMI ( r = 0.53) ( p < .00001). Among H. pylori ‐positive subjects, ghrelin correlated only with pepsinogen I levels ( r = 0.26, p = .04). Conclusions. H. pylori infection was associated with a reduction in circulating ghrelin levels independent of sex and BMI.
Background. The babA2 gene, which encodes a blood-group antigen-binding adhesin that mediates attachment of Helicobacter pylori to human Lewis(b) antigens on gastric epithelial cells, has been associated with a higher risk of peptic ulcer and gastric cancer. The purpose of this study was to ascertain the frequency of babA2 genotype in H. pylori strains of patients with peptic ulcer and to correlate with other virulence factors. Materials and Methods. vacA, cagA, and babA2 genotypes of H. pylori were determined by using polymerase chain reaction (PCR). DNA was extracted from positive urease test gastric samples of 150 patients with peptic ulcer. Antrum and corpus biopsies were taken for histologic examination according to the updated Sydney system classification. Results. babA2 genotype was present in 104 (69.3%) and cagA in 113 (75.3%) gastric samples. No significant correlation was observed between babA2 and vacAs1 genotype or between babA2 and cagA status. The correlation of vacAs1 genotype with positive cagA was statistically significant (p < .001). The babA2-positive strain was more frequently found from the gastric samples of men, than of women (p = .01). Strains harboring cagA, vacAs1, and babA2 genotypes had no association to the grading of gastritis, presence of glandular atrophy, or intestinal metaplasia. The simultaneous presence of cagA, vacAs1, and babA2 was found in 32.6% of the H. pylori strains. Conclusions. babA2 genotype is frequently found in H. pylori strains from peptic ulcer disease in Brazil, although it has no significant correlation to the worsening of the gastritis and to other virulence markers such as vacAs1 and cagA.
Background. A small proportion of patients suffering from chronic active gastritis are diagnosed with gastric Helicobacter species other than Helicobacter pylori. Circumstantial evidence has suggested that these bacteria, also referred to as "Helicobacter heilmannii"-like organisms (HHLO), may be transmitted through animals. The isolation of a Helicobacter bizzozeronii strain from a human patient confirmed this hypothesis. It was the aim of the present study to assess the presence of animal Helicobacter species and H. pylori in humans infected with HHLO, as diagnosed by histology. Methods. Paraffin-embedded gastric biopsy specimens of 108 HHLO-infected patients (42 women and 66 men) from three clinical centers were screened for the presence of animal gastric Helicobacter species by polymerase chain reaction (PCR), using assays targeting the 16S rDNA region of the three known canine and feline helicobacters (H. bizzozeronii, H. salomonis and H. felis), "Candidatus H. suis", and "Candidatus H. bovis". In addition, the presence of H. pylori was evaluated by multiplex PCR analysis. Results. In 63.4% of the stomachs (64/101) classification of the Helicobacter infection into the above mentioned groups was achieved. Non-pylori Helicobacter species commonly colonizing the stomachs of cats and dogs were found in 48.5% (49/101) of the patients. Fourteen (13.9%) samples tested positive for "Candidatus H. suis", and "Candidatus H. bovis" was demonstrated in 1 (0.9%) patient. The presence of H. pylori was established in 13 patients (12.9%). Eleven stomachs (10.9%) were infected with at least two different Helicobacter species. Conclusions. This study identifies animal Helicobacter species in the stomach of a large series of HHLO-infected patients, which may have clinical implications in a subset of patients with gastric disease.
Background. Helicobacter pylori is a curved microaerophilic Gram‐negative bacterium considered as a risk factor for gastric cancer. The aim of this study was to find an association between burning sensations, acid taste, halitosis, and lingual hyperplasia with the effect of H. pylori on the mouth. Materials and Methods. A total of 124 subjects with different gastric diseases were studied: 46 patients with burning, halitosis and lingual dorsum hyperplasia and 78 patients with other diseases. Results. The detection of H. pylori in the oral cavity by histopathologic diagnosis and molecular biology was confirmed in 40/46 (87%) patients with burning, halitosis, and lingual hyperplasia, and in 2/78 (2.6%) subjects with other diseases. χ 2 : 91.26 ( p < .001) Mantel–Haenszel. Conclusion. This trial showed an association between H. pylori and burning, halitosis, and lingual hyperplasia, and further considered this bacterium a risk factor for gastric infection.
Background. We tested whether Helicobacter pylori ‐infected dyspeptic mothers had a higher rate of H. pylori infection in their children, and whether such H. pylori ‐infected children were predisposed to iron deficiency or growth retardation. Materials and methods. A total of 163 children from 106 dyspeptic mothers (58 with and 48 without H. pylori infection) were enrolled to evaluate body weight, height, hemoglobin, serum ferritin, and H. pylori infection using the 13 C‐urea breath test. A questionnaire was used to evaluate demographic factors of each child. Results. The rate of H. pylori infection in children with H. pylori ‐infected dyspeptic mothers was higher than that of children with noninfected mothers (20.5% vs. 5.3%; p < .01, OR: 4.6, 95% CI: 1.5–14.2). The rate of H. pylori infection in children elevated as the number of their H. pylori ‐infected siblings increased ( p < .01). For children below 10 years of age, H. pylori infection was closely related to low serum ferritin and body weight growth ( p < .05). Conclusion. The children of H. pylori ‐infected dyspeptic mothers had an increased risk for such infection. The risk further increased once their siblings were infected. H. pylori infection in pre‐adolescent children may determine iron deficiency and growth retardation.
Background. Helicobacter pylori is the major pathogen causing chronic gastritis and peptic ulcer disease and is closely linked to gastric malignancy. We have previously shown that H. pylori ‐induced NF‐κB activation and interleukin (IL)‐8 secretion are mediated by Toll‐like receptor (TLR) 2 in epithelial cells. However, the TLR2‐mediated global gene expression profile of the epithelial cell during H. pylori infection is still unknown. The goal of this study was to identify TLR2‐regulated genes in epithelial cells induced by H. pylori. Materials and methods. The HEK293 and HEK‐TLR2 cells were cocultured with H. pylori 26695 for 6 hours. Total RNA was extracted and hybridized to the Affymetrix human U133A microarray chipset, which contains 22,283 total probe sets including 14,285 genes. Data analyses were performed using affymetrix suite 5 software. The expression of selected genes in gastric epithelial cells AGS and MKN45 was monitored by quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR). Results. Forty‐six genes, contained in 57 probe sets, were induced > 2‐fold and three genes (five probe sets) decreased > 2‐fold by H. pylori infection of HEK293 cells. Fifty‐four genes, contained in 69 probe sets, were induced > 2‐fold, whereas only 1 gene was repressed > 2‐fold in H. pylori ‐infected HEK‐TLR2 cells. Comparisons of genes induced in HEK293 or HEK‐TLR2 cells identified 28 genes whose expression was dependent on the presence of TLR2. Seventeen genes were selected and their expression was assessed using the quantitative RT‐PCR in gastric epithelial cells during H. pylori infection . Eight of the 17 genes showed distinct expression patterns in AGS and MKN45 cells after H. pylori stimulation. Conclusions. The current study investigated the TLR2‐mediated global gene changes after H. pylori stimulation in the epithelial cell system. This approach will be helpful in identifying genes whose expression is mediated by specific TLRs and in determining the cellular responses that are responsible for diverse signal pathways during H. pylori infection.
Background. Neuronal damage in idiopathic parkinsonism may be in response to ubiquitous occult infection. Since peptic ulceration is prodromal, Helicobacter is a prime candidate. Aim. To consider the candidature of Helicobacter in parkinsonism with cachexia. Methods. We explore the relationship between being underweight and inflammatory products in 124 subjects with idiopathic parkinsonism and 195 controls, and present the first case-series evidence of efficacy of Helicobacter eradication, in parkinsonism advanced to the stage of cachexia. Results. Association of a low body mass index with circulating interleukin-6 was specific to parkinsonism (p = .002), unlike that with antibodies against Helicobacter vacuolating-toxin and cytotoxicity-associated gene product (p = 3.5 years. The latter presented with postprandial bloating, and persistent nausea: following eradication, radioisotope gastric-emptying returned towards normal, and upper abdominal symptoms regressed. Reversibility of their cachexia/disability contrasts with the outcome of anti-Helicobacter therapy where eradication repeatedly failed (one case), and in non-Helicobacter gastritis (three cases). Anti-parkinsonian medication remained constant. Intestinal absorption and barrier function were normal in all. Conclusion. Categorization, according to presence or absence of Helicobacter infection, was a useful therapeutic tool in late idiopathic parkinsonism.
Background.Neuronal damage in idiopathic parkinsonism may be in response to ubiquitous occult infection. Since peptic ulceration is prodromal, Helicobacter is a prime candidate. Aim.To consider the candidature of Helicobacter in parkinsonism with cachexia. Methods.We explore the relationship between being underweight and inflammatory products in 124 subjects with idiopathic parkinsonism and 195 controls, and present the first case-series evidence of efficacy of Helicobacter eradication, in parkinsonism advanced to the stage of cachexia. Results.Association of a low body mass index with circulating interleukin-6 was specific to parkinsonism (p = .002), unlike that with antibodies against Helicobacter vacuolating-toxin and cytotoxicity-associated gene product (p < .04). Marked reversibility in both cachexia and disability of idiopathic parkinsonism followed Helicobacter heilmannii eradication in one case, Helicobacter pylori eradication in another, follow-up being greater than or equal to 3.5 years. The latter presented with postprandial bloating, and persistent nausea: following eradication, radioisotope gastric-emptying returned towards normal, and upper abdominal symptoms regressed. Reversibility of their cachexia/disability contrasts with the outcome of anti-Helicobacter therapy where eradication repeatedly failed (one case), and in non-Helicobacter gastritis (three cases). Anti-parkinsonian medication remained constant. Intestinal absorption and barrier function were normal in all. Conclusion.Categorization, according to presence or absence of Helicobacter infection, was a useful therapeutic tool in late idiopathic parkinsonism.