Interleukin-27 is abrogated in gastric cancer, but highly expressed in other Helicobacter pylori-associated gastroduodenal diseases.

BACKGROUND: IL-27 has dual roles in the immune response either stimulating Th1 or inhibiting Th17 cells. Because there is a particular link of IL-23/Th17 axis in the development of cancer and IL-27 has been considered a potential treatment for cancer, we evaluated the gastric and serum concentrations of IL-27 in two mutually exclusive Helicobacter pylori-associated diseases, gastric cancer (GC) and duodenal ulcer (DU). MATERIAL AND METHODS: We prospectively studied 110 H pylori-positive patients and 40 healthy blood donors. Serum and gastric concentrations of IL-27 and cytokines of the Th1/Th17 cells were assessed by ELISA. RESULTS: IL-27 was not detected in GC patients, but the cytokine concentration was very high in the patients with DU. IL-27 was also detected in the gastritis patients and in the H pylori-positive blood donors. IL27RA mRNA expression in peripheral blood mononuclear cells, evaluated by rt-PCR, was stimulated by H pylori strains. The cytokine concentration positively correlated with the Th1 and negatively with Th17 cell representative cytokine levels. Gastric IL-27 concentrations were positively correlated with increased degree of mononuclear and polymorphonuclear cells on the antral gastric mucosa of DU patients in consonance with the DU gastritis pattern. IL-12p70 and IFN-γ gastric concentrations were significantly higher in DU than in GC. Conversely, gastric concentrations of Th17 cell-associated cytokines (IL-1ß, IL-6, IL-17A, IL-23, and TGF-ß) were significantly higher in GC than in DU patients. CONCLUSION: Although H pylori infection is able to elicit IL-27 and IL-27Rα secretion, DU and GC have diametrically opposed cytokine patterns.

Cytokine profile of patients with chronic immune thrombocytopenia affects platelet count recovery after Helicobacter pylori eradication.

Helicobacter pylori eradication induces platelet recovery in a subgroup of patients with chronic immune thrombocytopenia (cITP), but the mechanisms involved are still not understood. We aimed to evaluate the effect of H. pylori eradication on platelet response and to identify the associated serum cytokine profile in 95 patients with cITP. Serum cytokine concentrations were determined by enzyme-linked immunosorbent assay prior to and 6 months after H. pylori eradication. Remission of cITP was observed in 17 (28·8%) of 59 patients in whom the bacterium was eradicated. Six months after treatment, a significant reduction in the concentrations of T-helper (Th) 1 and Th17 cells and an increase in T regulatory (Treg) and Th2-cell commitment cytokines were observed in patients who recovered, but not in those whose platelet count did not recover. Patients who had a platelet response to eradication of the bacteria had higher pre-treatment serum levels of γ-interferon (IFNG, IFN-γ), transforming growth factor-ß (TGFB1, TGF-ß) and interleukin 17 (IL17A, IL-17) than patients who did not respond, but only higher pre-treatment TGFB1 levels was independently associated with platelet response. In conclusion, amelioration of cITP after eradication of H. pylori was linked to a more efficient suppression of Th1 and Th17 response and a more pronounced Treg cell response.

First detected Helicobacter pylori infection in infancy modifies the association between diarrheal disease and childhood growth in Peru.

BACKGROUND: In endemic settings, Helicobacter pylori infection can occur shortly after birth and may be associated with a reduction in childhood growth. MATERIALS AND METHODS: This study investigated what factors promote earlier age of first H. pylori infection and evaluated the role of H. pylori infection in infancy (6-11 months) versus early childhood (12-23 months) on height. We included 183 children near birth from a peri-urban shanty town outside of Lima, Peru. Field-workers collected data on socioeconomic status (SES), daily diarrheal and breast-feeding history, antibiotic use, anthropometrics, and H. pylori status via carbon 13-labeled urea breath test up to 24 months after birth. We used a proportional hazards model to assess risk factors for earlier age at first detected infection and linear mixed-effects models to evaluate the association of first detected H. pylori infection during infancy on attained height. RESULTS: One hundred and forty (77%) were infected before 12 months of age. Lower SES was associated with earlier age at first detected H. pylori infection (low vs middle-to-high SES Hazard ratio (HR) 1.59, 95% CI 1.16, 2.19; p = .004), and greater exclusive breast-feeding was associated with reduced likelihood (HR 0.63, 95% CI 0.40, 0.98, p = .04). H. pylori infection in infancy was not independently associated with growth deficits (p = .58). However, children who had their first detected H. pylori infection in infancy (6-11 months) versus early childhood (12-23 months) and who had an average number of diarrhea episodes per year (3.4) were significantly shorter at 24 months (-0.37 cm, 95% CI, -0.60, -0.15 cm; p = .001). DISCUSSION: Lower SES was associated with a higher risk of first detected H. pylori infection during infancy, which in turn augmented the adverse association of diarrheal disease on linear growth.

Helicobacter pylori virulence genes detected by string PCR in children from an urban community in northeastern Brazil.

The accuracy of a nested PCR in gastric DNA obtained by a string test for the diagnosis of Helicobacter pylori infection in asymptomatic children was 94.0%. The cagA-positive toxigenic vacAs1m1 strains were the most prevalent strains, indicating that this population is colonized early by the strains associated with gastric cancer.

Single nucleotide polymorphisms of Helicobacter pylori dupA that lead to premature stop codons.

BACKGROUND: The detection of the putative disease-specific Helicobacter pylori marker duodenal ulcer promoting gene A (dupA) is currently based on PCR detection of jhp0917 and jhp0918 that form the gene. However, mutations that lead to premature stop codons that split off the dupA leading to truncated products cannot be evaluated by PCR. METHODS: We directly sequence the complete dupA of 75 dupA-positive strains of H. pylori isolated from patients with gastritis (n = 26), duodenal ulcer (n = 29), and gastric carcinoma (n = 20), to search for frame-shifting mutations that lead to stop codon. RESULTS: Thirty-four strains had single nucleotide mutations in dupA that lead to premature stop codon creating smaller products than the predicted 1839 bp product and, for this reason, were considered as dupA-negative. Intact dupA was more frequently observed in strains isolated from duodenal ulcer patients (65.5%) than in patients with gastritis only (46.2%) or with gastric carcinoma (50%). In logistic analysis, the presence of the intact dupA independently associated with duodenal ulcer (OR = 5.06; 95% CI = 1.22-20.96, p = .02). CONCLUSION: We propose the primer walking methodology as a simple technique to sequence the gene. When we considered as dupA-positive only those strains that carry dupA gene without premature stop codons, the gene was associated with duodenal ulcer and, therefore, can be used as a marker for this disease in our population.

Higher frequency of cagA EPIYA-C phosphorylation sites in H. pylori strains from first-degree relatives of gastric cancer patients.

BACKGROUND: To evaluate the prevalence of more virulent H. pylori genotypes in relatives of gastric cancer patients and in patients without family histories of gastric cancer. METHODS: We evaluated prospectively the prevalence of the infection by more virulent H. pylori strains in 60 relatives of gastric cancer patients comparing the results with those obtained from 49 patients without family histories of gastric cancer. H. pylori status was determined by the urease test, histology and presence of H. pylori ureA. The cytotoxin associated gene (cagA), the cagA-EPIYA and vacuolating cytotoxin gene (vacA) were typed by PCR and the cagA EPIYA typing was confirmed by sequencing. RESULTS: The gastric cancer relatives were significant and independently more frequently colonized by H. pylori strains with higher numbers of CagA-EPIYA-C segments (OR = 4.23, 95%CI = 1.53-11.69) and with the most virulent s1m1 vacA genotype (OR = 2.80, 95%CI = 1.04-7.51). Higher numbers of EPIYA-C segments were associated with increased gastric corpus inflammation, foveolar hyperplasia and atrophy. Infection by s1m1 vacA genotype was associated with increased antral and corpus gastritis. CONCLUSIONS: We demonstrated that relatives of gastric cancer patients are more frequently colonized by the most virulent H. pylori cagA and vacA genotypes, which may contribute to increase the risk of gastric cancer.

dupA polymorphisms and risk of Helicobacter pylori-associated diseases.

The dupA of Helicobacter pylori has been suggested as a virulence marker associated with the development of duodenal ulcer disease. However, the studies performed in different geographical areas have shown that there are variations in the prevalence of dupA and its association with H. pylori clinical outcomes. Our group did not observe associations between the presence of dupA and H. pylori clinical outcomes in Brazil. On the other hand, we observed 2 mutations in the sequence of dupA that lead to stop codons: a deletion of an adenine at position 1311 and an insertion of an adenine at position 1426 of the gene. Our aim was to evaluate associations of the presence of dupA with duodenal ulcer and gastric cancer, considering dupA-positive only those H. pylori strains that do not have the mutations in the gene sequence. We also evaluated the effect of infection with a strain carrying an intact dupA on the gastric mucosa histology and IL-8 gastric levels. Colonization with strains that had the intact dupA was negatively associated with gastric carcinoma (p=0.001, OR=0.32, 95% CI=0.16-0.66). The presence of dupA was also associated with an increased degree of antral mucosa inflammation (p=0.01) and with decreased corpus atrophy (p<0.01) as well as with increased gastric mucosa IL-8 levels (p=0.04). In conclusion, the infection with a H. pylori strain containing the dupA without the stop codon polymorphisms is associated with a lower risk of development of gastric carcinoma in Brazilian subjects.

Higher number of Helicobacter pylori CagA EPIYA C phosphorylation sites increases the risk of gastric cancer, but not duodenal ulcer.

BACKGROUND: Helicobacter pylori infection is one of the most common infections worldwide and is associated with gastric cancer and peptic ulcer. Bacterial virulence factors such as CagA have been shown to increase the risk of both diseases. Studies have suggested a causal role for CagA EPIYA polymorphisms in gastric carcinogenesis, and it has been shown to be geographically diverse. We studied associations between H. pylori CagA EPIYA patterns and gastric cancer and duodenal ulcer, in an ethnically admixed Western population from Brazil. CagA EPIYA was determined by PCR and confirmed by sequencing. A total of 436 patients were included, being 188 with gastric cancer, 112 with duodenal ulcer and 136 with gastritis. RESULTS: The number of EPIYA C segments was significantly associated with the increased risk of gastric carcinoma (OR=3.08, 95% CI=1.74 to 5.45, p<10-3) even after adjustment for age and gender. Higher number of EPIYA C segments was also associated with gastric atrophy (p=0.04) and intestinal metaplasia (p=0.007). Furthermore, patients infected by cagA strains possessing more than one EPIYA C segment showed decreased serum levels of pepsinogen I in comparison with those infected by strains containing one or less EPIYA C repeat. Otherwise, the number of EPIYA C segments did not associate with duodenal ulcer. CONCLUSIONS: Our results demonstrate that infection with H. pylori strains harbouring more than one CagA EPIYA C motif was clearly associated with gastric cancer, but not with duodenal ulcer.Higher number of EPIYA C segments was also associated with gastric precancerous lesions as demonstrated by histological gastric atrophic and metaplastic changes and decreased serum levels of pepsinogen I.

Low prevalence of H. pylori infection in HIV-positive patients in the northeast of Brazil.

BACKGROUND: This study conducted in Northeastern Brazil, evaluated the prevalence of H. pylori infection and the presence of gastritis in HIV-infected patients. METHODS: There were included 113 HIV-positive and 141 age-matched HIV-negative patients, who underwent upper gastrointestinal endoscopy for dyspeptic symptoms. H. pylori status was evaluated by urease test and histology. RESULTS: The prevalence of H. pylori infection was significantly lower (p < 0.001) in HIV-infected (37.2%) than in uninfected (75.2%) patients. There were no significant differences between H. pylori status and gender, age, HIV viral load, antiretroviral therapy and the use of antibiotics. A lower prevalence of H. pylori was observed among patients with T CD4 cell count below 200/mm3; however, it was not significant. Chronic active antral gastritis was observed in 87.6% of the HIV-infected patients and in 780.4% of the control group (p = 0.11). H. pylori infection was significantly associated with chronic active gastritis in the antrum in both groups, but it was not associated with corpus chronic active gastritis in the HIV-infected patients. CONCLUSION: We demonstrated that the prevalence of H. pylori was significantly lower in HIV-positive patients compared with HIV-negative ones. However, corpus gastritis was frequently observed in the HIV-positive patients, pointing to different mechanisms than H. pylori infection in the genesis of the lesion.

Increased Oxidative Stress in Gastric Cancer Patients and Their First-Degree Relatives: A Prospective Study from Northeastern Brazil.

BACKGROUND AND AIMS: First-degree relatives of gastric cancer patients are at increased risk of developing gastric cancer. Increased oxidative stress, including lipid peroxidation, has been associated with gastric carcinogenesis. Whether first-degree relatives of gastric cancer patients have increased oxidative stress remains unknown. We aimed to compare oxidative stress in patients with gastric cancer, their first-degree relatives, and dyspeptic controls. METHODS: A total of 155 patients undergoing upper endoscopy were prospectively enrolled, including 50 with gastric cancer, 49 first-degree relatives of gastric cancer patients, and 56 controls. Serum concentrations of malondialdehyde (MDA) and glutathione) and activities of superoxide dismutase (SOD) and catalase were measured. Multivariate analysis adjusting for sex, age, smoking status, and alcohol consumption was performed. RESULTS: Lipid peroxidation, as measured by concentration of MDA (nmol/mL), was higher (p = 0.04), and glutathione levels were lower (p < 0.001) in the gastric cancer group compared to controls. There was no difference in the catalase activity among the groups. There was no difference in glutathione and MDA concentration or catalase activity between the different stages of gastric cancer based on the TNM classification. Relatives of gastric cancer patients had higher glutathione concentration (µmol/mL) compared to gastric cancer patients (262.5 vs. 144.6; p = 0.018), while there was no difference in MDA concentration. Catalase and superoxide dismutase activity were lower in the gastric cancer group (3.82 vs. 0.91; p < 0.001 and 1.04 vs. 0.6; p < 0.001) compared to their first-degree relatives. Interestingly, MDA concentration in the first-degree relative group was higher than in the control group (7.9 vs. 5.1; p = 0.03). CONCLUSIONS: In this study, similarly to gastric cancer patients, their first-degree relatives were found to have increased oxidative stress compared to controls. Further studies are warranted to validate this observation and to better understand the role of oxidative stress as a possible biomarker in this population.

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 (13) C-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.

Helicobacter pylori transiently in the mouth may participate in the transmission of infection.

Helicobacter pylori infection is associated with peptic ulcer and gastric carcinoma. The oral cavity may be a reservoir for H. pylori; however, the results of studies on this subject are controversial. We employed single-step and nested polymerase chain reactions (PCR) to detect the presence of the vacA, ureA and 16S rDNA genes of H. pylori in the stomach, saliva and dental plaque of 30 subjects. The results were confirmed by sequencing. Nested 16S rDNA and ureA amplification was achieved in 80% of gastric, 30% of saliva and 20% of dental plaque specimens. Sequencing of 10, seven and four 16S rDNA products from stomach, saliva and dental plaque, respectively, showed > 99% identity with H. pylori. Sequencing of the other four oral cavity PCR products showed similarity with Campylobacter and Wolinella species. Additionally, the vacA genotype identified in the samples of different sites was the same within a given subject.H. pylori may be found in the oral cavity of patients with gastric infection, thus it could be a source of transmission. However, results obtained with detection methods based only on PCR should be interpreted with caution because other microorganisms that are phylogenetically very close to H. pylori are also present in the mouth.

Lack of association between Helicobacter pylori infection with dupA-positive strains and gastroduodenal diseases in Brazilian patients.

Duodenal ulcer-promoting gene (dupA) was recently described as a new putative Helicobacter pylori virulence marker associated with an increased risk for duodenal ulcer and reduced risk for gastric carcinoma in Japan and Korea. Since differences regarding the association among H. pylori markers and H. pylori-associated diseases have been demonstrated around the world, we evaluated the presence of the gene in 482 strains from Brazilian children (34 with duodenal ulcer and 97 with gastritis) and adults (126 with duodenal ulcer, 144 with gastritis and 81 with gastric carcinoma) by PCR using the described primers and an additional set of primers based on Brazilian strain sequences. The results were confirmed by sequencing. The presence of cagA was investigated by PCR and also included in the analysis. dupA was present in 445 (92.32%) and absent in 29 (6.02%) strains. All samples from children with and without duodenal ulcer were dupA-positive (p=1.0). No association was observed among the strains from adults with gastritis (92.36%), duodenal ulcer (87.30%, p=0.30) and gastric carcinoma (87.65%, p=0.31). Conversely, cagA-positve status remained independently associated with duodenal ulcer (children: odds ratios (OR)=5.58, 95% confidence intervals (CI)=1.67-18.50; adults: OR=3.33, 95% CI=2.14-5.19) and gastric carcinoma (OR=6.58, 95% CI=3.51-12.30) in multivariate analyses. The presence of dupA was significantly higher in strains from children than in those from adults (p=0.01). In conclusion, dupA is highly frequent and not associated with H. pylori-associated diseases in both Brazilian adults and children, which points to regional differences in the distribution of the gene.

Association between pre-sarcopenia, sarcopenia, and bone mineral density in patients with chronic hepatitis C.

BACKGROUND: Preserved skeletal muscle is essential for the maintenance of healthy bone. Loss of bone mineral density (BMD) and muscle strength, considered a predictor of BMD, have been demonstrated in patients with cirrhosis, but they are poorly studied in chronic hepatitis C (CHC) without cirrhosis. Thus, we aimed to evaluate the prevalence of low BMD and its association with body composition, muscle strength, and nutritional status in CHC. METHODS: One hundred and four subjects [mean age, 50.5 ± 11.3 years; 75.0% males; 67.3% non-cirrhotic; and 32.7% with compensated cirrhosis] with CHC, prospectively, underwent scanning of the lean tissue, appendicular skeletal muscle mass (ASM), fat mass, lumbar spine, hip, femoral neck, and whole-body BMD by dual-energy X-ray absorptiometry. Muscle strength was assessed by dynamometry. Sarcopenia was defined by the presence of both low, ASM/height2 (ASMI) and low muscle strength according to the European Working Group on Sarcopenia in Older People criteria. The cut-off points for low ASMI and low muscle strength, for women and men, were < 5.45 and < 7.26 kg/m2 and < 20 and < 30 kg, respectively. According to the adopted World Health Organization criteria in men aged > 50 years, the T-score of osteopenia is between -1.0 and -2.49 standard deviation (SD) below the young average value and of osteoporosis is ≥-2.5 SD below the young normal mean for men, and the Z-score of low bone mass is ≤-2.0 SD below the expected range in men aged < 50 years and women in the menacme. Nutritional status evaluation was based on the Controlling Nutritional Status score. RESULTS: Low BMD, low muscle strength, pre-sarcopenia, sarcopenia, and sarcopenic obesity were observed in 34.6% (36/104), 27.9% (29/104), 14.4% (15/104), 8.7% (9/104), and 3.8% (4/104) of the patients, respectively. ASMI was an independent predictor of BMD (P < 0.001). Sarcopenia was independently associated with bone mineral content (P = 0.02) and malnutrition (P = 0.01). In 88.9% of the sarcopenic patients and in all with sarcopenic obesity, BMI was normal. The mid-arm muscle circumference was positively correlated with ASMI (r = 0.88; P < 0.001). CONCLUSIONS: This is the first study to demonstrate that ASM is an independent predictor of BMD in CHC. Mid-arm muscle circumference coupled with handgrip strength testing should be incorporated into routine clinical practice to detect low muscle mass, which may be underdiagnosed when only BMI is used. These findings may influence clinical decision-making and contribute to the development of effective strategies to screen the musculoskeletal abnormalities in CHC patients, independently of the stage of the liver disease.

Cytokine expression profile over time in severely burned pediatric patients.

A severe burn leads to hypermetabolism and catabolism resulting in compromised function and structure of essential organs. The massive release of cytokines is implicated in this hypermetabolic response. The aim of the present study was to compare cytokine expression profiles from severely burned children without signs of infections or inhalation injury (n = 19) to the cytokine profiles from normal, noninfected, nonburned children (n = 14). The Bio-Plex suspension array system was used to measure the concentration of 17 cytokines. The expression of proinflammatory and anti-inflammatory cytokines was maximal during the first week after thermal injury. Significant increases were measured for 15 mediators during the first week after thermal injury: interleukin (IL) 1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12 p70, IL-13, IL-17, interferon gamma, monocyte chemoattractant protein 1, macrophage inflammatory protein 1beta, and granulocyte colony-stimulating factor (P < 0.05). Granulocyte-macrophage colony-stimulating factor was significantly increased during the second week after burn (P < 0.05). Within 5 weeks, the serum concentrations of most cytokines decreased, approaching normal levels. When compared with the cytokine levels measured in normal children, a total of 16 cytokines were significantly altered (P < 0.05). After severe burn, a specific cytokine expression profile is observed in patients without complications such as inhalation injury or sepsis. The cytokine concentrations decrease during 5 weeks after burn but remain elevated over nonburned values. Furthermore, the elevation in most serum cytokine levels during the first week after burn may indicate a potential window of opportunity for therapeutic intervention.

History of breastfeeding and Helicobacter pylori infection in children: results of a community-based study from northeastern Brazil.

The aim of this study was to evaluate the role of breastfeeding and the infection status of the mother in the acquisition of Helicobacter pylori infection in a poor urban community in northeastern Brazil. Helicobacter pylori status was evaluated by 13C-urea breath test in individuals under the age of 14 years and by ELISA in the mothers. The prevalence of H. pylori infection was 55.8% (197/353) in the children and it increased with age (P<0.0001). Of the children in whom breastfeeding status was known, 93.2% (316/339) were breastfed. The H. pylori prevalence did not differ between breastfed and never breastfed children (55% vs. 52%) even when children were breastfed for >6 months. The prevalence of infection was much higher in children whose mothers were H. pylori infected than in children whose mothers were not infected, resulting in a crude odds ratio (OR) of 3.11 (95% CI 1.57-6.19) and 2.40 after adjustment for potential confounders (95% CI 1.12-5.15). This study suggests that breastfeeding does not protect against acquisition of H. pylori in northeastern Brazil; conversely, an infected mother may have an important role in transmission of the disease to the child.

Gastroduodenal peptic ulcer and Helicobacter pylori infection in children and adolescents.

OBJECTIVES: To show important aspects of gastroduodenal peptic ulcer and of Helicobacter pylori infection in children and adolescents. SOURCES: Technical textbooks and MEDLINE and LILACS databases including publications between 1966 and 2006. SUMMARY OF THE FINDINGS: The etiology of peptic ulcer in children and adolescents may be primary, associated with H. pylori infection, or secondary, in which etiopathogenic mechanisms rely upon the underlying disease. The infection is acquired predominantly in childhood, with prevalence rates between 56.8 and 83.1% in children who live in the poorest Brazilian regions, amounting to nearly 10% in children aged less than 10 years in industrialized countries. The infection can be diagnosed by invasive methods, which investigate the presence of the bacterium, or of DNA, RNA or bacterial products in biopsy fragments of the gastric mucosa obtained at endoscopic examination; it can also be diagnosed through noninvasive methods, which include the detection of anti-H. pylori antibodies in serum, urine or saliva samples, detection of bacterial antigens in stool samples, and the carbon 13-labeled urea breath test. However, upper gastrointestinal endoscopy is the method of choice for the diagnosis of peptic ulcer, as it allows collecting fragments from the gastric mucosa during the procedure for the diagnosis of infection and for histopathological analysis. CONCLUSION: H. pylori infection is the major cause of peptic ulcer among children. Eradication of the bacterium with antimicrobial therapy results in the cure of the disease, and is therefore indicated for all children with H. pylori infection with an active, recurrent, healed, or complicated peptic ulcer.

Helicobacter pylori infection in adults from a poor urban community in northeastern Brazil: demographic, lifestyle and environmental factors.

We investigated the prevalence and the risk factors for infection with Helicobacter pylori in a randomly-selected population of adults from a low-income community in Northeastern Brazil. Helicobacter pylori infection was determined by ELISA. Risk factors were assessed using a structured interview. Two hundred and four individuals were included in the study, including 49 males and 155 females, ranging from 18 to 80 years old. Overall, 165 of 204 participants (80%) were H. pylori positive, without significant gender differences (p= 0.49). The infection rate was of 84.7% in subjects 18 to 30 years of age, increasing to 92% in subjects 46-60 years old. Above 60 years old, the prevalence decreased slightly. As a whole, the prevalence of infection did not increase significantly (p=0.147) with age. There were no significant differences in the prevalence of H. pylori infection, when patients were classified by age, smoking habit, educational level, alcohol consumption, the number of persons per room, the number of children per household, the number of adults per household, cup-sharing, household pets, toilet location, number of persons per bed and medical history of antibiotic and raw vegetable ingestion. In conclusion, no risk factors associated with infection was found in these adults, suggesting that the infection, even in a poor population, may be acquired predominantly during childhood; the relatively high prevalence that we observed may be more due to a cohort effect than to acquisition of infection during adulthood.

Prevalence of Helicobacter pylori infection in Fortaleza, Northeastern Brazil.

The prevalence of Helicobacter pylori infection was assessed in a randomly selected sample of individuals from low-income community in Fortaleza, Northeastern Brazil. Overall, 384 out of 610 participants (62.9%) were H. pylori positive. A 47.5% infection rate was found in subjects aged six months to 10 years old, increased to 73.3% in subjects aged 11-20 years and then continued to increase with age reaching up to 87% in those over 60 years old. After this age group, the prevalence decreased slightly. The prevalence of infection increased significantly with age (p<0.0001).

DNA damage in patients infected by Helicobacter pylori.

Helicobacter pylori (H. pylori) is considered to predispose carriers to gastric cancer but its role on gastric carcinogenesis is still unknown. The aim of this study was to investigate DNA damage by the comet assay in gastric epithelial cells from antrum and corpus in H. pylori-infected patients with gastritis of different degrees. H. pylori status, gastric histology, and DNA damage were studied in 62 H. pylori-infected and 18 non-infected patients, all of them non-smokers, non-alcoholics, and non-drug users. DNA damage was significantly higher in H. pylori-infected patients presenting gastritis than in non-infected patients with normal mucosa. A direct correlation between the levels of DNA damage and the intensity of gastritis was observed in H. pylori-infected patients. Association between DNA damage and age was also found. The levels of DNA damage were significantly higher in patients older than 50 years than in younger patients with the same degree of gastritis. Our results indicate that H. pylori infection is associated with DNA damage in gastric epithelial cells, which could be a biomarker of risk for gastric cancer in humans.