Increase of antigen-presenting cells in the gastric mucosa of Helicobacter pylori-infected children

BACKGROUND: Infection with Helicobacter pylori leads to an increase of T cells in the gastric mucosa of children. In contrast to peripheral blood, where monocytes are the most abundant antigen-presenting cells, CD14+ macrophages are very rare in infected gastric mucosa. We postulated that other types of antigen-presenting cells must be present in infected gastric mucosa. MATERIAL AND METHODS: Antral biopsies were obtained from 56 children. The cellular expression of major histocompatibility complex (MHC) class II molecules, CD1a/b, and CD23, which are involved in antigen presentation were analyzed by immunohistochemistry. In addition, T cells (CD4, CD8, CD25, and gamma/delta-TCR), B cells (anti-IgM), macrophages (CD14) and granulocytes (CD15) were quantified. RESULTS: Twenty-eight children were H. pylori-infected. Thirteen children were healthy, 15 had other gastric pathologies. T cells (p<.0001), B cells (p<.0001), CD23+ (p<.0001), and CD1a/b+ (p<.005) cells were significantly increased in the lamina propria of H. pylori-infected children, whereas macrophages were rare without significant differences among the groups. Within the epithelium, CD8+ T lymphocytes predominated clearly over CD4+ cells. H. pylori-negative children had only few MHC class II-positive cells within the gastric epithelium, whereas MHC class II antigens were strongly expressed on epithelial cells (p<.0001) of all H. pylori-infected children. CONCLUSION: Helicobacter pylori infection leads to an enhanced expression of antigen-presenting molecules together with a parallel rise of T cells in the lamina propria. This may represent an effort of the immune system to optimize local immune responses against H. pylori. We speculate that the epithelium participates in the initiation of a local immune response against H. pylori.     

Expression of adhesion and activation molecules on circulating monocytes in children with Helicobacter pylori infection

Objectives: The aim of this study was to assess the cell surface expression of adhesion (CD11a, CD11b, CD11c, CD18, CD54, and CD58) and activation (CD14, HLA‐DR, and CD16) molecules on the circulating monocytes in Helicobacter pylori (H. pylori)‐infected and noninfected children with gastritis, with the goal of comparing the results with those obtained from the controls. Materials and Methods: Ninety‐four children were studied: 47 of them with H. pylori infection (of those 25 children after the failure of eradication therapy) and 26 children with gastritis where H. pylori infection was excluded, as well as 21 controls. H. pylori infection status was assessed based on [¹³C] urea breath test, rapid urease test, and histology. Analysis of the monocyte surface molecule expression was carried out by flow cytometry. Results: H. pylori‐infected children and children who experienced a failure of the eradication therapy differed significantly in the expression of adhesion and activation molecule on circulating monocytes. A decrease, both in the proportion of CD11c‐ and CD14‐bearing monocytes, and the expression of CD11c and CD14 molecules on circulating monocytes, was found in children in whom the eradication therapy failed (p < .05). Low expression of CD11b (p = .04) and CD18 (p = .02) integrins on monocytes was also observed. Additionally, the percentage of HLA‐DR‐bearing monocytes was decreased (p = .04), while the CD16 density receptor was increased (p = .02). Compared with the controls, low percentage of CD16‐positive monocytes was noted in noninfected children with gastritis (p = .01). Conclusion: H. pylori eradication therapy in children causes inhibition of inflammatory response via a reduction in CD11b, CD11c, and CD18 beta2 integrin monocyte expression.     

Younger siblings play a major role in Helicobacter pylori transmission among children from a low-income community in the Northeast of Brazil

Background and Aims: To further evaluate intrafamilial transmission of H. pylori infection during childhood, we investigated the prevalence of H. pylori in family members from a poor H. pylori high‐prevalence urban community in the Northeast of Brazil. Methods: H. pylori infection was investigated in 570 members of 128 households, by ¹³C‐urea breath test in children and by ELISA in mothers and other adult relatives. Results: The overall prevalence of H. pylori infection (376/570) increased with age (p < .001) and ranged from 28.9%, in children aged 6 months to 5 years, to 82% in adults over 40 years. An H. pylori positive mother and the number of infected siblings are independent risk factors for childhood H. pylori infection (OR = 2.2, 95% CI = 1.0–4.6 and OR = 4.3, 95% CI = 2.3–8.1, respectively) The number of siblings, number of younger siblings, and number of infected younger siblings were also associated with the infection in the univariate analysis. The number of infected younger siblings remained independently associated with the infection (p = .000), even after controlling for all the above cited variables, in addition to the H. pylori status of siblings and mothers, age, number of people per room, and number of children in the household. Conclusion: The transmission of H. pylori occurs from infected mothers to their offspring and among siblings, notably from younger siblings to the older ones.     

Probiotics-containing yogurts suppress Helicobacter pylori load and modify immune response and intestinal microbiota in the Helicobacter pylori-infected children

Background: The benefits of probiotics to the pediatric Helicobacter pylori infection remain uncertain. We tested whether the H. pylori‐infected children have an altered gut microflora, and whether probiotics‐containing yogurt can restore such change and improve their H. pylori‐related immune cascades. Methods: We prospectively included 38 children with H. pylori infection confirmed by a positive ¹³C‐urea breath test (UBT) and 38 age‐ and sex‐matched noninfected controls. All of them have provided the serum and stool samples before and after 4‐week ingestion of probiotics‐containing yogurt. The serum samples were tested for the TNF‐α, IL‐10, IL‐6, immunoglobulin (Ig) A, G, E, pepsinogens I and II levels. The stool samples were tested for the colony counts of Bifidobacterium spp. and Escherichia coli. The follow‐up UBT indirectly assessed the H. pylori loads after yogurt usage. Results: The H. pylori‐infected children had lower fecal Bifidobacterium spp. count (p = .009), Bifidobacterium spp./E. coli ratio (p = .04), serum IgA titer (p = .04), and pepsinogens I/II ratio (p < .001) than in controls. In the H. pylori‐infected children, 4‐week yogurt ingestion reduced the IL‐6 level (p < .01) and H. pylori loads (p = .046), but elevated the serum IgA and pepsinogen II levels (p < .001). Moreover, yogurt ingestion can improve the childhood fecal Bifidobacterium spp./E. coli ratio (p = .03). Conclusions: The H. pylori‐infected children have a lower Bifidobacterium microflora in gut. The probiotics‐containing yogurt can offer benefits to restore Bifidobacterium spp./E. coli ratio in children and suppress the H. pylori load with increment of serum IgA but with reduction in IL‐6 in H. pylori‐infected children.     

Inhibitory effects of polyphenols on gastric injury by Helicobacter pylori VacA toxin

Background. Helicobacter pylori induces gastric damage and may be involved in the pathogenesis of gastric cancer. H. pylori‐vacuolating cytotoxin, VacA, is one of the important virulence factors, and is responsible for H. pylori‐induced gastritis and ulceration. The aim of this study is to assess whether several naturally occurring polyphenols inhibit VacA activities in vitro and in vivo. Materials and Methods. Effects of polyphenols on VacA were quantified by the inhibition of: 1, vacuolation; 2, VacA binding to AZ‐521 or G401 cells or its receptors; 3, VacA internalization. Effects of hop bract extract (HBT) containing high molecular weight polymerized catechin on VacA in vivo were investigated by quantifying gastric damage after oral administration of toxins to mice. Results. HBT had the strongest inhibitory activity among the polyphenols investigated. HBT inhibited, in a concentration‐dependent manner: 1, VacA binding to its receptors, RPTPα and RPTPβ; 2, VacA uptake; 3, VacA‐induced vacuolation in susceptible cells. In addition, oral administration of HBT with VacA to mice reduced VacA‐induced gastric damage at 48 hours. In vitro, VacA formed a complex with HBT. Conclusions. HBT may suppress the development of inflammation and ulceration caused by H. pylori VacA, suggesting that HBT may be useful as a new type of therapeutic agent for the prevention of gastric ulcer and inflammation caused by VacA.     

Effects of estradiol and progesterone on gastric mucosal response to early Helicobacter pylori infection in female gerbils

BACKGROUND: Gender differences have been shown regarding the changes in the inflammatory response, gastrin secretion, and gastric acidity during Helicobacter pylori infection. Aim: To investigate the role of estradiol and progesterone in the changes of the gastric mucosa induced by H. pylori during the early stage of infection in female gerbils. MATERIALS AND METHODS: Thirty-three adult ovariectomized female gerbils were infected with H. pylori (SS1); 7 days after infection they were treated with low and high doses of estradiol (50 and 250 microg/60 days pellet), progesterone (15 and 50 mg/60 days pellet) and vehicle. Non-ovariectomized infected gerbils were used as control. Gerbils were euthanized after 6 weeks of infection. Histologic evaluation, immunohistochemical detection of proliferation cell nuclear antigen (PCNA), gastrin, and apoptosis by terminal deoxynucleotide nick end labeling (TUNEL) assay were performed. Positive cells for PCNA, TUNEL, and gastrin were counted in 10 oriented glands per animal. Two-sided p = .05 was considered significant. RESULTS: Estradiol-treated groups showed more intense and extended acute and follicular gastritis compared to the vehicle group, whereas progesterone-treated groups presented less gastritis than the other groups. Proliferation and apoptosis indexes were significantly lower in the vehicle group when compared with those of the control; both indexes were increased in the high-dose estradiol and progesterone groups as compared with those of the vehicle. Grade I nonmetaplastic atrophy was observed in the vehicle and progesterone groups. The high-dose progesterone group showed a significant reduction in the number of gastrin cells. CONCLUSIONS: Estradiol and progesterone participate in the gastric mucosal response to early H. pylori infection in gerbils.     

Antibiotics resistance of Helicobacter pylori in children with upper gastrointestinal symptoms in Hangzhou,China

Background

The decreasing eradication rate of Helicobacter pylori is mainly because of the progressive increase in its resistance to antibiotics. Studies on antimicrobial susceptibility of H. pylori in children are limited. This study aimed to investigate the resistance rates and patterns of H. pylori strains isolated from children.

Materials and Methods

Gastric mucosa biopsy samples obtained from children who had undergone upper gastrointestinal endoscopy were cultured for H. pylori, and susceptibility to six antibiotics (clarithromycin, amoxicillin, gentamicin, furazolidone, metronidazole, and levofloxacin) was tested from 2012‐2014.

Results

A total of 545 H. pylori strains were isolated from 1390 children recruited. The total resistance rates of H. pylori to clarithromycin, metronidazole, and levofloxacin were 20.6%, 68.8%, and 9.0%, respectively. No resistance to amoxicillin, gentamicin, and furazolidone was detected. 56.1% strains were single resistance, 19.6% were resistant to more than one antibiotic, 16.7% for double resistance, and 2.9% for triple resistance in 413 strains against any antibiotic. And the H. pylori resistance rate increased significantly from 2012‐2014. There was no significant difference in the resistance rates to clarithromycin, metronidazole, and levofloxacin between different gender, age groups, and patients with peptic ulcer diseases or nonulcer diseases.

Conclusions

Antibiotic resistance was indicated in H. pylori strains isolated from children in Hangzhou, and it increased significantly during the 3 years. Our data strongly support current guidelines, which recommend antibiotic susceptibility tests prior to eradication therapy.     

Immune and proliferative cellular responses to Helicobacter pylori infection in the gastric mucosa of Mexican children

BACKGROUND: Helicobacter pylori infection occurs mostly during childhood, but few studies on this age group have addressed the innate immune and the proliferative response to this infection. Mexico has a high H. pylori prevalence in children, but a low risk of gastric cancer. The aim of this work was to study the cellular responses of the gastric mucosa to this infection in Mexican children. METHODS: Antral and corpus gastric biopsies were obtained from 44 H. pylori-infected children (mean age 12 +/- 3.2 years) and 44 uninfected children (mean age 10 +/- 3 years). Mucosal cellular responses were studied by immunohistochemistry, using anti-Ki67 antibodies for proliferation studies, antihuman tryptase for mast cells, and antihuman CD68 for macrophages. T and B lymphocytes were stained with a commercial integrated system. The intensity of cellular responses was estimated histologically using the software KS300. RESULTS: Epithelium proliferation and infiltration of macrophages and T and B lymphocytes were significantly higher in H. pylori-infected than in uninfected children. A balanced increase of CD4, CD8, and CD20 lymphocytes was observed in infected children. However, activated mast cells were decreased, and infiltration of neutrophil and mononuclear cells was low. Epithelial proliferation was associated with polymorphonuclear infiltration but not with infiltration of macrophages or lymphocytes. Inflammation and proliferation was higher in CagA (+)-infected children. CONCLUSIONS: Mexican children respond to H. pylori infection with a low inflammatory response, a balanced increase of T and B lymphocytes, and a high regenerative activity.     

Maintenance of Helicobacter pylori cultures in agar stabs

Background: Helicobacter pylori requires frequent passage at 37 °C with reduced oxygen tension to maintain viability, and recovery from frozen stocks can be unpredictable and slow. Agar stab cultures were assessed as a possible means of maintaining viability without the need to passage every 4–7 days. Materials and Methods: Agar stabs prepared from either Brucella or Brain Heart Infusion media were inoculated deeply with H. pylori strains or H. felis and grown under varying conditions for up to 13 weeks. Subcultures were prepared from these stabs at various intervals to test for viability. Results: Established cultures in agar stabs failed to survive at room temperature but did survive at 37 °C with 10% CO₂ for up to 56 days. H. felis remained viable for up to 28 days. No difference was observed between the two media formulations. Conclusion: H. pylori grown in agar stabs remains viable for prolonged periods of time without the need to subculture and may represent an improved method for storing H. pylori for infrequent use.     

Decreasing trend of Helicobacter pylori infection in children with gastrointestinal symptoms from Buenos Aires, Argentina

Background: Helicobacter pylori infection is declining in developed and developing countries. The aim of this study was to retrospectively evaluate over an 8‐year period the rate of H. pylori infection in children with gastrointestinal symptoms from Buenos Aires, Argentina. Materials and Methods: We reviewed the records of children referred from 2002 to 2009 to the gastroenterology unit of the Children Hospital “Superiora Sor Maria Ludovica” for evaluation of upper gastrointestinal signs and symptoms in which the ¹³C‐urea breath test was performed to diagnose H. pylori infection and a sociodemographic questionnaire was obtained. Results: Records of a total of 1030 children and adolescents with a mean age of 9.99 years were included in the analysis. We found an H. pylori prevalence of 41.2% (95% CI, 36.9–46.0%) for the triennium 2002–2004, dropping to 26.0% (95% CI, 20.7–31.8%) in the triennium 2007–2009. Conclusion: Our results showed a significant decrease in H. pylori infection rates from children referred for upper gastrointestinal symptoms evaluation from 2002 to 2009, following the H. pylori epidemiologic trend reported in other countries.     

Effects of alpha tocopherol and ascorbic acid on Helicobacter pylori colonization and the severity of gastric inflammation

Background and Aim: We aimed to evaluate the changes in histopathologic features, concentrations of vitamins C and E in gastric mucosa, and total antioxidant capacity of the body after ingestion of ascorbic acid and alpha tocopherol in patients with Helicobacter pylori. Material and Method: Patients with H. pylori‐positive nonulcer dyspepsia were included in this study. Tissue samples were taken from the lesser and greater curvature in both prepyloric antrum and corpus for histopathologic examination and measurement of vitamins C and E concentrations. Blood samples were obtained for measurement of the total antioxidant capacity of the body. The patients were given vitamin C 500 mg BID and vitamin E 200 IU BID for 4 weeks orally. At the end of the 4th week, the initial procedures were repeated. Histopathologic examination of the tissue samples were carried out by two pathologists. Results: The mean vitamins C and E concentrations in gastric mucosa at the 4th week were higher than those at the beginning (p = .000 and p = .006, respectively). Mean total antioxidant capacity of the body at the beginning and that at the 4th week were similar (p = .689). H. pylori intensity in the antrum at the beginning was higher than that at the 4th week for both pathologists (p = .007 and p = .039). Neutrophilic activity in the antrum at the beginning was higher than that at the 4th week for both pathologists (p = .000 and p = .025). Neutrophilic activity in the corpus at the beginning was higher than that at the 4th week for pathologist 1 (p = .033), and they were similar for pathologist 2 (p = .763). Conclusion: The findings that H. pylori intensity and neutrophilic activity decrease through increasing gastric ascorbic acid and alpha tocopherol concentrations suggest that supplementation with vitamins C and E increases the eradication rates via impairing the microenvironment created by the bacteria and facilitating the diffusion of antibiotics into gastric mucosa.     

ERK介导幽门螺杆菌HSP60感染胃上皮细胞的IL-8分泌

目的：探讨幽门螺杆菌热休克蛋白60（H．pylori—HSP60）感染胃上皮细胞后ERK与白介素-8（IL-8）分泌的关系。方法：利用ELISA技术,对活菌（IntactH．pylori）、死菌（Heat—killedH．pylori）及H．pylori—HSP60刺激胃上皮细胞KATOIII的IL_8蛋白分泌水平进行分析,观察IL-8随以上抗原浓度梯度的变化及ERK抑制剂PD98059对其分泌量的影响;利用Westernblot技术,观察KATOⅢ胞中磷酸化ERK随IntactH．pylori、Heat—killedH．pylori及H．pylori—HSP60刺激时间的变化状况。结果：IL-8的分泌随着IntactH．pylori、Heat—killedH．pylori及H．pylori—HSP60刺激浓度的升高而增高;H．pylori刺激KATOⅢ胞1h后ERK开始表达,其中IntactH．pylori在9h时表达达到高峰,Heat·killedH．pylori在24h时达到高峰,而H．pylori-HSP60刺激KATOⅢ胞6h后ERK开始表达,9h时达到高峰;PD98059抑制了H．pylori—HSP60诱导的IL-8的分泌。结论：ERK介导了H．pylori—HSP60感染的胃上皮细胞的IL-8的分泌。     

Impact of Helicobacter pylori on the development of vitamin B12 deficiency in the absence of gastric atrophy

Background. Cobalamin (vitamin B₁₂) deficiency is associated with Helicobacter pylori infection. This study examined how serum vitamin B₁₂ levels relate to gastric mucosa H. pylori density and histology, and to hematological findings in patients with minimal or no gastric atrophy. A second aim was to confirm that H. pylori eradication therapy increases serum B₁₂. Materials and Methods. Biopsies of the gastric mucosa from a population of dyspeptic patients were graded for level of chronic inflammation, neutrophil activity, atrophy, and H. pylori density. A total of 145 H. pylori‐infected patients with minimal or no atrophy were included in the study. Serum cobalamin level, hemoglobin level, and mean corpuscular volume were measured in the 145 patients before eradication therapy, and in 65 of the subjects after treatment. The hematologic findings before and after eradication therapy and correlations between serum vitamin B₁₂ level and histologic parameters, hematologic findings, and patient age were statistically analyzed. Results. There was no significant correlation between serum cobalamin level and patient age. Before treatment all the histopathological scores were inversely correlated with serum vitamin B₁₂ level (p < .01) on univariate analysis. Only H. pylori density was significantly associated with B₁₂ level on multivariate analysis. Serum hemoglobin and cobalamin levels were significantly increased after treatment, regardless of H. pylori eradication status (p < .001). Conclusion. The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with nonulcer dyspepsia and minimal or no gastric atrophy.     

Effects of aspirin on the development of Helicobacter pylori-induced gastric inflammation and heterotopic proliferative glands in Mongolian gerbils

Background: Helicobacter pylori infection is a major cause of gastritis and gastric carcinoma. Aspirin has anti‐inflammatory and antineoplastic activity. The aim of the present study was to determine the effects of aspirin on H. pylori‐induced gastritis and the development of heterotopic proliferative glands. Methods: H. pylori strain SS1 was inoculated into the stomachs of Mongolian gerbils. Two weeks after inoculation, the animals were fed with the powder diets containing 0 p.p.m. (n = 10), 150 p.p.m. (n = 10), or 500 p.p.m. (n = 10) aspirin. Mongolian gerbils were killed after 36 weeks of infection. Uninfected Mongolian gerbils (n = 10) were used as controls. Histologic changes, epithelial cell proliferation and apoptosis, and prostaglandin E₂ (PGE₂) levels of gastric tissue were determined. Results: H. pylori infection induced gastric inflammation. Administration of aspirin did not change H. pylori‐induced gastritis, but alleviated H. pylori‐induced hyperplasia and the development of heterotopic proliferative glands. Administration of aspirin accelerated H. pylori‐associated apoptosis but decreased H. pylori‐associated cell proliferation. In addition, the increased gastric PGE₂ levels due to H. pylori infection were suppressed by treatment with aspirin, especially at the dose of 500 p.p.m. Conclusions: Aspirin alleviates H. pylori‐induced hyperplasia and the development of heterotopic proliferative glands. Moreover, aspirin increases H. pylori‐induced apoptosis. We demonstrated the antineoplastic activities of aspirin in H. pylori‐related gastric carcinogenesis.     

Profiling and identification of eubacteria in the stomach of Mongolian gerbils with and without Helicobacter pylori infection

Background. Mongolian gerbils are frequently used to study Helicobacter pylori‐induced gastritis and its consequences. The presence of an indigenous bacterial flora with suppressive effect on H. pylori may cause difficulties with establishing this experimental model. Aim. The aim of the present study was to determine bacterial profiles in the stomach of Mongolian gerbils with and without (controls) H. pylori infection. Methods. Gastric tissue from H. pylori ATCC 43504 and CCUG 17874 infected and control animals were subjected to microbial culturing and histology. In addition, gastric mucosal samples from H. pylori ATCC 43504 infected and control animals were analyzed for bacterial profiling by temporal temperature gradient gel electrophoresis (TTGE), cloning and pyrosequencing of 16S rDNA variable V3 region derived PCR amplicons. Results. Oral administration of H. pylori ATCC 43504, but not CCUG 17874, induced colonization and gastric inflammation in the stomach of Mongolian gerbils. Temporal temperature gradient gel electrophoresis (TTGE) and partial 16S rDNA pyrosequencing revealed the presence of DNA representing a mixed bacterial flora in the stomach of both H. pylori ATCC 43504 infected and control animals. In both cases, lactobacilli appeared to be dominant. Conclusion. These findings suggest that indigenous bacteria, particularly lactobacilli, may have an impact on the colonization and growth of H. pylori strains in the stomach of Mongolian gerbils.     

The bactericidal and morphological effects of peroxynitrite on Helicobacter pylori

Peroxynitrite (ONOO-) is correlated with the pathogenesis of Helicobacter pylori-induced peptic ulcer diseases. We aimed to investigate the time- and concentration-dependent bactericidal and morphological effects of ONOO- on H. pylori. Authentic ONOO- was synthesized as quenched-flow method. A stock culture of H. pylori NCTC 11637 was exposed to different concentrations of ONOO- (0.1-40 micromol/L) or decomposed ONOO- or fresh medium. Samples were taken at 0, 15, 30, 60, and 120 minutes, for the evaluation of viable bacteria and bacterial morphology with gram strain and transmission electron microscopy. Decomposed ONOO- showed no bactericidal activity against H. pylori. ONOO- application caused a decrease in the number of viable bacteria within the first 15 minutes. The significant conversion of H. pylori from spiral form to coccoid form was determined with 10 micromol/L of ONOO-, and higher concentrations caused lysis of the cells. Separation of cell wall, bleb formation, vacuolization, decrease of secretory granules, and lysis of bacteria were the morphological effects of ONOO- on H. pylori. Because the morphology of the bacteria is one of the important factors in virulence; peroxynitrite-related morphological effects might have an impact in the progress of the H. pylori-induced peptic ulcer diseases.     

High rate of Helicobacter pylori reinfection in children and adolescents

AIMS: Primary Helicobacter pylori infection occurs predominantly in childhood. The aims of this study were to establish the rate of H. pylori reinfection after successful eradication in children and adolescents and to determine the risk factors associated with reinfection. PATIENTS AND METHODS: This retrospective study involved 45 children (20 girls, 25 boys) who met the following criteria: eradication of H. pylori confirmed at least 4 weeks after the completion of therapy, and the search for reinfection at least one year after control of eradication of H. pylori. Demographic data, socioeconomic status and living conditions were recorded. RESULTS: Forty-five children aged 1.2-17.6 years (median, 10.9 years) at the time of H. pylori treatment were reviewed 1 to 9 years after H. pylori eradication. Eight children (18%) had been reinfected (5.4% to 6% per patient-year). Six of 25 (24%) children older than 10 years at the time of diagnosis became reinfected. None of the studied risk factors was associated with reinfection. However, having a sibling younger than 5 years was found in four of seven (57%) reinfected children versus five of 24 (21%) nonreinfected children (p = .08). CONCLUSION: Children become reinfected more frequently than adults. Adolescents become reinfected, whereas acquisition of primary H. pylori infection occurs predominantly in early childhood. Close contact with young children, especially siblings, younger than 5 years could be a more important risk factor than the age of the patient at the time of treatment for the high rate of reinfection in childhood.     

Twice-a-day quadruple therapy for eradication of Helicobacter pylori in the elderly

BACKGROUND: Midday and evening twice-a-day quadruple therapy appears to be the most effective therapy for Helicobacter pylori infection in Northern Sardinia, a site where antibiotics resistance is common. Aim: The objective of our study was to estimate the efficacy, side-effects, and compliance of a quadruple therapy containing esomeprazole in a group of dyspeptic elderly patients. PATIENTS AND METHODS: Consecutive elderly patients positive for H. pylori infection and not previously treated for eradication were enrolled. Therapy consisted of esomeprazole 20 mg, tetracycline 500 mg, metronidazole 500 mg, and bismuth subcitrate tablets 240 mg, all twice-a-day with the midday and evening meals, for 10 days. Efficacy was evaluated using 13C-urea breath testing. Compliance was assessed after completing treatment and at follow up. Side effects were graded based on daily activities. RESULTS: Ninety-five dyspeptic patients (range 65-81 years), 52 men and 43 women, were enrolled. The intention-to-treat cure rate was 91% (81 of 89; 95% CI = 88-99%) and, 95% (81 of 85; 95% CI = 83-96%) per-protocol analysis. Compliance was excellent. Mild-moderate side effects occurred in 27 patients. CONCLUSIONS: Esomeprazole containing quadruple therapy was highly successful for initial eradication of H. pylori in elderly patients.